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Periactin

Generic Periactin is used to relieve cold- and allergy-related symptoms such as hay fever, nasal inflammation, stuffy nose, red and inflamed eyes, hives, and swelling. Generic Periactin is approved by FDA. Generic Periactin blocks the effects of the naturally occurring chemical histamine in your body.

Other names for this medication:

Similar Products:
Atarax, Phenergan, Flonase, Allegra

 

Also known as:  Cyproheptadine.

Description

Generic Periactin is used to treat fever, nasal inflammation, stuffy nose, red and inflamed eyes, hives, swelling and other symptoms of cold and allergy.

Generic Periactin blocks the effects of the naturally occurring chemical histamine in your body.

Periactin is also known as Cyproheptadine, Ciplactin, Periactine, Ciproral.

Generic name of Generic Periactin is Cyproheptadine.

Brand name of Generic Periactin is Periactin.

Dosage

Generic Periactin can be taken in tablets (4mg) and syrup. You should take it by mouth.

Take Generic Periactin by mouth with or without food.

Measure the syrup form of Generic Periactin with a special dose-measuring spoon or cup.

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

Overdose

If you overdose Generic Periactin and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Generic Periactin overdosage: extreme sleepiness, confusion, weakness, ringing in the ears, blurred vision, large pupils, dry mouth, flushing, fever, shaking, insomnia, hallucinations, seizure.

Storage

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

Side effects

The most common side effects associated with Periactin 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.

Contraindications

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

Try to be careful with Generic Periactin if you're pregnant or you plan to have a baby, or you are a nursing mother. Generic Periactin can harm your baby.

Do not take cyproheptadine if you have taken a monoamine oxidase inhibitor (MAOI) such as isocarboxazid (Marplan), phenelzine (Nardil), or tranylcypromine (Parnate) in the last 14 days.

Be careful in taking Generic Periactin if you have glaucoma or pressure in the eye, stomach ulcer, enlarged prostate, bladder problems, difficulty urinating, hyperthyroidism, hypertension, any problems with heart, asthma.

Be careful with taking Generic Periactin if you use anxiety or sleep medicines such as alprazolam (Xanax), diazepam (Valium), chlordiazepoxide (Librium), temazepam (Restoril), or triazolam (Halcion); anti-depression medications such as amitriptyline (Elavil), doxepin (Sinequan), nortriptyline (Pamelor), fluoxetine (Prozac), sertraline (Zoloft), or paroxetine (Paxil); any other medications that make you feel drowsy, sleepy, or relaxed.

Avoid machine driving while taking Generic Periactin.

Avoid alcohol.

Do not stop taking Generic Periactin suddenly.

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Fifty percent of patients with migraine were prescribed daily prophylactic medicines, reflecting a referral bias. The most commonly prescribed agents were amitriptyline (preferred for the older patients) and cyproheptadine (preferred for the younger patients). The overall positive response rates were 89% for amitriptyline and 83% for cyproheptadine during a 6-month follow-up. Headache frequencies were reduced with amitriptyline by 62% and with cyproheptadine by 55%. Long-term follow-up of this population is ongoing, and prospective studies are needed.

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On the basis of low dose inhaled corticosteroid, orally administered Loratadine significantly improves the therapeutic efficacy of asthma in patients with allergic asthma and rhinitis.

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Adults with symptomatic SAR were randomized in a double-blind manner to receive desloratadine, 5 mg, or placebo for 14 days. Patient-rated SAR symptoms were recorded twice daily (morning and evening). On days 1 and 15, SAR symptoms were scored jointly (investigator and patient), nasal airflow was measured using 4-phase rhinomanometry, and QOL and the overall condition of SAR were rated. Overall treatment response was scored on day 15. Adverse events were recorded.

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Delirium status of surgical patients was evaluated postoperatively at the time of admission to the intensive care unit (ICU) using the Confusion Assessment Method (CAM-ICU) scale. Patients without delirium were assigned to the cyproheptadine or placebo group based on the simple randomization method. Patients received cyproheptadine or placebo tablet at a dose of 4 mg 3 times per day for 7 days. Patients were monitored daily for incidence of delirium.

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Breastfeeding women may suffer from migraine. While we have many drugs for its treatment and prophylaxis, the majority are poorly studied in breastfeeding women. We conducted a review of the most common anti-migraine drugs (AMDs) and we determined their lactation risk.

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A patient with active Cushing's disease who became pregnant following treatment with cyproheptadine is described. Despite stopping the cyproheptadine treatment at 3 mth gestation, the previous amelioration of the clinical and biochemical features of the adrenal hyperfunction was maintained and the pregnancy progressed satisfactorily. Moreover, serial evaluation of maternal glucose tolerance proved to be normal and it is suggested that this matabolic aspect is an important determinant in the outcome of pregnancies occurring in patients with Cushing's syndrome.

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This double-blind, double-dummy, randomized, 2-phase, multicenter study was designed primarily to compare the therapeutic responses to loratadine and fexofenadine in patients who failed initial therapy with the other drug.

