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Micronase (Glyburide)

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Generic Micronase is used for treating type 2 diabetes. It is used along with diet and exercise. It may be used alone or with other antidiabetic medicines.

Other names for this medication:

Similar Products:
Glucophage, Actos, Glucotrol, Avandia


Also known as:  Glyburide.


Generic Micronase is used for treating type 2 diabetes. It is used along with diet and exercise. It may be used alone or with other antidiabetic medicines.

Generic Micronase is a sulfonylurea antidiabetic medicine. It works by causing the pancreas to release insulin, which helps to lower blood sugar.

Brand name of Generic Micronase is Micronase.


Take Generic Micronase by mouth with food.

If you are taking 1 dose daily, take Generic Micronase with breakfast or the first main meal of the day unless your doctor tells you otherwise.

High amounts of dietary fiber may decrease Generic Micronase 's effectiveness, resulting in high blood sugar.

Generic Micronase works best if it is taken at the same time each day.

Continue to take Generic Micronase even if you feel well.

If you want to achieve most effective results do not stop taking Generic Micronase suddenly.


If you overdose Generic Micronase and you don't feel good you should visit your doctor or health care provider immediately.


Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Throw away any unused medicine after the expiration date. Keep out of reach of children.

Side effects

The most common side effects associated with Micronase are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Generic Micronase if you are allergic to Generic Micronase components.

Do not take Generic Micronase if you're pregnant or you plan to have a baby, or you are a nursing mother. Generic Micronase can ham your baby.

Do not take Generic Micronase if you have certain severe problems associated with diabetes (eg, diabetic ketoacidosis, diabetic coma).

Do not take Generic Micronase if you have moderate to severe burns or very high blood acid levels (acidosis) you are taking bosentan.

Do not take Generic Micronase if you are taking bosentan.

Be careful with Generic Micronase if you are taking any prescription or nonprescription medicine, herbal preparation, or dietary supplement.

Be careful with Generic Micronase if you have allergies to medicines, foods, or other substances.

Be careful with Generic Micronase if you have had a severe allergic reaction (eg, a severe rash, hives, itching, breathing difficulties, dizziness) to any other sulfonamide medicine, such as acetazolamide, celecoxib, certain diuretics (eg, hydrochlorothiazide), glipizide, probenecid, sulfamethoxazole, valdecoxib, or zonisamide.

Be careful with Generic Micronase if you have a history of liver, kidney, thyroid, or heart problems.

Be careful with Generic Micronase if you have stomach or bowel problems (eg, stomach or bowel blockage, stomach paralysis), drink alcohol, or have had poor nutrition.

Be careful with Generic Micronase if you have type 1 diabetes, very poor health, a high fever, a severe infection, severe diarrhea, or high blood acid levels, or have had a severe injury.

Be careful with Generic Micronase if you have a history of certain hormonal problems (eg, adrenal or pituitary problems, syndrome of inappropriate secretion of antidiuretic hormone [SIADH]), low blood sodium levels, anemia, or glucose-6-phosphate dehydrogenase (G6PD) deficiency.

Be careful with Generic Micronase if you will be having surgery.

Be careful with Generic Micronase if you are taking bosentan because liver problems may occur; the effectiveness of both medicines may be decreased; beta-blockers (eg, propranolol) because the risk of low blood sugar may be increased; they may also hide certain signs of low blood sugar and make it more difficult to notice; angiotensin-converting enzyme (ACE) inhibitors (eg, enalapril), anticoagulants (eg, warfarin), azole antifungals (eg, miconazole, ketoconazole), chloramphenicol, clarithromycin, clofibrate, fenfluramine, insulin, monoamine oxidase inhibitors (MAOIs) (eg, phenelzine), nonsteroidal anti-inflammatory drugs (NSAIDs) (eg, ibuprofen), phenylbutazone, probenecid, quinolone antibiotics (eg, ciprofloxacin), salicylates (eg, aspirin), or sulfonamides (eg, sulfamethoxazole) because the risk of low blood sugar may be increased; calcium channel blockers (eg, diltiazem), corticosteroids (eg, prednisone), decongestants (eg, pseudoephedrine), diazoxide, diuretics (eg, furosemide, hydrochlorothiazide), estrogens, hormonal contraceptives (eg, birth control pills), isoniazid, niacin, phenothiazines (eg, promethazine), phenytoin, rifamycins (eg, rifampin), sympathomimetics (eg, albuterol, epinephrine, terbutaline), or thyroid supplements (eg, levothyroxine) because they may decrease Generic Micronase 's effectiveness, resulting in high blood sugar; gemfibrozil because blood sugar may be increased or decreased; cyclosporine because the risk of its side effects may be increased by Generic Micronase.

Avoid alcohol.

Do not stop taking Generic Micronase suddenly.

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1 This study examined the contribution of cytochrome P450 metabolites of arachidonic acid in mediating ischaemia/reperfusion (I/R)-induced cardiac dysfunction in normal and diabetic rats. 2 We first compared the metabolism of arachidonic acid in microsomes prepared from the hearts of control rats and rats treated with streptozotocin (55 mg kg(-1)) to induce diabetes. The production of dihydroxyeicosatrienoic acids and epoxyeicosatrienoic acids (EETs) were similar in microsomes prepared from the hearts of control and diabetic rats, but the production of 20-hydroxyeicosatetraenoic acid (20-HETE) was two-fold higher in diabetic hearts than in control animals. 3 We then compared the change in left ventricular pressure (P(max)), left ventricular end-diastolic pressure, coronary flow and coronary vascular resistance in isolated perfused hearts obtained from control and diabetic animals after 40 min of global ischaemia (I) followed by 30 min of reperfusion (R). The decline in cardiac function was three- to five-fold greater in the hearts obtained from diabetic vs. control animals. 4 Pretreatment of the hearts with N-hydroxy-N'-(4-butyl-2-methyl-phenyl)-formamidine (HET0016, 1 microm), a selective inhibitor of the synthesis of 20-HETE, for 30 min before I/R resulted in significant improvement in the recovery of cardiac function in the hearts obtained from diabetic but not in control rats. Perfusion with an inhibitor of soluble epoxide hydrolase, 1-cyclohexyl-3-dodecyl urea (CDU), before I/R improved the recovery of cardiac function in hearts obtained from both control and diabetic animals. Perfusion with both HET0016 and CDU resulted in significantly better recovery of cardiac function of diabetic hearts following I/R than that seen using either drug alone. Pretreatment of the hearts with glibenclamide (1 microm), an inhibitor of ATP-sensitive potassium channels, attenuated the cardioprotective effects of both CDU and HET0016. 5 This is the first study to suggest that acute blockade of the formation of 20-HETE and/or reduced inactivation of EETs could be an important strategy to reduce cardiac dysfunction following I/R events in diabetes.

