Trandate is used to treat severe high blood pressure (hypertension). Lowering high blood pressure Trandate helps prevent strokes, heart attacks and kidney problems.
Other names for this medication:
Also known as: Labetalol.
Trandate is a drug which is used for treating high blood pressure. It is related to carvedilol (Coreg). Nerves that are part of the adrenergic nervous system travel to most arteries where they release an adrenergic chemical norepinephrine. The norepinephrine attaches to receptors on the muscles of the arteries and causes the muscles to contract, narrowing the arteries, and increasing the blood pressure. Trandate blocks receptors of the adrenergic nervous system. When Trandate attaches to and blocks the receptors, the arterial muscles relax, and the arteries expand, resulting in a fall in blood pressure.
Generic name of Trandate is Labetalol.
Trandate is also known as Labetalol, Normodyne.
Brand name of Trandate is Trandate.
Take this medicine with food or milk.
If you want to achieve most effective results do not stop taking Trandate suddenly.
If you overdose Trandate 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, light and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.
The most common side effects associated with Trandate are:
Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.
Do not take Trandate if you are allergic to Trandate components.
Be careful with Trandate if you're pregnant or you plan to have a baby, or you are a nursing mother.
Be careful with Trandate if you have a history of liver problems, heart problems, pheochromocytoma, diabetes, any allergies.
Do not take Trandate if you have a lung disease (asthma, COPD), advanced heart block, severe bradycardia, severe heart failure, post-CABG surgery.
This drug may make you dizzy for up to 3 hours after it is given. You should remain lying down during this time period in order to prevent falls.
You should get up slowly when rising from a seated or lying position.
Be very careful if you are driving machine.
Diabetic patients should be careful with Trandate.
Do not stop taking Trandate suddenly.
Dynamic forearm exercise was performed in healthy subjects before and after intravenous labetalol, 1 mg/kg body weight. Labetalol produced a sustained fall in arterial blood pressure. Forearm blood flow decreased by 17.2% partly due to the reduced driving pressure and partly due to an increased vascular resistance. Forearm oxygen uptake decreased by 14.6%, suggesting an increased mechanical efficiency. Lactate release from the exercising forearm decreased by 17.6%. Forearm uptake of glucose and free fatty acids remained unchanged.
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High blood pressure (BP) complicates approximately 10% of all pregnancies. Hypertension in pregnancy falls into four categories: (1) preeclampsia-eclampsia, (2) chronic hypertension of whatever cause, (3) preeclampsia-eclampsia superimposed to chronic hypertension or renal disease, and (4) transient or late hypertension (gestational hypertension). Preeclampsia, the association of hypertension, proteinuria, and edema, accounts for more than 50% of all the hypertensive disorders of pregnancy and is a major cause of fetal and maternal morbidity and mortality. Unfortunately, distinguishing between preeclampsia and other causes of hypertension on clinical grounds can be difficult because of the lack of specific tests for differential diagnosis. Increased vascular resistance has been claimed as the primary cause of preeclampsia; however, a variable hemodynamic profile with relatively high cardiac outputs, normal filling pressures, and inappropriately high systemic vascular resistances is now reported by most investigators. Imbalance between vasodilator and vasoconstrictor eicosanoids may account for platelet activation and increased responsiveness to pressor peptides. Altered prostacyclin (PGI2) to thromboxane A2 (TxA2) ratio in maternal uteroplacental vascular bed may favor local platelet activation and vasoconstriction contributing to placental insufficiency and fetal distress. Alternatively, recent evidence seems to suggest that fetal umbilical placental circulation may be the site of the primary vascular injury. Whether low-dose aspirin prevents preeclampsia because it inhibits the excessive maternal TxA2 or whether the partial inhibition of fetal TxA2 is also of therapeutic value remains to be established. Treatment of severe hypertension in pregnancy is probably important to prevent cardiac failure or cerebrovascular accidents in the mother. The need for pharmacological therapy of mild to moderate hypertension is still debated, since no formal studies are available to clarify whether pharmacological treatment in such instances effectively reduces maternal or fetal risk. For the treatment of preeclampsia, hydralazine and nifedipine may be used when delivery is not applicable. Labetalol and diazoxide are effective for hypertensive emergencies. Life-threatening hypertension that does not respond to more conventional therapy is an indication for the use of sodium nitroprusside. For chronic hypertension, alpha-methyldopa remains the treatment of choice; if ineffective, hydralazine or beta-blockers are suitable. Effectiveness and safety of other molecules remain elusive.