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The purpose of this study was to compare the effect of two serotonergic receptor antagonists on the contractile responses mediated by 5-hydroxytryptamine (5-HT) in isolated canine coronary arteries. After removing the endothelium and blocking neuronal uptake with cocaine, the coronary artery contracted when exposed to nanomolar concentrations of 5-HT; at micromolar concentrations the amine caused relaxation. A relatively high concentration of the selective S2-serotonergic antagonist, ketanserin (10(-6) M), attenuated peak contractions caused by 5-HT by an average of only 52% and caused no significant change in sensitivity to the amine. In contrast, the antagonist behaved competitively in the canine femoral artery. Cyproheptadine (10(-6) M) also was a noncompetitive serotonergic antagonist in the coronary artery. The relatively nonselective S1- and S2-serotonergic receptor antagonist, methiothepin, competitively antagonized coronary contractions caused by 5-HT with an estimated pA2 of 8.0. The rightward shifts of coronary serotonergic contractions caused by methiothepin were not significantly different whether or not ketanserin (10(-6) M) was present in the assay to block S2-serotonergic receptors. Unlike ketanserin, methiothepin (10(-6) M) nearly abolished coronary artery contractions caused by aggregating platelets. These results indicate that serotonergic coronary contractions are resistant to S2-serotonergic blockade, and suggest that they are mediated at least in part by receptors which are different from the S2-serotonergic subtype.

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In 1993, the Food and Drug Administration (FDA) approved 25 new molecular entities (NMEs), 23 of which are for therapeutic use and two are diagnostic agents. Eleven of the NMEs for therapeutic use, as well a new biological agent intended for therapeutic use, were both approved and marketed in the United States in 1993. In addition, 11 other NMEs that the FDA approved before 1993 (most in late 1992) were marketed during the year. Thus, a total of 23 therapeutic agents reached the U.S. market for the first time in 1993, a considerably lower number than the 30 new therapeutic agents marketed in 1992 and the record number 31 new agents marketed in 1991. Many of the 13 therapeutic agents approved in 1993 but not marketed before the end of the year have become available in early 1994. Of the 23 new therapeutic agents first marketed in 1993, 22 are considered in this series. The one agent not reviewed is flosequinan, which was withdrawn from the market after being available only several months because of a concern about toxicity. This review considers the new agents' most important properties and, when possible, compares them with other available agents with similar properties. When additional information is needed, more comprehensive references and the product literature should be consulted.

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The effect of intracisternal injection of thyrotropin-releasing hormone (TRH) on small intestinal transit of a charcoal bolus was investigated in 14-, 21-, 28- and 35-day-old and adult rats. Intracisternal TRH (15 micrograms in 2 microliters) was administered, and transit (distance traveled by the charcoal) was measured 120 min later. In all age groups, intracisternal TRH increased charcoal transit significantly (P less than 0.05) as compared to saline-treated controls. This increase in transit was not mimicked by intravascular TRH, and it was blocked in all age groups by prior intraperitoneal injection of atropine (2 micrograms/g body weight). Vagotomy blocked TRH-induced increases in small intestine transit in rats of 28 days and older. Prior intraperitoneal injection of the antiserotonin compound, cyproheptadine (1 microgram/g body weight) reduced TRH-induced increases in small intestine transit in all age groups. These results demonstrate that centrally administered TRH stimulates small intestine transit through both cholinergic and serotonergic mechanisms in rats as early as 14 days of age.

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The symptoms of allergic rhinitis vary in severity over the course of the day and often are worse in the morning. This review focuses on data from clinical studies of the antihistamine desloratadine to establish whether it effectively controls the morning symptoms of allergic rhinitis. Studies of desloratadine in patients with allergic rhinitis that used instantaneous scoring to assess the severity of morning symptoms were selected for inclusion from published literature (peer-reviewed articles and abstracts presented at professional meetings). When administered once daily, desloratadine is effective in alleviating the morning symptoms of allergic rhinitis, including nasal congestion. Its action is sustained over the 24-hour dosing interval. A comparison of morning and evening dosing of desloratadine revealed equivalent relief of morning symptoms, illustrating that the effect of desloratadine is independent of the time of dosing. Clinical studies indicate that desloratadine is nonsedating and well tolerated, with no evidence of adverse cardiac effects. For many patients with allergic rhinitis, symptoms are most severe in the morning. To maximize the benefits for patients, pharmacologic agents used in the management of allergic rhinitis should be effective in controlling these peak morning symptoms. The sustained 24-hour action of desloratadine and its effective control of morning symptoms make it a valuable tool for improving the quality of life of patients with allergic rhinitis.