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Bowel distention after colonoscopy has been considered as a cause of blood flow disturbance. Carbon dioxide (CO2), with its higher absorbability and vasodilating effect, may reduce parietal blood flow disturbance of distended colon when used for intraluminal insufflation instead of air. The purpose of this study was to assess parietal blood flow of the colon distended with intraluminal air/CO2 insufflation.

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Diabetes diagnosis was made by three separate fasting blood glucose values of 16.2, 18.1, and 29.9 mM, and HbA1C of 10.1% (normal 4.2-5.9). The patient became euglycemic 5 mo after diagnosis while on no treatment. An oral glucose tolerance test was then normal, and C-peptide stimulation showed supra-normal response.

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An open-label, parallel-group, randomized, multicenter trial was conducted to compare efficacy and safety of repaglinide versus nateglinide, when used in a combination regimen with metformin for treatment of type 2 diabetes.

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The present study was carried out to look at the influence of the K+ channel opener cromakalim, compared with suramin and prazosin, on the contractile response evoked by single-pulse field stimulation and exogenous agonists in epididymal and prostatic portions of rat vas deferens. In the epididymal portion suramin abolished the first phase of the response to single shock, prazosin deeply affected the second phase and a combination of both antagonists almost completely abolished both phases. Cromakalim was able to inhibit in a concentration-dependent manner the first purinergic phase (pD2 = 5.90 +/- 0.11), leaving practically unaffected the second, adrenergic phase. This inhibitory effect of cromakalim on the electrically evoked response was counteracted by glibenclamide. Cromakalim and prazosin, but not suramin, affected the response to exogenous noradrenaline. Suramin but not cromakalim was able to antagonize responses to alpha, beta-methylene-ATP. In the prostatic portion because of a less clear discrimination between adrenergic and purinergic phases of the electrically evoked response, the picture was less clear although the trend was identical. Cromakalim was not able to antagonize the response to ATP. It is concluded that in rat vas deferens cromakalim inhibits purinergic transmission by acting prejunctionally.

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The purpose of the study was the comparison of the effect of the oral therapy of non-insulin-dependent diabetes mellitus (NIDDM) with either a sulphonylurea or biguanide derivative on plasma amylin level. In 10 healthy individuals the fasting plasma amylin level was 1.56 +/- 0.27 pmol/l (mean +/- SEM) and 6 min after i.v. injection of 1 mg glucagon a fourfold increase was observed. In 10 patients with NIDDM receiving glibenclamide (CAS 10238-21-8) the fasting plasma amylin level was twofold higher than in healthy control (2.72 +/- 0.38 pmol/l; p < 0.025) but following glucagon administration it increased only twofold. In 15 patients treated with metformin (CAS 657-24-9) the fasting plasma amylin level was similar to that in healthy individuals (1.64 +/- 0.25 pmol/l), but after glucagon stimulation the increment of plasma amylin was minimal and the relevant mean value was significantly lower when compared with those in healthy individuals and with NIDDM patients treated with glibenclamide. In 10 untreated obese patients with newly diagnosed NIDDM the administration of glibenclamide (14 days) resulted in the increase of basal (2.47 +/- 0.23 and 3.16 +/- 0.29 pmol/l; p < 0.1), and glucagon stimulated (3.34 +/- 0.39 and 4.56 +/- 0.38; p < 0.05) plasma amylin concentrations, whereas other 10 patients receiving metformin showed a decrease in fasting plasma level of this peptide before (2.64 +/- 0.59 and 1.28 +/- 0.38 pmol/l; p < 0.1), and after glucagon injection (5.02 +/- 0.55 and 2.83 +/- 0.65 pmol/l; p < 0.02). With the respect to the trophic effect of amyloid deposits in the pancreatic islets and to a hypothetic effect of amylin increasing insulin resistance, the present results emphasize the particular usefulness of metformin in the pharmacological treatment of NIDDM. All contraindications and side effects of metformin should be taken into account before drug administration.

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We demonstrate that glibenclamide and glimepiride modulate FXR activation in a reporter-gene assay and induce FXR target genes in HepG2 cells. Within the docking experiments and molecular dynamics simulation, we found glibenclamide interacting with the ligand-binding domain of FXR and with helix 12.

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The authors examined the role of adenosine triphosphate-sensitive potassium (K(ATP)) channels, adenosine A1 receptor, and alpha and beta adrenoceptors in desflurane-induced preconditioning in human myocardium, in vitro.

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The cardiac sarcolemmal ATP-sensitive potassium channel (K(ATP)) consists of a Kir6.2 pore and an SUR2 regulatory subunit, which is an ATP-binding cassette (ABC) transporter. K(ATP) channels have been proposed to play protective roles during ischemic preconditioning. An SUR2 mutant mouse was previously generated by disrupting the first nucleotide-binding domain (NBD1), where a glibenclamide action site was located. In the mutant ventricular myocytes, a non-conventional glibenclamide-insensitive (10 microM), ATP-sensitive current (I(KATPn)) was detected in 33% of single-channel recordings with an average amplitude of 12.3+/-5.4 pA per patch, an IC(50) to ATP inhibition at 10 microM and a mean burst duration at 20.6+/-1.8 ms. Newly designed SUR2 isoform- or variant-specific antibodies identified novel SUR2 short forms in the sizes of 28 and 68 kDa in addition to a 150-kDa long form in the sarcolemmal membrane of wild-type (WT) heart. We hypothesized that channels constituted by these short forms that lack NBD1 confer I(KATPn). The absence of the long form in the mutant corresponded to loss of the conventional glibenclamide-sensitive K(ATP) currents (I(KATP)) in isolated cardiomyocytes and vascular smooth muscle cells but the SUR2 short forms remained intact. Nested exonic RT-PCR in the mutant indicated that the short forms lacked NBD1 but contained NBD2. The SUR2 short forms co-immunoprecipitated with Kir6.1 or Kir6.2 suggesting that the short forms may function as hemi-transporters reported in other eukaryotic ABC transporter subgroups. Our results indicate that different K(ATP) compositions may co-exist in cardiac sarcolemmal membrane.