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The alpha- and beta-blocking effects of labetalol are such that during and following exercise the haemodynamic benefits of beta-blockade outweigh the unfavourable effects, because the latter are diminished by the concomitant minor degree of alpha-blockade.
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Much more stable hemodynamic parameters during surgery in patients treated with remifentanil; labetalol was administered in 10% of patients in group F; no significant differences as regards the adverse effects and VAS. Faster awakening time was obtained in the remifentanil group as compared with the fentanyl group.
This 32-yr-old man presented with uncontrolled hypertension for a few years for which he was treated with nifedipine. He subsequently defaulted follow-up. The patient presented again approximately three months from the day of surgery and was diagnosed to have a pheochromocytoma. The endocrinologist prescribed phenoxybenzamine and propanolol in addition to the nifedipine but the patient stopped taking both drugs six weeks prior to surgery due to their side effects. The patient was admitted the evening before surgery to the intensive care unit for rapid control of his blood pressure. Blood pressure was optimized with an infusion of labetolol and volume expansion titrated under central venous catheter and intraarterial blood pressure guidance throughout the night. On the morning of surgery, a magnesium sulfate infusion was started. The laparoscopic surgery proceeded uneventfully and the patient was hemodynamically stable. There were two transient periods of hypotension after induction and at removal of tumour respectively which were corrected with a brief adrenaline infusion. No adverse outcome was noted.
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Two simple and sensitive spectrofluorimetric methods have been developed for the determination of labetalol (LBT). In method A, the native fluorescence was measured at 432 nm after excitation at 312 nm. The second method (method B) is based on the formation of a ternary complex between zinc (II), eosin and LBT. The fluorescence intensity of the ternary complex was measured at 452 nm after excitation at 317 nm. Optimum conditions for the determination were also investigated. The linear range and detection limit for method A and B were found to be 1.25-30 µg/ml; 0.24 µg/ml and 0.5-4 µg/ml; 0.08 µg/ml, respectively. The proposed methods are simple, practical and relatively free of interference from coexisting substances. The methods have been applied to assess LBT in commercial tablets and human urine samples with good precision and accuracy.
The effects of atropine administration during anticholinesterase poisoning on heart rate, blood pressure and electrocardiographic changes (ECG) were studied in the cat. Administration of atropine intravenously during anticholinesterase poisoning caused a significant increase in heart rate and blood pressure; ECG changes were also seen. The simultaneous intravenous administration of atropine and labetalol during anticholinesterase poisoning abolished the increase in blood pressure and heart rate; ECG readings remained normal. It is suggested that labetalol may be a useful adjuvant in the treatment of anticholinesterase poisoning especially in patients with compromised heart function.
The clinical effects, the exercise test answer, the left ventricular function by polygraphyc test after administration at middle term of Metoprolol and Labetalol have been evaluated in 20 patients with moderate and non complicated essential hypertension. The study was a double blind cross-over between Metoprolol and Labetalol (270 mg/die per os). Both drugs induced a reduction of PAOS and PAOD. The exercise test induced in all patients a decrease of PAOS and PAOD, showing an improvement of strain tolerance. The normalization of PEP and non modification of LVET seem to confirm that the treatment with Metoprolol and with Labetalol, neither induces significant modification of left ventricular function.
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There were no differences in blood loss and quality of surgical field among the study groups. Patients in the hypocapnia group demonstrated the highest, and in the hypercapnia group, the lowest, requirements for remifentanil, labetalol, and administration of the antihypertensive medications in general. The computed tomography-graded severity of sinonasal disease and duration of surgery were the only independent predictors of intraoperative blood loss.
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This is a case of a 28-yr-old man who underwent general anaesthesia for emergency repair of a right lid laceration and lacrimal apparatus. Following induction of anaesthesia and local nasal application of phenylephrine (0.25%) he developed transient elevation of blood pressure, which was treated immediately with labetalol. Subsequently the patient developed acute pulmonary oedema which responded to treatment with morphine and furosemide. The diagnosis of pulmonary oedema was confirmed by blood gas studies, chest x-ray and serial echocardiograms. Subsequent investigation revealed that he was a cocaine user, as the urine tested positive for cocaine. Considering that the patient was young and otherwise healthy and that the hypertension was transient, it is unlikely that phenylephrine was the main cause of pulmonary oedema. Cardiac morbidity was most likely precipitated by the interaction of phenylephrine-induced hypertension with a cocaine-depressed myocardium.