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The Pp.Cr on application (0.01-5.0 mg/ml) to isolated rabbit jejunum preparation exhibited relaxation through decrease in magnitude and frequency of spontaneous contractions. The Pp.Cr also exerted a relaxant (0.01-5.0 mg/ml) effect on K+ (80 mM) induced contractions in isolated rabbit jejunum preparations and caused shifting of the Ca2+ curves (1.0-3.0 mg/ml) toward right in a manner similar to that of verapamil (3 μM), possibly suggesting presence of Ca2+ channel blocking activity. Subsequently, Pp.Cr in a concentration-dependent fashion (0.01-10.0 mg/ml) caused relaxation of CCh (1 μM) and K+ (80 mM) induced contractions in isolated rabbit tracheal preparations in a manner comparable to that of dicyclomine, suggesting that the observed relaxant effect is likely to be mediated through antimuscarinic and/or Ca2+ channel blocking activities. Moreover, when evaluated against isolated rabbit aortic preparations, the Pp.Cr in concentrations up to 10 mg/ml exhibited a contractile response that was found to be abolished subsequent to pretreatment of isolated tissue preparation with cyproheptadine (1 μM), phentolamine (1 μM), and losartan (1 μM), suggesting that Pp.Cr may have some α-adrenergic, muscarinic, serotonergic, and angiotensin II activities.

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Rats were trained to discriminate intraperitoneally administered mescaline from saline in a two-lever operant chamber for food reinforcement. Reward was contingent upon responses made greater than 15 sec apart (DRL-15) on the appropriate lever paired with either drug or saline administration. Following the establishment of discriminative response control by mescaline, the animals were tested for stimulus generalization produced by mescaline after: (a) blockade of periphreral and central serotonin (5-HT) receptors with cinanserin, methysergide, or cyproheptadine; (b) blockade of peripheral 5-HT receptors with xylamidine tosylate; and (c) depletion of brain 5-HT with the tryptophan hydroxylase inhibitor p-chlorophenylalanine (PCPA). The results show that all three central 5-HT antagonists greatly reduced the discriminability of mescaline while the peripheral antagonist, xylamidine tosylate, was without effect. Furthermore, these agents at the doses employed did not effect the discriminability of saline. Depletion of 5-HT with PCPA potentiated the effects of a sub-threshold dose of mescaline and slightly reduced the discriminability of saline. The results indicate that mescaline produces its discriminative stimulus properties by directly stimulating central serotonergic receptors.

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Thus, our study shows that the biogenic amines play a significant role in C. procera latex-induced inflammation and antihistaminic drugs could be effectively used to inhibit inflammatory response elicited by exposure to latex.

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A series of compounds with actions on the central nervous system was tested for antagonism of clonidine-induced sleep in chicks and clonidine-induced mydriasis in rats for the purpose of evaluating these methods as tests for demonstrating an in vivo alpha 2-adrenoceptor blocking effect of a novel compound. Clonidine-induced mydriasis was found to be the most selective method. The order of potency for compounds fully antagonizing clonidine-induced mydriasis was MSD 26 greater than physostigmine = idazoxan greater than aptazapine greater than piperoxan greater than yohimbine greater than mianserin greater than tolazoline. Partial antagonism was found for quipazine and sulpiride. Misleading results can arise from the involvement of cholinergic mechanisms in the control of the pupil diameter. The order of potency for compounds antagonizing clonidine-induced sleep in chicks was apomorphine greater than yohimbine greater than idazoxan greater than aptazapine = MSD 26 greater than quipazine greater than methysergide greater than piperoxan = mianserin = bepridil = metergoline = cyproheptadine = desipramine greater than tolazoline greater than dexchlorpheniramine, although antagonism was not complete for all of these compounds. Misleading results can arise from effects on arousal of the chicks but cholinergic mechanisms do not play a disturbing role so that the method with chicks can be a useful supplement to the mydriasis method. The enantiomers of mianserin and of a compound related to mianserin, Org 3770, were tested in the 2 methods and the alpha 2-blocking effect of these compounds was found to be residing in the S(+)-enantiomers.

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The data presented show that along with acid-peptic aggression an important role in pathogenesis of stress ulceration in the stomach and duodenum belongs to energy and immune deficiency which makes the correction of these alterations necessary. The timely and valuable conservative therapy including histamine H2-receptor blocking agents in addition to antacids and endoscopic electrocoagulation in case of profuse bleeding from stress ulcers allows to obtain hemostasis and healing of the ulcers more than in 90% of cases. When choosing the surgical method of treatment the preference should be given to atraumatic organ-preserving operations.

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Studies by the method of splenic exocolonies with serotonin receptor blockers methysergide and cyproheptadine showed that S2 receptors are involved in the stimulatory effect of serotonin on hemopoietic bone marrow stem cells.

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A 14.7 year-old boy had almost complete suppression of growth as a result of mild pituitary-dependent Cushing's disease. There was complete clinical remission during treatment with cyproheptadine (12 mg/day) and this was maintained when treatment was stopped after 18 months.