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hCG may contribute to the reduction in arterial tone seen early in human pregnancy. Its vascular effects are in part mediated by the activation of adenosine 5'-triphosphate-sensitive potassium channels, suggesting a protein kinase A dependent signaling pathway.

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Under the normoxia condition, the values of the third pulmonary artery rings tension were relatively stable, but under the hypoxia hypercapnia condition, we observed a biphasic pulmonary artery contractile response compared with N group (P < 0.05, P < 0.01). When the third pulmonary artery rings incubated by Gly, it's phase II persistent vasoconstriction was enhanced compared with the H group (P < 0.05, P < 0.01), and the phase I vasoconstriction was also heightened. Moreover, under the hypoxia hypercapnia condition, U0126 could significantly relieve the phase II persistent vasoconstriction compared with HD group (P < 0.05, P < 0.01) induced by Gly, but the phase I acute vasoconstriction and the phase I vasodilation had no changes (P > 0.05).

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The role of ATP-sensitive K+ channels (KATP) in ischemia and reperfusion (I/R) was studied in isolated rat lungs. I/R produced a sixfold increase in endothelial permeability as measured by the capillary filtration coefficient. Cromakalim (10 microM) given at 46 min after reperfusion reversed the filtration coefficient increase. This effect was not blocked by either a protein kinase A inhibitor (adenosine-3',5'-cyclic monophosphothioate; 100 microM) or an adenosine antagonist [8-(p-sulfophenyl)-theophylline; 20 microM]. Cromakalim given before ischemia or at the beginning of reperfusion protected the endothelial barrier from injury. Glibenclamide (500 microM) given before the ischemic period, at the beginning of reperfusion, or 46 min after reperfusion did not alter the changes in microvascular permeability produced by I/R. Glibenclamide blocked the ability of cromakalim to reverse endothelial damage but not the ability of either isoproterenol (10 microM) or an adenosine A2-receptor agonist, CGS-21680 (300 nM). We conclude that opening of KATP channels does not produce endothelial injury in I/R. The activation of KATP channels can both protect against and reverse the endothelial damage associated with I/R. This novel mechanism(s) is independent from known pathways that employ cAMP-protein kinase system and adenosine.

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Glibenclamide, a hypoglycemic sulfonylurea, has shown antiarrhythmic effects in acutely ischemic myocardium. The aim of the present study was to evaluate the effectiveness of the drug in preventing ventricular fibrillation in diabetic patients with acute myocardial infarction.

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Inside-out patches were exposed to zero, or low, [ATP] to activate KATP channels. Glibenclamide did not affect single channel conductance, but reversibly reduced channel open probability from either side of the membrane. Internal (cytoplasmic) glibenclamide inhibited with half-maximal inhibitory [glibenclamide] = 6 microM, Hill coefficient = 0.35. Complete channel inhibition was not observed, even at 300 microM [glibenclamide]. The response to step increases of internal [glibenclamide] could be resolved into two phases of channel inhibition (t1/2,fast < 1 sec, t1/2, slow = 10.5 +/- 0.9 sec, n = 8). Step decrease of [glibenclamide] caused a single resolvable phase of reactivation (t1/2 = 20.4 +/- 0.7 sec, n = 16). Channel inhibition by internal glibenclamide could be relieved by ADP, but only in the presence of Mg2+.

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Recently, gabapentin-lactam (GBP-L) was shown to be neuroprotective in vivo. It has been suggested that GBP-L may act by opening mitochondrial ATP-sensitive potassium (K(ATP)) channels. We tested this hypothesis by quantifying the effect of GBP-L on the survival of purified retinal ganglion cells (RGCs).

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Several studies have suggested that glibenclamide may be used safely and effectively in women with gestational diabetes mellitus (GDM). The aim of our study was to assess effectiveness and safety of glibenclamide for GDM in UK clinical practice.

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The localization of a putative ATP-regulated K+ channel in normal rat and neurological mutant mice was studied by light microscopic quantitative autoradiography using a tritiated glibenclamide, an antidiabetic sulfonylurea. Glibenclamide binding sites presented a heterogeneous distribution in the rat central nervous system. Their density was particularly important in substantia nigra reticulata, septohippocampal nucleus, globus pallidus, neocortex, molecular layer of cerebellum, CA3 field and dentate gyrus of hippocampus. Conversely hypothalamic areas, medulla oblongata and spinal cord contained only low amounts of glibenclamide receptors. The ontogenesis of sulfonylurea binding sites was a postnatal phenomenon and seemed to correlate with the maturation of neuronal connectivity. In the cerebellum of neurological mutant mice, the autoradiographic patterns were different to that of wild-type cerebellum. In particular, in the molecular layer of weaver cerebellum, a decrease of 82% of binding site density suggested a presynaptic position of glibenclamide receptors in parallel fibers.

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Sexual enhancement medication presents a large market for counterfeit versions. We report here a case of hypoglycemia caused by an illicit sexual enhancement medication containing an extremely large amount of the sulfonylurea drug glibenclamide together with a moderate amount sildenafil citrate.

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Type 2 diabetes mellitus is associated with abnormal MBF response to CPT, which can be significantly improved by euglycaemic control with glyburide and metformin. The close association between the decrease in plasma glucose concentration and the improvement in coronary vasomotor function in response to CPT suggests a direct adverse effect of raised plasma glucose concentration on diabetes-related coronary vascular disease.