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Vagal stimulation is preferentially central and directly linked to the electric excitation of the lateral dorsal motor nucleus of the vagus nerve. Younger patients with no cardiac history are more at risk. This could be explained by the fact that juvenile tissue conducts electricity more rapidly than senescent (the difference being probably due to the fibrosis and adipose tissue which reduce its conductive capacity). Finally, it is appropriate to question the direct therapeutic aspect of vagal stimulation which constitutes an experimental treatment of resistant depression.
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A zone of hypoperfusion surrounding acute intracerebral hemorrhage (ICH) has been interpreted as regional ischemia. To determine if ischemia is present in the periclot area, the authors measured cerebral blood flow (CBF), cerebral metabolic rate of oxygen (CMRO2), and oxygen extraction fraction (OEF) with positron emission tomography (PET) in 19 patients 5 to 22 hours after hemorrhage onset. Periclot CBF, CMRO2, and OEF were determined in a 1-cm-wide area around the clot. In the 16 patients without midline shift, periclot data were compared with mirror contralateral regions. All PET images were masked to exclude noncerebral structures, and all PET measurements were corrected for partial volume effect due to clot and ventricles. Both periclot CBF and CMRO2 were significantly reduced compared with contralateral values (CBF: 20.9 +/- 7.6 vs. 37.0 +/- 13.9 mL 100 g(-1) min(-1), P = 0.0004; CMRO2: 1.4 +/- 0.5 vs. 2.9 +/- 0.9 mL 100 g(-1) min(-1), P = 0.00001). Periclot OEF was less than both hemispheric OEF (0.42 +/- 0.15 vs. 0.47 +/- 0.13, P = 0.05; n = 19) and contralateral regional OEF (0.44 +/- 0.16 vs. 0.51 +/- 0.13, P = 0.05; n = 16). In conclusion, CMRO2 was reduced to a greater degree than CBF in the periclot region in acute ICH, resulting in reduced OEF rather than the increased OEF that occurs in ischemia. Thus, the authors found no evidence for ischemia in the periclot zone of hypoperfusion in acute ICH patients studied 5 to 22 hours after hemorrhage onset.
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Hypertensive emergencies, though uncommon in children, are potentially life threatening. While targeting blood pressure reduction to below the 90th percentile for age, gender and height, mean arterial blood pressure should be gradually lowered by one-fourth of the planned reduction over 8-12 h, a further fourth over the next 8-12 h, and the final 50% over the 24 h after that. Frequent invasive or non-invasive blood pressure monitoring is essential, as is monitoring for sensorial alteration and loss of papillary reflexes. Few antihypertensive agents have been examined in children. Continuous intravenous infusions of short acting drugs such as nitroprusside, labetalol and nicardipine are preferred to intravenous boluses of hydralazine or diazoxide. If severe symptoms are absent, oral agents such as nifedipine, clonidine, minoxidil, hydralazine, labetalol, captopril, and prazosin may be used. Nicardipine and labetalol are particularly suited in emergencies with intracranial bleeding or ischemic stroke, while furosemide, sodium nitroprusside and nitroglycerine are useful in congestive cardiac failure. Therapy with oral antihypertensive drugs should be instituted within 6-12 h of parenteral therapy, and the latter gradually withdrawn over the next 12-48 h. Oral agents have limited application as primary therapy, except when administration of intravenous infusion is likely to be delayed. This article provides a summary of the clinical approach to evaluation and management of severe symptomatic hypertension in children.
The effects of labetalol, an alpha- and beta-adrenoceptor blocking drug, on blood pressure, heart rate, plasma renin activity (PRA) and plasma aldosterone were studied in 17 adult patients with essential hypertension. Following a total dose of 1 g labetalol administered over a 48-hour period, there was a rapid and significant fall in systolic and diastolic BP averaging 16,5 +/- 7,9%/14,8 +/- 7,5% respectively supine, 18,7 +/- 8,3%/17,8 +/- 7,2% standing and 23,9 +/- 7,1%/16,8 +/- 10,3% after moderate exercise; 24 hours after labetalol was discontinued, the BP had gone up but was still below pretreatment values. Bradycardia remained slight throughout. During treatment a significant decrease in PRA (mean : 45%) was observed in all patients and found to correlate in standing position with changes in standing and post-exercise mean arterial pressure. There was no significant changes in plasma aldosterone. Side-effects were mild and limited to tingling of the scalp in 5 patients. No clinical symptoms of postural hypotension were recorded.