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The guinea-pig ileum longitudinal muscle-myenteric plexus preparation, preincubated with 3H-choline or 3H-noradrenaline, was mounted in an organ bath and superfused with Tyrode's solution. Alaproclate (2-(4-chlorophenyl)-1,1-dimethyl 2-aminopropanoate) (0.01-0.5 mmol/l) reduced (IC50 = 0.1 mmol/l) and at about 0.5 mmol/l completely blocked the electrically evoked 3H-acetylcholine secretion. The depressing effect of alaproclate (0.2 mmol/l) was not counteracted by atropine (0.01, 1 or 10 mumol/l), hexamethonium (0.1 mmol/l), phentolamine (1 mumol/l) yohimbine (1 mumol/l), haloperidol (1 mumol/l), 8-phenyltheophylline (10 mumol/l), cyproheptadine (1 mumol/l), metitepine (1 mumol/l), bicuculline (10 mumol/l), picrotoxinin (0.1 mmol/l), forskolin (25 mumol/l), 3-isobutyl-1-methylxanthine (5 mmol/l), nifedipine (1 mumol/l), verapamil (1 mumol/l), dilitiazem (1 mumol/l), high calcium (6 mmol/l), high potassium (10 or 15 mmol/l), tetraethylammonium (2 mmol/l), 4-aminopyridine (0.5 mmol/l), apamin (0.5 mumol/l), barium (0.5 mmol/l) or quinine (0.1 mmol/l). Among the potassium channel blockers tested only quinine (at 0.5 or 1 mmol/l), in the same manner as lidocaine, reduced the evoked secretion of 3H-acetylcholine. The results are in agreement with the hypothesis that the effect of alaproclate on the evoked 3H-acetylcholine secretion is not mediated by a neurotransmitter receptor, or a potassium channel sensitive to tetraethylammonium, 4-aminopyridine, apamin, or barium or quinine, but is due to a local anaesthetic effect. In contrast to the evoked secretion, the spontaneous release of 3H-acetylcholine was enhanced by high concentrations of alaproclate (0.4-1 mmol/l). The mechanism underlying the effect of alaproclate on the spontaneous release remains to be established. Alaproclate (0.25 or 0.5 mmol/l) also enhanced the spontaneous release and reduced the electrically evoked 3H-noradrenaline secretion.

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Nonsedating antihistamines (nsAHs) are recommended as first-line therapeutics for the treatment of mast cell-driven disorders, including allergic rhinitis and urticaria. However, their superiority over first-generation AHs (fgAHs) has recently been called into question, mainly because of the lack of supporting head-to-head therapeutic studies.

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This was a retrospective open-label study conducted to evaluate the safety and efficacy of cyproheptadine in children with refractory upper gastrointestinal symptoms (eg, nausea, early satiety, vomiting, retching after fundoplication, abdominal pain). Response was graded as resolution if symptoms resolved and medication was discontinued, as significant improvement if symptoms resolved with no further interventions, and as failure with any other outcome.

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Fenfluramine, an anorectic used in the treatment of obesity, in a final concentration of 1 mM strongly inhibited both phases of insulin release by the perfused rat pancreas. Insulin secretion resumed promptly after cessation of the drug infusion. This concentration of the drug markedly increased glucagon output. The blockade of alpha-adrenergic receptors and the use of antiserotonin agents did not alter the inhibitory effect of fenfluramine on insulin secretion. It is concluded that in the perfused rat pancreas 1 mM fenfluramine acutely inhibits glucose-induced insulin secretion and potentiates glucagon output. The direct effect of fenfluramine on insulin secretion is not related to alpha-adrenergic activity, nor is it mediated by serotonin.

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The effect of intestinal anaphylaxis on goblet cell mucus release was tested in rats immunized with small doses of egg albumin and alum and challenged intraduodenally with antigen. The alteration in vascular and mucosal permeability which accompanies intestinal anaphylaxis was reflected by increased retention of 125I-labelled rat serum albumin in gut wall segments and increased amounts of protein-bound radioactivity in the intestinal secretion from the segments. Intestinal goblet cell mucus was labelled in vivo with 35S. Infusion of antigen, into the duodenum of actively immunized rats led to the appearance of 35S-labelled high molecular weight glycoprotein, presumably of goblet cell origin, in the intestinal secretions. Goblet cell mucus release was dependent on the dose of antigen infused, was antigen-specific and was inhibited by pretreatment of rats with cyproheptidine. Enhanced release of goblet cell mucus was observed in normal rats prepared by intravenous injection of rat antiserum rich in IgE anti-egg albumin antibodies and challenged by intraduodenal infusion of antigen. Prior heating of the antiserum inhibited passive transfer of the reaction; this finding is consistent with the heat lability of IgE antibodies. The latter class of antibodies are presumed to be responsible for intestinal anaphylaxis and its associated mucus release in the model system examined.