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1. We studied the relation of nitric oxide-mediated relaxation of smooth muscle to changes in membrane potential of cells in the proximal colon of rats. 2. The resting membrane potential and electrical field stimulation (EFS)-induced junction potentials were recorded from the circular and longitudinal muscle cells. 3. Localized distension with a small balloon caused relaxation of the circular muscle on the anal side of the distended region (descending relaxation). Relaxation of the longitudinal muscle was also induced by EFS. 4. Inhibitory junction potentials ( were recorded from all circular muscle cells tested, but rarely from the longitudinal muscle cells. 5. The were recorded only in the presence of atropine but relaxations of both muscles were induced even in the absence of atropine. 6. Apamin (100 nM) completely abolished the recorded in both circular and longitudinal muscle cells, but had no significant effect on the relaxations of either. 7. In contrast to apamin, Ng nitro-L-arginine (10 microM) inhibited the relaxations of both muscles, but did not affect the 8. Exogenously added nitric oxide (0.1-10 microM) induced relaxations of both muscles concentration-dependently, but did not affect the membrane potentials at these concentrations. 9. These data strongly suggest that nitric oxide-mediated relaxation of rat proximal colon is not associated with the of the cell membrane.

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In anesthetized rats, we used a cranial window to examine effects of topical norepinephrine on diameter of the basilar artery in vivo. Topical application of norepinephrine increased the diameter of the basilar artery. NG-nitro-L-arginine methyl ester, an inhibitor of nitric oxide synthase, inhibited vasodilatation to acetylcholine but did not attenuate dilator responses to norepinephrine. Indomethacin also did not attenuate vasodilatation in response to norepinephrine. Dilatation of the basilar artery to norepinephrine was inhibited by propranolol and the beta 1-antagonist atenolol but not by the beta 2-antagonist butoxamine. Thus dilatation of the basilar artery in response to norepinephrine is produced by activation of beta 1-receptors and is not mediated by endothelium-derived relaxing factor or prostanoids. Glibenclamide, a selective inhibitor of ATP-sensitive K+ channels, partially inhibited vasodilatation in response to norepinephrine. Forskolin, a direct activator of adenylate cyclase, also increased the diameter of the basilar artery, and glibenclamide attenuated the dilatation. Thus dilatation of rat basilar artery in response to norepinephrine is mediated, in part, by activation of ATP-sensitive K+ channels, and activation of these K+ channels may be achieved by an adenosine 3',5'-cyclic monophosphate-dependent mechanism.

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Cystic fibrosis (CF) is caused by defects in the CF transmembrane conductance regulator (CFTR) that functions as a chloride channel in epithelial cells. The most common cause of CF is the abnormal trafficking of CFTR mutants. Therefore, understanding the cellular machineries that transit CFTR from the endoplasmic reticulum to the plasma membrane (PM) is important. The coat protein complex I (COPI) has been implicated in the anterograde and retrograde transport of proteins and lipids between the endoplasmic reticulum and the Golgi. Here, we investigated the role of COPI in CFTR trafficking. Blocking COPI recruitment to membranes by expressing an inactive form of the GBF1 guanine nucleotide exchange factor for ADP-ribosylation factor inhibits CFTR trafficking to the PM. Similarly, inhibiting COPI dissociation from membranes by expressing a constitutively active ADP-ribosylation factor 1 mutant arrests CFTR within disrupted Golgi elements. To definitively explore the relationship between COPI and CFTR in epithelial cells, we depleted beta-COP from the human colonic epithelial cell HT-29Cl.19A using small interfering RNA. Beta-COP depletion did not affect CFTR synthesis but impaired its trafficking to the PM. The arrest occurred pre-Golgi as shown by reduced level of glycosylation. Importantly, decreased trafficking of CFTR had a functional consequence as cells depleted of beta-COP showed decreased cAMP-activated chloride currents. To explore the mechanism of COPI action in CFTR traffic we tested whether CFTR was COPI cargo. We discovered that the alpha-, beta-, and gamma-subunits of COPI co-immunoprecipitated with CFTR. Our results indicate that the COPI complex plays a critical role in CFTR trafficking to the PM.

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Miniglucagon, or glucagon-[19-29], is partially processed from glucagon in its target tissues where it modulates the glucagon action. In the islets of Langerhans, the glucagon-producing A cells contain miniglucagon at a significant level (2-5% of the glucagon content). We studied a possible control of insulin release by miniglucagon using as a model the MIN6 cell line. Miniglucagon, in the 10(-14) to 10(-9) M range, inhibited insulin release induced by glucose, glucagon, tGLP-1, or glibenclamide by 85-100% with an IC50 close to 1 pM. While no change in the cyclic AMP content was noted, Ca2+ influx was reduced in parallel with the inhibition of insulin release. Use of pharmacological modulators of L-type voltage-sensitive Ca2+ channels and bacterial toxins indicates that miniglucagon blocks insulin release by closing this type of channel via a pertussis toxin-sensitive G protein. Miniglucagon is a novel, possibly physiologically relevant, local regulator of islet function.

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A randomized, double-blind, crossover study of cholestyramine (8 g twice daily) compared with placebo for a period of 6 weeks each.

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Pharmacologic inhibition of the K(ATP) channel with sulfonylureas or the adenosine receptor with methylxanthines has been shown to attenuate ischemic preconditioning (IPC). Both classes of compounds are widely used clinically, and several reports have demonstrated adverse outcomes in patients taking sulfonylureas. Recently inhibition of the sodium/hydrogen exchanger isozyme-1 (NHE-1) has been shown to be equal to IPC at providing myocardial protection in dogs and may be an alternative to IPC in patients taking sulfonylureas or methylxanthines. However, no experiments have examined the pharmacologic overlap between IPC and NHE-1 inhibitor-mediated cardioprotection in dogs. With an in vivo canine infarct model in which the left anterior descending coronary artery was occluded for 60 min and reperfused for 3 h, neither the K(ATP) channel antagonist glibenclamide nor the adenosine-receptor antagonist PD 115199 attenuated NHE-1 inhibitor-mediated reduction in infarct size expressed as a percentage of the area at risk produced by EMD 85131 (Control, 24.2 +/- 3.6%; EMD 85131, 6.4 +/- 2.3%; PD 115199 + EMD 85131, 6.6 +/- 2.4%; glibenclamide + EMD 85131, 3.5 +/- 1.2%). NHE-1 inhibition and IPC do not overlap pharmacologically, and NHE-1 inhibition may be an alternative for cardioprotection in patients taking sulfonylureas or methylxanthines.