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While there is general agreement on the natural history, pathology, and pathophysiology of hypertension, there continues to be controversy over the selection of specific antihypertensive agents. All antihypertensive agents will, by definition, lower blood pressure, and factors beyond side effects and other difficulties associated with therapy form the basis of selecting specific agents. One of these factors is the effect of a given drug on core organ function. Propranolol was the first beta-adrenoceptor-blocking agent introduced for the treatment of hypertension. Initiation of therapy with propranolol may result in a decline in blood pressure more at the expense of cardiac function due to a concomitant rise in total peripheral resistance. Furthermore, propranolol may result in a decline in both glomerular filtration rate (GFR) and renal blood flow (RBF). In contrast, cardioselective beta-blockers or those with intrinsic sympathomimetic activity may not adversely affect renal function. It had been predicted that nadolol, a noncardioselective beta-blocker without intrinsic sympathomimetic activity, should result in decreased renal function. In contrast, observations demonstrated a preservation or improvement in both RBF and GFR, suggesting the presence of an alternative effective mechanism. Recent additions to the beta-adrenolytic group of antihypertensive agents include drugs with concurrent beta-blockade and vasodilation. This vasodilatation may be achieved through agonist properties resulting in lesser increases in vasomotor tone and smaller, if any, decreases in cardiac output. Alternatively, vasodilation may be achieved by concomitant alpha-adrenoceptor blockade, such as with labetalol. This agent preserves GFR and RBF during therapy of hypertension, in patients with normal as well as diminished renal function and hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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There is a major controversy over the relative value of anti-hypertensive drugs in hypertension in pregnancy. Our purpose was to study two different beta-adrenolytic drugs, atenolol, a cardioselective beta blocker, and labetalol, an alpha-beta blocker. Fifty-six hypertensive (BP greater than 140/90 mmHg) pregnant women were treated either with atenolol or labetalol. The patients were divided into two subgroups for which there were no statistical differences with regard to age, number of previous pregnancies, initial level of blood pressure and uricemia, proteinuric pre-eclampsia, beginning of therapeutic trial and delivery. The average daily dosage was 144.6 +/- 47.8 mg day-1 with atenolol and 614 +/- 47.8 mg day-1 with labetalol. This study shows: the same anti-hypertensive effect of the two drugs with control of blood pressure in 82% of the cases; a birth-weight significantly higher with labetalol (3280 +/- 555 g) than with atenolol (2750 +/- 630 g) (P less than 0.001); two still-births with atenolol; no adverse effects of the drugs during pregnancy and the neo-natal period; the trans-placental passage of atenolol and labetalol as shown by plasma dosages in the mothers and the new-born. It is concluded that atenolol and labetalol are safe and they are usually effective in the control of the hypertension complicating pregnancy. But labetalol appears to be better able to prevent the appearance of fetal growth retardation.
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Cardiac phaeochromocytoma is a rare cause of endocrine hypertension. We report a case of a 25-year-old woman, who presented with severe hypertension and intermittent chest pain. The patient denied typical phaeochromocytoma spells of palpitation, headache, and diaphoresis. The 24-hr urinary excretion of norepinephrine was increased sevenfold above the upper limit of normal; however, the excretion of total metanephrines, epinephrine, and dopamine were normal. Computed tomography (CT) scan of the abdomen was normal. An 131I-labelled metaiodobenzylguanidine (MIBG) scan was falsely negative while the patient was taking labetalol. The cardiac phaeochromocytoma was localized with indium-111-pentetreotide scintigraphy and chest magnetic resonance imaging scan. Repeat 123I-MIBG scintigraphy was positive after discontinuing labetalol. The cardiac phaeochromocytoma was located in the right atrial groove, adjacent to the tricuspid valve, and contained multiple feeder arteries from the right coronary artery. After treatment with volume expansion, alpha-methyl-p-tyrosine, and alpha- and beta-adrenergic blockade, surgical resection was performed. While under cardiopulmonary bypass, coronary bypass grafting and tricuspid annuloplasty were performed to facilitate the complete surgical resection of the 4.5-cm tumour. The surgical course was uncomplicated, with complete cure of hypertension and normalization of catecholamine excretion. Post-operative cardiac function, as measured by echocardiogram, was normal. Although cardiac phaeochromocytoma may be highly vascular, invasive and difficult to resect, it can be cured.