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A rapid HPLC procedure for analytical quality control of pharmaceutical preparations containing the antihistaminic drug substance loratadine and/or its analog desloratadine (which is also an active metabolite of loratadine) was developed using a microemulsion as the eluent. The separation was performed on a column packed with cyanopropyl bonded stationary phase adopting UV detection at 247 nm using a flow rate of 1 ml/min. The optimized microemulsion mobile phase consisted of 0.1M sodium dodecyl sulphate, 1% octanol, 10% n-propanol and 0.3% triethylamine in 0.02 M phosphoric acid, pH 3.0. The developed method was validated in terms of specificity, linearity, lower limit of quantification, lower limit of detection, precision and accuracy. With the proposed method satisfactory resolution between loratadine and desloratadine (resolution factor=3.85). The method requires a minimum of sample handling and is rapid (10 min), and reproducible (R.S.D.<2.0%). The mean recoveries of the analytes in pharmaceutical preparations were in agreement with those obtained from a reference method, as revealed by statistical analysis of the obtained results using the Student's t-test and the variance ratio F-test. Pseudoephedrine, the co-formulated drug substance, did not interference with the assay and was successfully separated using the developed HPLC method.

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Mizolastine is a nonsedating H1 histamine receptor antagonist with additional antiallergic properties currently marketed in Europe for the treatment of seasonal and perennial allergic rhinitis (PAR) and urticaria.

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periactin syrup dosage 2016-06-02

Poisoning with opioid analgesics including tramadol represents a challenge. Tramadol may induce respiratory depression, seizures and serotonin syndrome, possibly worsened when in combination to benzodiazepines. Our objectives were to investigate tramadol-related neurotoxicity, consequences of diazepam/tramadol combination, and mechanisms of drug-drug interactions in rats. Median lethal-doses were determined using Dixon-Bruce's up-and-down method. Sedation, seizures, electroencephalography and plethysmography parameters were studied. Concentrations of tramadol and its metabolites were measured using liquid-chromatography-high-resolution-mass-spectrometry. Plasma, platelet and brain monoamines were measured using liquid-chromatography coupled to fluorimetry. Median buy periactin lethal-doses of tramadol and diazepam/tramadol combination did not significantly differ, although time-to-death was longer with combination (P=0.04). Tramadol induced dose-dependent sedation (P<0.05), early-onset seizures (P<0.001) and increase in inspiratory (P<0.01) and expiratory times (P<0.05). The diazepam/tramadol combination abolished seizures but significantly enhanced sedation (P<0.01) and respiratory depression (P<0.05) by reducing tidal volume (P<0.05) in addition to tramadol-related increase in respiratory times, suggesting a pharmacodynamic mechanism of interaction. Plasma M1 and M5 metabolites were mildly increased, contributing additionally to tramadol-related respiratory depression. Tramadol-induced early-onset increase in brain concentrations of serotonin and norepinephrine was not significantly altered by the diazepam/tramadol combination. Interestingly neither pretreatment with cyproheptadine (a serotonin-receptor antagonist) nor a benserazide/5-hydroxytryptophane combination (enhancing brain serotonin) reduced tramadol-induced seizures. Our study shows that diazepam/tramadol combination does not worsen tramadol-induced fatality risk but alters its toxicity pattern with enhanced respiratory depression but abolished seizures. Drug-drug interaction is mainly pharmacodynamic but increased plasma M1 and M5 metabolites may also contribute to enhancing respiratory depression. Tramadol-induced seizures are independent of brain serotonin.

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[3H]Loratadine was incubated with human liver microsomes to determine which cytochrome P450 (CYP) enzymes are responsible for its oxidative metabolism. Specific enzymes were identified by correlation analysis, by inhibition studies (chemical and immunoinhibition), and by incubation with various cDNA-expressed human P450 enzymes. Descarboethoxyloratadine (DCL) was the major metabolite of loratadine detected following incubation with pooled human liver microsomes. Although DCL can theoretically form by hydrolysis, the conversion of loratadine to DCL by human liver microsomes was not inhibited by the esterase inhibitor phenylmethylsulfonyl fluoride (PMSF), and was dependent on NADPH. A high correlation (r2 = 0.96, N = 10) was noted between the rate of formation of DCL and testosterone 6 beta-hydroxylation, a CYP3A-mediated reaction buy periactin . With the addition of ketoconazole (CYP3A4 inhibitor) to the incubation mixtures, the residual rate of formation of DCL correlated (r2 = 0.81) with that for dextromethorphan O-demethylation, a CYP2D6 reaction. Rabbit polyclonal antibodies raised against the rat CYP3A1 enzyme (5 mg IgG/nmol P450) and troleandomycin (0.5 microM), a specific inhibitor of CYP3A4, decreased the formation of DCL by 53 and 75%, respectively, when added to 1.42 microM loratadine microsomal incubations. Quinidine (5 microm), a CYP2D6 inhibitor, inhibited the formation of DCL approximately 20% when added to microsomal incubations of loratadine at concentrations of 7-35 microM. Incubation of loratadine with cDNA-expressed CYP3A4 and CYP2D6 microsomes catalysed the formation of DCL with formation rates of 135 and 633 pmol/min/nmol P450, respectively. The results indicated that loratadine was metabolized to DCL primarily by the CYP3A4 and CYP2D6 enzymes in human liver microsomes. In the presence of a CYP3A4 inhibitor, loratadine was metabolized to DCL by the CYP2D6 enzyme. Conformational and electrostatic analysis of loratadine indicated that its structure is consistent with substrate models for the CYP2D6 enzyme.