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micronase tablets 2015-12-23

Glybenclamide is used as a pharmacological tool in studies of mitochondrial functions supposing its main role to block buy micronase ATP-dependent potassium (KATP) channel. The aim of this study was to test whether glybenclamide might interact with the mitochondrial chloride channels. Mitochondrial membranes, isolated from rat heart muscle, were incorporated into lipid bilayer membrane and single chloride channel currents were measured in 250/50 mM KCl cis/trans solutions. The observed chloride channels (N=11) with mean conductance 120±14 pS were sensitive to glybenclamide, which decreased the open probability (IC50=129 μM) and affected the channel gating kinetics (IC50=12 μM) by perturbing its open state. It did not influence the channel conductance or reversal potential. These results indicate that glybenclamide interacts with chloride channels what should be taken into consideration, when glybenclamide is used as a specific inhibitor of KATP channels.

micronase 5 mg 2015-06-07

Succinic acid methyl esters are currently under investigation as potential insulinotropic tools in animal models of non-insulin-dependent diabetes mellitus. The in vivo administration of these esters may result in the undesirable generation of methanol through their intracellular hydrolysis. As a first attempt to circumvert this drawback, we have now investigated whether the esterification of the carboxylic group of succinic acid monomethyl ester by D-glucose or 3-O-methyl-D-glucose affects its insulin-otropic action. Both the 6-O-D-glucosyl and 6-O-(3-O-methyl)-D-glucosyl esters were found to stimulate insulin release in pancreatic islets and the isolated perfused pancreas. The 6-O-D-glucosyl ester also stimulated insulin release after intravenous administration to anaesthetized rats. These findings suggest that the undersirable generation of methanol from the buy micronase methyl esters of succinic acid could eventually be avoided by using other esters of this dicarboxylic acid, whilst keeping the benefit of their insulinotropic action.

micronase dosing 2016-06-05

Prospective randomized buy micronase laboratory study.

micronase medication 2015-02-22

To buy micronase examine perinatal outcomes in women with gestational diabetes mellitus treated with glyburide compared to insulin injections.

micronase generic name 2015-06-04

Renal ischemia reperfusion (IR) injury has been a major source of concern during the past decades and angiotensin converting enzyme (ACE) inhibitors have been successfully used to prevent this injury. There have buy micronase been some controversial reports about the involvement of K(ATP) channels in the mechanism of action of ACE inhibitors. In this study, we examined the effect of K(ATP) channel blocker (Glibenclamide) on preventive effect of captopril on renal IR injury.

micronase drug information 2017-09-25

The present study investigated the mechanisms of melatonin-induced inhibition of the ileal smooth muscle contraction. Rat isolated ileal smooth muscle strips were stimulated in an buy micronase organ bath using carbachol (CAR) or potassium chloride (KCl) depolarization. Under these conditions, melatonin produced a concentration-dependent inhibition of muscle contraction (mean inhibitory concentration, IC50: 17.3 x 10(-6) M), which was not blocked by either tetrodotoxin (10(-6) M), hexamethonium (10(-4) M), or phentolamine (10(-6) M). The inhibitory effect of melatonin during CAR stimulation was blocked in a concentration-dependent manner by the presence of apamin (4.8 x 10(-9) M), a K(+)-channel blocker. By contrast, other K(+)-channel blockers such as 4-aminopyridine (10(-4) M to 5 x 10(-3) M), tetraethylammonium (10(-4) to 10(-1) M), and glibenclamide (10(-5) M) were ineffective. Additionally, the Ca(2+)-channel antagonists nitrendipine (IC50: 2.4 x 10(-9) M) and verapamil (IC50: 1.1 x 10(-7) M) also blocked the inhibitory action of melatonin. These results suggest that melatonin may interact with an apamin-sensitive, possibly Ca(2+)-activated, K+ channel and thus cause an inhibition of ileal smooth muscle contractions.

dosage of micronase 2017-05-12

Earlier observations have indicated that repolarization-delaying agents may, under certain circumstances, have the propensity to induce polymorphous ventricular tachyarrhythmias (PVTs) (i.e., torsade de pointes). We have studied whether the potassium channel opener pinacidil and two of its pyridylcyanoguanidine analogues (P1075 buy micronase and P1188) have any antiarrhythmic effects on clofilium-induced PVTs and triggered responses in rabbits in vivo and in vitro.

micronase drug interactions 2015-05-13

The sulfonylurea receptor (SUR), an ATP-binding cassette (ABC) protein, assembles with a potassium channel subunit (Kir6) to form the ATP-sensitive potassium channel (K(ATP)) complex. Although SUR is an important regulator of Kir6, the specific SUR domain that associates with Kir6 is still unknown. All functional ABC proteins contain two transmembrane domains but some, including SUR and MRP1 (multidrug resistance protein 1), contain an buy micronase extra N-terminal transmembrane domain called TMD0. The functions of any TMD0s are largely unclear. Using Xenopus oocytes to coexpress truncated SUR constructs with Kir6, we demonstrated by immunoprecipitation, single-oocyte chemiluminescence and electrophysiological measurements that the TMD0 of SUR1 strongly associated with Kir6.2 and modulated its trafficking and gating. Two TMD0 mutations, A116P and V187D, previously correlated with persistent hyperinsulinemic hypoglycemia of infancy, were found to disrupt the association between TMD0 and Kir6.2. These results underscore the importance of TMD0 in K(ATP) channel function, explaining how specific mutations within this domain result in disease, and suggest how an ABC protein has evolved to regulate a potassium channel.

