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.
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With infusion of labetalol and remifentanil after a bolus dose we can induce effective controlled hypotension under general anesthesia. Remifentanil is a short-acting narcotic drug; then, patient satisfaction was better and recovery time was shorter. From the economic aspect, labetalol prefers to remifentanil.
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Eleven patients with essential hypertension participated in a double-blind cross-over comparison of labetalol (L) and propranolol (P). Each drug was given for 5--8 weeks. The dose reducing the supine diastolic blood pressure when given b.d. to or below 90 mm Hg was titrated out. At the end of each period, isometric exercise (sustained handgrip) and calf plethysmography were performed. L (mean daily dose 636 mg) was slightly more effective in lowering supine and standing blood pressure than P (mean dose 276 mg). There was no significant difference between the drugs in their effect on the blood-pressure response to handgrip. However, compared with no treatment, L attenuated the blood-pressure rise at near-maximal handgrip; this has not been reported with other beta-blockers. Resting vascular resistance and basal vascular tone were significantly lower (20%, p less than 0.05) during treatment with labetalol than when the patients were taking propranolol. - The differences may be explained by the alpha-receptorblocking action of labetalol.
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This study investigated the influence of gestational diabetes mellitus on the kinetic disposition and stereoselective metabolism of labetalol administered intravenously or orally.
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Stereoselective interaction of drugs with human serum transferrin in capillary zone electrophoresis is described. The substances passed a pseudo-stationary protein zone applied in a coated capillary and the possible chiral separation of the optical isomers was followed. Drugs with different structures were screened and the enantiomers of bupivacaine, propranolol and promethazine as well as the diastereomers of labetalol were resolved. Racemic mixtures of atenolol and pindolol enantiomers could not be resolved under these conditions.
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The beta-blockers in clinical use have been classified into 2 major divisions, nonselective or selective agents, and those with or without intrinsic sympathomimetic activity (ISA). These properties confer differing pharmacological properties with some relevance to the treatment of hypertension. A beta-blocker with significant beta 2-ISA can be regarded as a multiple-action drug. A third division of beta-blockers is a newer development; these agents, besides blocking the beta-receptor, possess important peripheral vasodilator activity. Labetalol was the first drug of this group and prizidolol followed, but has been withdrawn because of toxicity. Several other agents now under evaluation include bucindolol and medroxolol, and carvedilol and dilevalol (1 of the isomers of labetalol), which have been the most widely studied in hypertension. Combined action results in important haemodynamic differences compared with pure beta-blockade. Notably, peripheral resistance is reduced, and there is less reduction in, or no effect on, cardiac output. The 3 following mechanisms have been described as responsible for peripheral vasodilatation: alpha-receptor blockade, beta 2-agonism, and a dilator action independent of either the alpha- or beta-receptors. Evidence for these various mechanisms is more readily obtainable from animal experiments, but some confirmatory evidence has been obtained in man. Inhibition of alpha-stimulation has been found with labetalol and to a small degree with medroxalol and carvedilol. beta 2-Mediated vasodilatation has been shown by dilevalol and medroxolol, and evidence of vasodilatation independent of alpha- or beta-receptors has been obtained with carvedilol. More evidence is required to confirm the exact contribution of each of these mechanisms.(ABSTRACT TRUNCATED AT 250 WORDS)
The high incidence of cardiovascular morbidity and mortality in hypertensive patients with left ventricular hypertrophy shows the great interest in understanding the pathophysiology of this process. Many reports suggest the role of catecholamines in generating left ventricular hypertrophy. The aim of this study is to evaluate the effect of labetalol on myocardial norepinephrine content in hypertensive subjects with left ventricular hypertrophy by using an isotopic norepinephrine marker, the 123I-meta-iodobenzylguanidine (123I-MIBG). Eight male and female hypertensive patients with left ventricular hypertrophy were investigated after a 30 day placebo period. Resting, ambulatory and effort blood pressure was measured. Echocardiographic parameters allowed measure of left ventricular mass index according to Devereux. And we considered left ventricular hypertrophy as left ventricular mass index greater than 120 g/m2. Cardiac and mediastinal radioactivity is detected 4 h after a 4 mCi i.v. injection of 123I-MIBG and MIBG myocardial uptake is definite as the cardiac/mediastinal ratio (N : 1.78 +/- 0.19). All subjects received at the beginning of the study (D0) 2 tablets of labetalol 200 mg, increased to 4 tablets if diastolic blood pressure during follow-up remained above 95 mmHg. Patients again underwent these explorations after 3 months of treatment (D90). Labetalol decreases in considerable manner MIBG myocardial uptake as it has been shown that it decreases tissular norepinephrine content in experimental studies. Therefore, MIBG myocardial uptake seems to be a reliable tool in evaluating drugs effect on cardiac sympathetic nervous system.