Blood pressure (BP) elevations may correspond to different clinical situations. Hypertensives emergencies are situations that require immediate reduction in BP because of acute or rapidly progressing target organ damage: accelerated malignant hypertension, hypertensive encephalopathy, acute myocardial infarction, acute aortic dissection, acute left ventricular failure, and eclampsia. Hypertensive urgencies are those with marked elevated BP in which it is desirable to reduce BP progressively within few hours, such as severe hypertension, progressive target organ damage, perioperative hypertension. Cerebrovascular accidents have to be individualized. In most patients in the immediate post-stroke period, BP should not be lowered. Caution is advised in lowering BP in these patients because excessive falls may precipitate cerebral ischemia. In situations without symptoms or progressive target organ it is necessary to exclude proximate causes of elevated BP such as pain and elevated BP alone rarely requires antihypertensive treatment. Among parenteral antihypertensive (AH) drugs labetalol, nicardipine, urapidil, and nitroprussiate are generally used, and the choice of AH drug depends on the clinical situation. It is not required to normalize BP immediately but to reduce mean BP no more than 25%, then toward 160/100 mmHg as recommended by JNC VI, in order to avoid an impairment of renal, cerebral or coronary ischemia. Oral long-acting dihydropyridines are often subsequently administrated, except in myocardial ischemia. Therapeutic attitudes vary considerably according to the clinical situation: abstention, immediate decrease or progressive decrease in BP have to be decided.
We explored the sympatholytic property of dexmedetomidine, especially its role in intraocular pressure (IOP) reduction, haemodynamic stability, and attenuation of extubation response.
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The incidence of perioperative stroke was 55 of 57,218 (0.09%). Preoperative metoprolol was associated with an approximately 4.2-fold increase in perioperative stroke (P < 0.001; 95% CI, 2.2-8.1). Analysis of matched cohorts revealed a significantly higher incidence of stroke in patients taking preoperative metoprolol compared with atenolol (P = 0.016). However, preoperative metoprolol was not an independent predictor of stroke in the entire cohort, which included patients who were not taking β blockers. The use of intraoperative metoprolol was associated with a 3.3-fold increase in perioperative stroke (P = 0.003; 95% CI, 1.4-7.8); no association was found for intraoperative esmolol or labetalol.
Rhinoplasty is one of the most common surgeries of the plastic surgery and as well as ear, throat and nose. Intra-operative bleeding during surgery is one of the most important factors that may impair the surgeon's job. Providing a clean blood-free surgical filed makes the operation faster, easier and with a better quality. One way to achieve this goal is to induce hypotension. This study aimed to compare the impacts and outcomes of administration of labetalol or nitroglycerin for this purpose.
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Preeclampsia is an exaggerated maternal inflammatory state with over-expression of placental soluble fms-like tyrosine kinase 1 (sFlt-1). It is also associated with shallow trophoblast invasion and inadequate transformation of uterine spiral arteries. Antihypertensive drugs administrated in preeclampsia to control blood pressure have been reported to regulate placental and circulating cytokine production from women with preeclampsia. Whether they could modulate the interaction between trophoblast and endothelial cells are not investigated.
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1 Nineteen pregnant patients whose mean arterial pressure (MAP) was persistently greater than or equal to 103.3 mmHg were given labetalol or methyldopa. 2 Singificant falls (P less than 0.001) in BP only occurred in the group treated with labetalol, and daily BP control was better in this group. 3 Two severely hypertensive patients were successfully treated with intravenous labetalol. 4 There was a higher incidence of spontaneous labour in the labetalol group and a significant difference (P less than 0.05) in the Bishop score of the cervix between the two groups. 5 There were no apparent detrimental effects on the foetus antenatally, during labour or post partum. 6 Slight breathlessness in one patient treated with labetalol was the only side-effect observed but drowsiness, headache and postural hypotension were reported in patients receiving methyldopa.
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Drug-induced sexual dysfunction is well known to occur with antihypertensive drugs in men. There are much less data on the effects of drugs on female sexual function. The physiology of the female sexual response has similarities to that of the male sexual response and there are therefore good reasons for suspecting that antihypertensive drugs are likely to adversely affect sexual function in women. Present evidence suggests that clonidine, methyldopa, guanethidine and reserpine are associated with adverse effects on sexual function. In healthy volunteers, labetalol appears to reduce vaginal lubrication, but there are no studies in patients receiving the drug therapeutically. Thiazide diuretics may be associated with the worsening of sexual problems, which interestingly appear to be ameliorated by weight reduction. Present evidence on the effects of vasodilators is limited but the evidence suggests that sexual function in women receiving calcium antagonists is not altered by changing to an angiotensin converting enzyme (ACE) inhibitor. Although present evidence suggests that effects on female sexual function may not be very great, it should be recognised that there are very few data in this area. Further work is clearly necessary.
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A total of 1184 consecutive adults with acute severe hypertension (systolic blood pressure [SBP] ≥ 180 mm Hg, diastolic blood pressure ≥ 110 mm Hg), without a neurologic reason for admission, receiving two or more intermittent intravenous antihypertensive doses or a continuous intravenous infusion within 24 hours of hospitalization.
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