micronase drug class 2016-09-16

The expression meglitinide analogs was introduced in 1995 to cover new molecules proposed as non-sulfonylurea insulinotropic agents and displaying structural analogy with meglitinide, such as repaglinide, nateglinide, and mitiglinide. Meglitinide analogs display, as judged by conformation analysis, a U-shaped configuration similar to that of antihyperglycemic sulfonylureas such as glibenclamide (glyburide) and glimepiride. In rat pancreatic islets incubated in the presence of 7.0 mmol/L D-glucose, repaglinide and mitiglinide demonstrate comparable concentration-response relationships for stimulation of insulin release, with a threshold value < 10 nmol/L and a maximal secretory response at about 10 nmol/L. Several findings indicate that meglitinide analogs provoke the closing of adenosine triphosphate-sensitive potassium channels, with subsequent gating of voltage-sensitive calcium channels. The effects of meglitinide analogs upon the binding of [3H]glibenclamide to islet cells membranes reinforces this concept. At variance, however, with other meglitinide analogs, the ionic and secretory response to repaglinide (10 micromol/L) is not rapidly reversible in perifused rat islets. In experiments conducted in vivo in control and diabetic rats, repaglinide provokes a greater and more rapid increase in plasma insulin concentration and an earlier fall in glycemia than glibenclamide or glimepiride. Onset of effect is also more rapid and duration of effect shorter with nateglinide versus glibenclamide. In clinical studies, single or repeated daily administration of repaglinide increased plasma insulin concentration in a dose-dependent manner, with an incremental peak reached about 2 hours after repaglinide intake. Plasma concentrations of repaglinide are about 5.0 microg/L 2-2.5 hours after oral intake of the drug. Despite the slow reversibility of repaglinide action in vitro, this drug offers advantages over glibenclamide in terms of the possible occurrence of hypoglycemia if a meal is missed. In volunteers receiving a single oral dose of nateglinide (120mg) 10 minutes before a standardized 800 Kcal breakfast, the plasma insulin concentration was higher 5, 10, and 20 minutes after meal intake than when they received a single dose of repaglinide (0.5 or 2.0mg) or placebo 10 minutes before breakfast. Peak plasma concentrations buy micronase of nateglinide were reached within 2 hours in most volunteers. Peak plasma concentrations of mitiglinide were reached 30 minutes after a single oral dose in a representative volunteer. Mitiglinide significantly suppressed meal-induced elevations in blood glucose concentrations in a study of patients with type 2 diabetes. In conclusion, two obvious differences among these meglitinide analogs should be underlined. First, on a molar basis, nateglinide is somewhat less potent than repaglinide or mitiglinide, as an insulinotropic agent. The maximal secretory responses evoked by these three meglitinide analogs are, however, identical to one another. Secondly, and as already mentioned, the functional effects of nateglinide and mitiglinide are more rapidly reversible than those of repaglinide, for instance in perifused rat islets. The meglitinide analogs offer the advantage over the long-acting antihyperglycemic sulfonylurea glibenclamide of minimizing the risk of undesirable hypoglycemia.

micronase 10 mg 2016-11-18

The extent to which ATP-sensitive K(+) channels contribute to reactive hyperemia in humans is unresolved. We examined the role of ATP-sensitive K(+) channels in regulating reactive hyperemia induced by 5 min of forearm ischemia. Thirty-one healthy subjects had forearm blood flow measured with venous occlusion plethysmography. Reactive hyperemia could be reproducibly induced (n = 9). buy micronase The contribution of vascular ATP-sensitive K(+) channels to reactive hyperemia was determined by measuring forearm blood flow before and during brachial artery infusion of glibenclamide, an ATP-sensitive K(+) channel inhibitor (n = 12). To document ATP-sensitive K(+) channel inhibition with glibenclamide, coinfusion with diazoxide, an ATP-sensitive K(+) channel opener, was undertaken (n = 10). Glibenclamide did not significantly alter resting forearm blood flow or the initial and sustained phases of reactive hyperemia. However, glibenclamide attenuated the hyperemic response induced by diazoxide. These data suggest that ATP-sensitive K(+) channels do not play an important role in controlling forearm reactive hyperemia and that other mechanisms are active in this adaptive response.

micronase dosage 2016-06-14

Caveolae are 50- to 100-nm cell surface plasma membrane invaginations present in terminally differentiated cells. They are characterized by the presence of caveolin-1, sphingolipids, and cholesterol. Caveolin-1 is thought to play an important role in the regulation of cellular cholesterol homeostasis, a process that needs to be properly controlled to limit and prevent cholesterol accumulation and eventually atherosclerosis. We have recently generated caveolin-1-deficient [Cav-1(-/-)] mice in which caveolae organelles are completely eliminated from all cell types, except cardiac and skeletal muscle. In the present study, we examined the metabolism of cholesterol in wild-type (WT) and Cav-1(-/-) mouse embryonic fibroblasts (MEFs) and mouse peritoneal macrophages (MPMs). We observed that Cav-1(-/-) MEFs are enriched in esterified cholesterol but depleted of free cholesterol compared with their wild-type counterparts. Similarly, Cav-1(-/-) MPMs also contained less free cholesterol and were enriched in esterified cholesterol on cholesterol loading. In agreement with buy micronase this finding, caveolin-1 deficiency was associated with reduced free cholesterol synthesis but increased acyl-CoA:cholesterol acyl-transferase (ACAT) activity. In wild-type MPMs, we observed that caveolin-1 was markedly upregulated on cholesterol loading. Despite these differences, cellular cholesterol efflux from MEFs and MPMs to HDL was not affected in the Cav-1-deficient cells. Neither ATP-binding cassette transporter G1 (ABCG1)- nor scavenger receptor class B type I (SR-BI)-mediated cholesterol efflux was affected. Cellular cholesterol efflux to apolipoprotein A-I was not significantly reduced in Cav-1(-/-) MPMs compared with wild-type MPMs. However, ABCA1-mediated cholesterol efflux was clearly more sensitive to the inhibitory effects of glyburide in Cav-1(-/-) MPMs versus WT MPMs. Taken together, these findings suggest that caveolin-1 plays an important role in the regulation of intracellular cholesterol homeostasis and can modulate the activity of other proteins that are involved in the regulation of intracellular cholesterol homeostasis.

micronase drug form 2017-10-14

Women with singleton gestations enrolled for outpatient services diagnosed with GDM and without history of pregnancy-related hypertension at enrollment buy micronase or in a prior pregnancy were identified in a database. Women with GDM controlled by diet only (n = 3918), glyburide (n = 873), or insulin without prior exposure to oral hypoglycemic agents (n = 2229) were included. Pregnancy outcomes were compared for obese versus nonobese women within each treatment group and also compared across treatment groups within the obese and nonobese populations.

micronase buy cheap 2015-10-09

Compared to baseline, mean reduction in HbA1-c at the endpoint was significant among patients of group I, group II and group III (p ≤ 0.05, p ≤ 0.02 and p < 0.005 respectively) and same was the case for FPG (p ≤ 0.05, p < 0.04, p < 0.003 respectively buy micronase ), but the improvement in 2 hour OGTT was significant only in group III (p < 0.03). The decrease in PSA was observed only among group I and group II with the later showing significant reduction from baseline (p < 0.01). In group III, the level slightly increased. Parameters including blood lipids, atherogenic index, body weight and SBP improved among patients of group I and group II but deteriorated among group III patients.