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22 patients with untreated, essential hypertension (diastolic blood-pressure greater than or equal to 140 mmHg) and in most cases also showing neurological symptoms were given a single oral dose of 400 mg labetalol. All patients displayed a gradual decrease of the blood-pressure down to a diastolic pressure about 110 mmHg with relief of the symptoms. There were no signs of neurological deficit due to the reduction of blood-pressure.
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Dexmedetomidine attenuates the hemodynamic stress response to laryngoscopy and intubation more effectively compared with labetalol without any deleterious effects. Furthermore, dexmedetomidine decreases dose of propofol for induction of anesthesia as guided by bispectral index.
The median time taken to achieve target blood pressure was 30 minutes (interquartile range, IQR 22.5-67.5 minutes) versus 45 minutes (IQR 30-60 minutes) for nifedipine and labetalol, respectively (P=0.59). Repeated measures analysis of variance indicated that in the first hour both systolic (F=87.6, P<0.001) and diastolic (F=55.8, P<0.001) blood pressure significantly decreased, but there was no difference between the nifedipine and labetalol groups for both systolic (F=0.12, P=0.74) and diastolic (F=0.92, P=0.34) blood pressure trends over time. Crossover treatment was required in 20% of women from each group.
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Women with acute severe intrapartum hypertension had a significantly higher risk of severe maternal morbidity compared to women without severe hypertension. Significantly lower antihypertensive treatment rates and higher severe maternal morbidity rates were seen in lower-delivery volume hospitals.
1 The pharmacokinetics of labetalol were studied in twelve hypertensive patients, ten of whom were not receiving other therapy. 2 Following intravenous administration there was a three- to fourfold variation in terminal elimination half-life, volume of distribution and total plasma clearance. The mean elimination half-life was 3.25 hours. 3 Following oral administration the drug was absorbed rapidly. Systemic availability varied from 11-86% (mean 33%). 4 Plasma levels correlated poorly with the acute effect on BP, raising the possibility of labetalol acting in a deep tissue compartment or alternatively an active metabolite contributing to its effect.
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Among the 1009 patients (1.2%) exposed to AD during pregnancy, 675 (66.9%) were incident users. Among the incident users, 31% received non-recommended drugs; this proportion decreased to 18% among women who started treatment in the third trimester. Women with at least four concomitant diseases had an elevated risk of receiving non-recommended drugs in pregnancy (OR 2.68; 95% CI 1.10-6.73).
Comparative trials have demonstrated that four currently available oral agents can lower blood pressure rapidly and predictably. Nifedipine, the most extensively studied, and clonidine have served traditionally as the oral agents of choice for the treatment of HUs. All the agents can lower blood pressure effectively within the first few hours after dosing, but their use also has been associated with adverse effects. Nifedipine and captopril are the two agents with the most rapid onset, within 0.5-1 hour, and may treat hypertensive emergencies as well as urgencies. Clonidine and labetalol have maximal blood pressure lowering effects at 2-4 hours.
This article describes two cases of PSS: one following traumatic brain injury and the other following cardiac arrest.