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The efficacy of montelukast alone vs montelukast-loratadine was studied in a 10-week, multicenter, randomized, double-blind, 2 x 2 crossover study. After a 2-week placebo run-in period, patients received montelukast sodium (10 mg) plus loratadine (20 mg), or montelukast sodium (10 mg) plus placebo once daily for 2 weeks. After a 2-week placebo washout period, patients were crossed over buy periactin to receive 2 weeks of the other active treatment regimen, followed by another 2-week placebo washout period.

periactin drug interactions 2016-11-28

Six hundred and eighty-eight SAR patients were randomized to receive fexofenadine HCl 120 mg, loratadine 10 mg or placebo, once daily for 2 weeks. The key parameters were the change from buy periactin baseline in: mean 24-h reflective total symptom scores (TSS); sum of four individual symptom scores, excluding nasal congestion; instantaneous TSS; individual symptom scores including nasal congestion; and Rhinoconjunctivitis Quality of Life Questionnaire (RQLQ). Adverse events were recorded.

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A reversed passive Arthus reaction was elicited in the rat pleural cavity. The kinetics of this inflammatory response indicate that exudate volume (cells and fluid) reaches a maximum level approximately 2 to 4 hr postantibody challenge. The neutrophil is the major cellular constituent of the pleural exudate during the first 12 hr of this reaction, reaching peak values at 4 hr; whereas, the monocyte predominates between 15 and 24 hr. Lymphocytes, eosinophils, and mast cells were also identified in the pleural exudates. The serotonin antagonists, cyproheptadine and methylsergide, and the antihistamine, chlorpheniramine, demonstrated marginal activity in the Arthus pleurisy model. The histamine antagonist, metiamide, was inactive. The nonsteroidal anti-inflammatory agents, flurbiprofen, ibuprofen, indomethacin, and benoxaprofen caused a modest suppression of exudate volume (18-32%) and cell accumulation (28-34%). The fluid and cellular components of the Arthus reaction were significantly inhibited by dexamethasone, triamcinolone, paramethasone, and prednisolone buy periactin . The oral gold preparation, auranofin, had a pronounced effect on exudate volume; whereas, other antirheumatic agents such as D-penicillamine, azathioprine, and chloroquine had no effect on the Arthus pleurisy reaction. The immunomodulator, levamisole, suppressed exudate volume, but had no effect on cell accumulation in the pleural cavity.

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The results are suggestive of a buy periactin high anti-inflammatory to sedation index of SUN-1334H among leading antihistamines.

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The flexor reflex of acute buy periactin (40-48 h after mid-thoracic spinal transection) and chronic (at least 2 months after transection) spinal rats was evoked by tetanic electrical stimulation of both hindfeet and recorded on a polygraph using a transducer connected to the left hindfoot. The flexor reflex in the chronic spinal rat was more responsive to electrical stimulation and to the actions of drugs studied than was the flexor reflex in the acute spinal rat. In chronic spinal rats, d-amphetamine, methoxamine, LSD, tryptamine, and 5-hydroxytryptophan (5-HTP) facilitated the flexor reflex and induced spontaneous movements. These facilitative effects were seen in acute spinal rats only when much larger i.p. doses of amphetamine, methoxamine, and LSD were used. Small i.v. doses of tryptamine also produced the facilitation. The facilitation caused by LSD and tryptamine, but not 5-HTP, in chronic spinal rats was antagonized by cyproheptadine. These observations suggest that chronic spinal rats were more sensitive to the drugs than acute spinal rats and support the hypothesis that the mode of action of LSD is similar to that of tryptamine but different from that of 5-HTP since cyproheptadine antagonized the facilitative effects of LSD and tryptamine but not those of 5-HTP.

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The involvement of adrenergic, serotonergic and cholinergic mechanisms in the diurnal surge of plasma prolactin (Prl) secretion has been examined using ovariectomized, polyestradiol phosphate-treated (PEP) rats bearing aortic catheters. An afternoon surge in plasma Prl was observed to peak at 15.00 h buy periactin and 17.00 h followed by declining levels at 19.00 and 21.00 h. This pattern was observed between 5 and 21 days after PEP administration. The alpha-adrenergic blocker, phenoxybenzamine (Phenox), completely prevented the Prl surge. The beta-blocker, propranolol (Propra), appeared to delay the onset and intensity of the diurnal Prl surge so that maximum levels were observed at 19.00 and 21.00 h. The serotonergic blocker, methysergide (MES), delayed the maximum diurnal Prl level until 21.00 h, while cyproheptadine (Cypro), another serotonergic blocker, significantly inhibited the surge. The muscarinic cholinergic agonist, arecoline (Arec), when administered at 12.00 h, delayed the surge, while the repeated administration of Arec completely blocked the surge. Atropine (Atro) (10 m/kg at 12.00 h and 5 mg/kg every 2 h thereafter) did not have any effect on the Prl surge, but when administered simultaneously with Arec, prevented the inhibitory effect of Arec on Prl release. The data suggested that the adrenergic and serotonergic systems have a positive input in the occurrence and magnitude of the surge and that the cholinergic system does not appear to have a physiologic role in tonically inhibiting Prl release, but may function under certain special conditions.