micronase 50 mg 2015-03-28

All three drugs were equally effective on the total prandial insulin secretion (area under buy micronase the curve [AUC] -15 to 240 min). However, clear differences were noted in the early insulin secretion (AUC -15 to 30 min); both repaglinide and glipizide increased secretion in nondiabetic subjects by approximately 61 and 34%, respectively, compared with placebo. In the diabetic patients, the difference versus placebo was 37 and 47%, respectively. The difference between glipizide and glibenclamide reached significance in both groups of subjects, whereas repaglinide was more effective than glibenclamide only in the healthy nondiabetic subject group. All three drugs were effective in decreasing total glucose AUC in the nondiabetic and diabetic population. In the nondiabetic subjects, however, repaglinide was significantly more effective than glibenclamide. The differences disappeared in the diabetic subjects, probably as a result of increased prevalence of insulin resistance in this group.

micronase cost 2016-09-09

In patients with type 2 diabetes, intensive blood-glucose control with insulin or sulphonylurea therapy decreases progression of microvascular disease and may also Vasaka Capsule reduce the risk of heart attacks. This study investigated whether intensive glucose control with metformin has any specific advantage or disadvantage.

micronase brand name 2015-07-25

These results suggest that K+ channel activation selectively relaxes SAH-induced vasospasm. We speculate that the ability of K+ Cardura Online channel activators to selectively relax the spasm may be due, at least in part, to the underlying inhibition of K+ channels after SAH.

micronase tablets 2016-06-02

These results show that isoflurane impairs insulin secretion and glucose utilization. The mechanism of action responsible for these effects may involve a decrease in glucose-induced inhibition of adenosine Allegra Dosage triphosphate-sensitive potassium channel activity in pancreatic beta cells.

micronase 5 mg 2016-05-06

The nitric oxide (NO) donor SIN-1 (3-morpholinosydnonimine) induced a concentration-dependent inhibition of the secretory response to glucose. The negative insulinotropic action of SIN-1 was attenuated by the hypoglycemic sulfonylurea Vantin Drug glibenclamide. Moreover, the NO donor enhanced 86Rb outflow from perfused islets and reduced the glucose-induced increase in 45Ca outflow. The present data provide further evidence that NO donors impair the secretory response to glucose, at least in part, by activating the ATP-sensitive K+ channels.

micronase dosing 2016-07-30

Rats were subjected to Cipro Renal Dosing hemorrhagic shock (HS) for 2 hours. The spinotrapezius muscle was prepared for microscopy and the responses of arterioles in the muscle to norepinephrine (NE) were tested. The resting membrane potentials of isolated arterial strips were measured with a microelectrode. Membrane potential and intracellular Ca2+ ([Ca2+]i) changes in isolated arteriolar smooth muscle cells (ASMCs) were determined with fluorescent probes and a confocal microscopy.

micronase medication 2017-09-24

Activation of ATP-sensitive potassium (K(ATP)) channels can regulate smooth muscle function through membrane potential hyperpolarization. A critical issue in understanding the role of K(ATP) channels is the relationship between channel activation and the effect on tissue function. Here, we explored this relationship in urinary bladder smooth muscle (UBSM) from the detrusor by activating K(ATP) channels with the synthetic compounds N-(4-benzoylphenyl)-3,3,3-trifluoro-2-hydroxy-2-methylpropionamide (ZD-6169) and levcromakalim. The effects of ZD-6169 and levcromakalim on K(ATP) channel currents in isolated UBSM cells, on action potentials, and on related phasic contractions of isolated UBSM strips were examined. ZD-6169 and levcromakalim at 1.02 and 2.63 microM, respectively, caused half-maximal activation (K1/2) of K(ATP) currents in single UBSM cells (see Heppner TJ, Bonev A, Li JH, Kau ST, and Nelson MT. Pharmacology 53: 170-179, 1996). In contrast, much lower concentrations (K(1/2) = 47 nM for ZD-6169 and K1/2 = 38 nM for levcromakalim) caused inhibition of action potentials Stromectol Online and phasic contractions of UBSM. The results suggest that activation of <1% of K(ATP) channels is sufficient to inhibit significantly action potentials and the related phasic contractions.

micronase generic name 2015-03-26

Apoptosis was induced by adding various concentrations of GB (0.001 to 200 µM) to a glucolipotoxic condition using 33 mM glucose, and the effects of varied concentrations Sustiva Medication of palmitate were evaluated via annexin V staining. The markers of ER stress and pro-apoptotic markers were assessed by Western blotting and semi-quantitative reverse transcription-polymerase chain reaction. Additionally, the anti-apoptotic markers were evaluated.

micronase drug information 2017-11-26

Cardioprotective effects of isoflurane are partially mediated by the sarcolemmal adenosine triphosphate-sensitive potassium (sarcK ATP ) channel. The authors tested the hypothesis that isoflurane sensitizes sarcK ATP channels to Eldepryl Tablets a potassium channel opener, pinacidil, adenosine- and phospholipid-mediated pathways.

dosage of micronase 2017-10-28

There is insufficient evidence to recommend momordica charantia for type 2 diabetes mellitus. Further studies are therefore required to address the Zyrtec Max Dose issues of standardization and the quality control of preparations. For medical nutritional therapy, further observational trials evaluating the effects of momordica charantia are needed before RCTs are established to guide any recommendations in clinical practice.

micronase drug interactions 2015-01-01

Adenosine-5'-triphosphate (ATP) released from damaged cells can affect functions of adjacent cells. Injuries of peripheral tissue stimulate nerves, but effect of ATP on the nerve bundles is still speculative. Peripheral nerves are surrounded by perineurium, therefore the response of perineurium may be a first event of nerve stimulation at tissue injuries. The aim of the present study is to clarify whether the perineurium responds to ATP. To this end, we analyzed the dynamics of the intracellular calcium concentration ([Ca2+]i) of perineurial cells by confocal microscopy. ATP induced a [Ca2+]i increase of perineurial cells. Ca2+ channel blockers and removing of extracellular Ca2+, but not thapsigargin pretreatment, abolished ATP-induced [Ca2+]i dynamics. This indicated that the [Ca2+]i increase was due to an Neurontin And Alcohol influx of extracellular Ca2+. Adenosine-5'-diphosphate also elicited an increase of [Ca2+]i, but P1 receptor agonists had few effects on [Ca2+]i dynamics. Suramin (an antagonist of P2X and P2Y receptors) totally inhibited ATP-induced [Ca2+]i dynamics, but reactive blue 2 (a P2Y receptor antagonist) did not. Uridine-5'-triphosphate (a P2Y receptor agonist) induced no significant change in [Ca2+]i, but alpha,beta-methylene ATP (a P2X receptor agonist) caused a [Ca2+]i increase. In conclusion, perineurial cells respond to extracellular ATP mainly via P2X receptors.