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Rupatadine fumarate is a second-generation antihistamine provided with a potent, long-lasting and balanced in vivo dual platelet-activating factor (PAF) and histamine antagonist activity and buy periactin it uniquely combines both activities at a high level of potency. Rupatadine has a rapid onset of action and a long-lasting effect, so a once-daily dosing is permitted, moreover is well tolerated by young adults and the elders. Rupatadine does not present the side effects of first-generation H1-antihistamines, such as somnolence, fatigue, headache, impaired memory and learning, sedation, increased appetite, dry mouth, dry eyes, visual disturbances, constipation, urinary retention and erectile dysfunction.

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While capable of inhibiting histamine and LTC(4) release by human basophils, desloratadine is buy periactin more effective at targeting the signals regulating IL-4 and IL-13 generation in these cells. This inhibitory effect on cytokine generation provides additional evidence that this antihistamine exerts anti-inflammatory properties.

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This study consists of 40 patients (28 females, 12 males, mean age 29.8 years; range 17 to 44 years) referred to ear, nose, and throat outpatient clinic between May 2010 and September 2010. A six-week randomized, double-blind, cross-sectional study was performed in two arms: In group 1, 20 patients received desloratadine (5 mg/d) alone; in group 2, 20 patients received desloratadine (5 mg) plus montelukast (10 mg) combination therapy. Quality of life was assessed on the day before starting treatment and buy periactin on the last day of each treatment period using the Rhinoconjunctivitis Quality of Life Questionnaire and Nighttime Symptom Scores.

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These results indicate that hydroxyzine is more effective than nsAHs when given as recommended in suppressing histamine-induced or allergic skin reactions. Our results suggest that higher doses of nsAHs than those currently recommended are required for the treatment of skin responses to obtain antihistaminic buy periactin and antiallergic effects that are equivalent to those of fgAHs.

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Rats were trained to discriminate between saline and either 0.3, 1.0, 3.0 or 6.0 mg/kg of diazepam in a two-choice, discrete-trial avoidance procedure. Diazepam, chlordiazepoxide, flurazepam and pentobarbital occasioned dose-related increases in diazepam-appropriate responding in all four training dose groups. Increasing the training dose of diazepam from 0.3 to 1.0 mg/kg resulted in approximately a 3-fold shift to the right in the dose-effect curves for each of these four drugs. However, increasing the training dose to 3.0 or 6.0 mg/kg did not result in additional, concomitant shifts in these dose-effect curves. Moreover, the dose-effect curves of nine additional benzodiazepine analogs also did not differ markedly in rats trained with either 1.0 or 3.0 mg/kg of diazepam. The nonbenzodiazepines ethanol, phencyclidine, cyproheptadine and ketocyclazocine failed to produce diazepam-like discriminative stimuli in rats trained with either 0.3, 1.0 or 3.0 mg/kg of Paracetamol Maximum Dose diazepam. In rats trained with 1.0 mg/kg of diazepam, Ro 11-6896, but not its inactive stereoisomer Ro 11-6893, occasioned diazepam-appropriate responding. Furthermore, the selective benzodiazepine antagonist CGS8216 blocked the effects of diazepam but not the diazepam-like effects of pentobarbital. These results demonstrate that the discriminative effects of diazepam are qualitatively similar across this 20-fold range of training doses; quantitatively, the discriminative effects of diazepam appear to reach a maximum and plateau above a training dose of 1.0 mg/kg in rats.(ABSTRACT TRUNCATED AT 250 WORDS)

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The intracerebroventricular (icv) administration of histamine but not N-telemethylhistamine and 1-methyl-4-imidazole acetic acid induced catalepsy in mice. Histamine H1-receptor blockers such as cyproheptadine, mepyramine and diphenhydramine reduced histamine-induced catalepsy. However, astemizole which is known to be without central effects, did not reduce histamine-induced catalepsy. The icv pretreatment with histamine H2-receptor blockers, such as metiamide and cimetidine, also had no effect. Moreover, various antidepressants, both imipramine- and atypical-type drugs Sinemet 200 Mg antagonized histamine-induced catalepsy to various degrees in this experiment. Thus, the induction of catalepsy by icv administration of histamine was mediated through histamine H1-receptors, and suggested that antidepressants reduced histamine-induced catalepsy via this mechanism. Histamine-induced catalepsy is a possible new animal model of depression which can also be used for evaluation of atypical antidepressants.

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In the rabbit, intracerebroventricular administration of dibutyryl cyclic AMP (DBC) produces fever which is selectively antagonised by phenoxybenzamine. This indicates the involvement of central Zetia Tablets alpha-adrenoceptors in DBC-induced fever. The decrease in DBC hyperthermia after 6-hydroxydopamine (6-OH-DA) supports the viewpoint that DBC-induced fever is dependent on the presence of noradrenaline (NA) in the central nervous system. The accentuation of NA hyperthermia by theophylline suggests that NA fever may be mediated by cAMP. It is unlikely that DBC-induced hyperthermia in the rabbit is mediated via prostaglandins since indomethacin does not inhibit this response to DBC.

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A retrospective review of the psychiatric records of nine patients with posttraumatic stress disorder (PTSD) was conducted to determine the efficacy of cyproheptadine in relieving nightmares. The treatment dose was 4 to 12 mg at Strattera Positive Reviews bedtime. The response varied from complete remission to a decrease in the intensity and frequency of nightmares.

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Although corticosteroids are the mainstay Flagyl 600 Mg of treatment in allergic rhinitis, montelukast may be considered as an additional agent especially in treatment of patients with impaired quality of life and it may be used to reduce nasal symptom scores.

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A 5mg oral dose Effexor Tablets of desloratadine once daily for 10 days.

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A retrospective cohort study of injury was carried out in 12,106 patients whose initial antihistamine prescription was for diphenhydramine and in 24,968 patients whose initial antihistamine prescription was for loratadine. Data were taken from a health care claims database that included employees, dependents, and retirees who filed claims from January 1991 through December 1998. Rates of six serious injuries in the diphenhydramine cohort after and before the first prescription were compared with rates in the loratadine cohort after and before the first prescription.

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Cocaine (2.5-10 mg/kg) caused a dose-related increase in the amplitude of the acoustic startle reflex in rats. In contrast, procaine (5-40 mg/kg) caused a dose-related decrease in startle, indicating that the effects of cocaine could not be ascribed to its local anesthetic effects. Cocaine's excitatory effects were blocked by pretreatment with haloperidol (0.5 mg/kg) but not by cyproheptadine or prazosin. The excitatory effects of cocaine (10 mg/kg) were markedly attenuated by pretreatment with reserpine (5 mg/kg 24 and 18 h earlier) but not by alpha-methyl-p-tyrosine (100 mg/kg 1 h earlier). In contrast, comparably sized excitatory effects of d-amphetamine were blocked by alpha-methyl-p-tyrosine and greatly enhanced by pretreatment with reserpine. Neither pretreatment blocked excitatory effects of apomorphine on startle. The data indicate that cocaine increases startle by acting through reserpine-sensitive pools of dopamine and provide further support for the conclusion that acoustic startle is enhanced by activation of dopamine receptors.

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Ebastine (CAS 90729-43-4), cetirizine (CAS 83881-51-0) and loratadine (CAS 79794-75-5) are second generation H1-antihistamines of proven efficacy for treating allergy. Recent clinical studies have found ebastine to be more effective than cetirizine or loratadine in alleviating the symptoms of seasonal allergic rhinitis. The objective of this study was to compare the efficacy of these compounds in three guinea-pig modeles of bronchoconstriction, elicited either by histamine, allergen or leukotriene C4 in order to shed light onto the mechanisms that might explain differences found in clinical studies. In the present experiments, ebastine and cetirizine were equipotent against aerosol histamine-induced bronchospasm in guinea pigs (ED50 115 and 100 micrograms/kg p.o., respectively), while loratadine was three-fold less potent. In the same model the effects of ebastine, loratadine and cetirizine lasted 21, 19 and 15 h, respectively. Ebastine (ED50 334 micrograms/kg p.o.) was the most potent compound in inhibiting allergen-induced bronchospasm in conscious guinea pigs. In vitro studies in tracheally perfused guinea pig lungs demonstrated that ebastine and loratadine inhibited with equal potency the bronchoconstriction induced by leukotriene C4 whilst cetirizine was significantly less potent. Finally, in another in vivo study, ebastine reverted the changes in pulmonary resistance induced by leukotriene C4 in anaesthetised guinea pigs, whereas cetirizine and loratadine were devoid of activity in this model. In accordance with the clinical data, ebastine proved to be the substance with the widest range of application in animal experiments, too.

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Patient eyes treated with Patanol were significantly less itchy than those treated with systemic Claritin alone at critical time points 3, 7, and 10 minutes after the onset of action challenge (p < 0.05), and at 3 and 7 minutes after the duration of action challenge (p < 0.05).

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Headshaking may have many causes. A large subset of horses have similar clinical signs including shaking the head in a vertical plane, acting as if an insect were flying up the nostrils, and rubbing the muzzle on objects. Seasonality and worsening of clinical signs with exposure to light are also common features of this syndrome. Geldings and Thoroughbreds appear to be overrepresented. Cyproheptadine treatment was beneficial in more than two thirds of treated horses.