micronase drug class 2015-04-14

Doxorubicin is a chemotherapeutic drug used to treat solid and haematopoietic tumours. Its use is limited by a major side effect of cardiotoxicity. It was reported that doxorubicin-induced cardiotoxicity is mediated through oxidative stress coupled with impaired NO bioavailability and NF-κB activation. Nicorandil, a mitochondrial ATP-dependent potassium (KATP ) channel opener, was reported to be cardioprotective on ischaemic myocardium. However, the effect of nicorandil against doxorubicin-induced cardiotoxicity has not yet been clarified. Accordingly, six groups of rats were used. The first three groups were injected with vehicle, nicorandil (3 mg/kg) orally and doxorubicin (a single intraperitoneal injection of 20 mg/kg), respectively. Group four was treated with nicorandil, whereas group five was treated with glibenclamide and then nicorandil starting 2 days before doxorubicin and continued for five consecutive days. Group six was treated with glibenclamide alone. At the end of the experiment, the rats were killed. Cardiac enzyme indexes were measured in serum. Heart tissues were processed for determination of nitrite/nitrate, NF-κB protein expression, glutathione (GSH), lipid peroxide (TBARS) levels and superoxide production. In addition to body-weight reduction, doxorubicin produced cardiotoxicity as indicated from the increase in lactate dehydrogenase (LDH), creatine kinase (CK) activities, TBARS, superoxide production, NF-κB expression and caspase-3 activity. Moreover, doxorubicin decreased GSH and nitrite/nitrate levels. Histopathological examination of doxorubicin-treated hearts revealed degenerative changes. On the other hand, nicorandil protected cardiac tissues against doxorubicin cardiotoxicity as demonstrated from normalization of cardiac biochemical and oxidative stress parameters and amelioration of histopathological changes. Glibenclamide, a blocker of the KATP channel, reversed most of the cardiac effects of nicorandil.

micronase 10 mg 2015-12-04

Warm-up phenomenon, one of the clinical models of ischemic preconditioning, refers to an increased tolerance to myocardial ischemia during the second of two consecutive exercise tests.

micronase dosage 2015-03-22

Nitric oxide (NO) is known to be an important relaxant of contractile activity in various muscles including the human uterine arteries. It has been suggested that NO plays a role in modulation of vascular action of arginin vasopressin (AVP), a strong vasoconstrictor of the human uterine arteries. Therefore, the purposes of this study were to investigate an involvement of endogenous NO in regulation of responses of the human intrauterine arteries to AVP and examine the effect of exogenous NO on contractions of the human intrauterine arteries evoked by AVP. Pretreatment of the artery rings with L-NA, an inhibitor of NO synthase significantly increased the resting force and enhanced the artery responses to AVP. The opposite effect has been observed after administration of 10(-6) mol/L sodium nitroprusside (SNP). Pretreatment of the artery rings with 10(-7) M CTX, a blocker of Ca(2+)-sensitive potassium channels with large conductance, did not change significantly their responses to AVP. Glibenclamide (1.5.10(-6) mol/L), a blocker of ATP-dependent potassium channels and apamin (10(-8) M), a specific blocker of Ca(2+)-sensitive potassium channels with small conductance strongly enhanced the maximum responses of the artery rings to AVP. Pretreatment with CTX significantly decreased the relaxation induced by SNP while apamin attenuated the sensitivity to SNP resulted in rightward shift of the concentration-response curve to SNP. In conclusion, this study indicates that: NO plays a role in regulation of both the vascular tone of the human intramyometrial arteries and their response to AVP. Ca(2+)-sensitive K(+) channels with small and large conductance are involved in the SNP-induced relaxation of these arteries. The pathways of this relaxation cannot be sufficiently explained at this moment and need further investigation.

micronase drug form 2017-08-01

Twelve dogs were anesthetized with 8% end-tidal desflurane for baseline anesthesia. A flow probe was placed on the left anterior descending (LAD) artery. A probe that measured PmO2 was inserted into the middle myocardium in the LAD region. After baseline measures, six dogs received i.v. 1 mg kg(-1) of glyburide and six dogs received sham vehicle treatment. After the glyburide or sham treatment, each dog received an i.v. infusion of adenosine 0.1 microg kg(-1) x min(-1), sodium nitroprusside (SNP) 2-4 microg kg(-1) x min(-1) and 14% end-tidal desflurane in random order.

micronase buy cheap 2015-11-01

Oxygen is a potent stimulus for pulmonary vasodilation. Potassium channels have been implicated as both sensors and effectors for oxygen-induced changes in pulmonary vascular tone. We have examined the effect of potassium channel blockers on oxygen-induced vasodilation in isolated pulmonary arterioles from fetal rats at term.

micronase 50 mg 2016-05-18

A total of 144 male patients were referred for suspected drug-induced hypoglycaemia. Sildenafil and glibenclamide, or their metabolites, were detected in the urine specimens of 68 (47%) patients, none of whom had been prescribed either drug by a registered medical practitioner. Among these subjects, 24 (35%) denied any use of sexual enhancement products despite repeated questioning. Eight patients had repeated exposure resulting in re-admission. The sources of these sexual enhancement products included pharmacies in Mainland China, friends, local pharmacies, peddlers, or were unknown. Three patients died, one remains in a vegetative state and one suffered cognitive impairment; the remaining 63 recovered fully. Twenty-five unused sexual enhancement products of seven different kinds were recovered for analysis. The median (range) of sildenafil and glibenclamide per unit dose was 64 (0.05-198) mg and 70 (0-158) mg, respectively.