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Labetalol is a competitive antagonist of alpha 1-, beta 1-, and beta 2-adrenergic receptors. The hemodynamic effects of the drug include reduced blood pressure, heart rate, and peripheral resistance, with little change in resting cardiac output or stroke volume. In open trials and controlled studies, labetalol was an effective antihypertensive. Labetalol compared favorably with beta-blockers alone or in combination with vasodilators, for the treatment of hypertension. Reductions in heart rate are less pronounced with labetalol as compared with propranolol. Labetalol produces rapid reductions in blood pressure when administered intravenously for severe hypertension. The most frequent adverse reactions to the drug include fatigue, postural symptoms, headache, and gastrointestinal complaints. Labetalol may prove advantageous when vasodilation in addition to beta-blockade is desired, or for selected patients experiencing adverse effects attributable to beta-blockade. Until the clinical profile of labetalol is better defined, the use of the drug should be limited.
Hypertensive disorders occur in approximately 6% to 8% of all pregnancies and are a significant source of maternal and fetal morbidity. Little is known about the range of agents routinely used in practice. We used Medicaid claims from 2000 to 2007 to identify completed pregnancies. We included women who were Medicaid beneficiaries from at least 3 months prior to last menstrual period to 1 month postdelivery, and were successfully linked to infant records. Maternal exposure to antihypertensive medications was derived from Medicaid pharmacy claim files, and duration of exposure was assigned based on the days' supply dispensed. We identified 1,106,757 Medicaid patients in our cohort, of whom 48,453 (4.4%) were exposed to antihypertensive medications during pregnancy. The prevalence of antihypertensive use increased from 3.5% to 4.9% during the study period. Antihypertensive medication users were older than nonusers, more likely to be white or black, and more likely to have comorbid diabetes mellitus and renal disease. Overall, 1.9% of pregnant women were exposed during the first trimester, 1.7% during the second trimester, and 3.2% during the third trimester. The range of antihypertensive medications to which patients were exposed was highly heterogeneous and frequently included agents other than methyldopa or labetalol. Angiotensin-converting enzyme inhibitor exposure, which is contraindicated in late pregnancy, occurred in 928 (4.9%) antihypertensive medication users in the second trimester and 383 (1.1%) in the third trimester. Antihypertensive use during pregnancy is relatively common and increasing. The wide range of agents used during pregnancy includes medications considered contraindicated during pregnancy.
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A woman with Kawasaki disease complicated by coronary aneurysms underwent two consecutive pregnancies without further difficulty. She was maintained on therapeutic enoxaparin, alpha-methyldopa, and labetalol, with labor induction, passive second stage, and continued anticoagulation for 6 weeks postpartum. During gestations she was assessed with echocardiography, electrocardiography, and cardiac event monitor and managed by a maternal-fetal medicine and cardiology team.
Activation of adrenergic receptors (AR) has been reported to enhance the growth and invasion of various malignancies. The effects of AR agonists on malignant hepatocyte proliferation and migration have yet to be determined.
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A 20-year follow-up study of central hemodynamics in essential hypertension at rest and during exercise in 61 men with uncomplicated essential hypertension has clearly shown that hemodynamic disturbances depend on the age of the subjects and the severity of the hypertensive state and that a shift in the hemodynamic alterations take place over time. During 10- and 20-year follow-up, central hemodynamics changed towards a low cardiac-index (CI)-high total peripheral-resistance index (TPRI) pattern. With increasing age there was a gradual reduction in CI as well as stroke index (SI). The arteriovenous oxygen difference increased, particularly during exercise. The 20-year treatment with conventional drugs (beta-blockers and/or diuretics) did not prevent a marked increase in TPRI and a marked reduction in CI and SI in subjects initially 40-49 years of age. In recent years, beta-blockers with vasodilating activity have been introduced in the treatment of hypertension (labetalol, prizidilol, dilevalol and carvedilol). The hemodynamic effects of these compounds clearly differ from the changes induced during acute and chronic conventional beta-blocking treatment. In contrast to usual beta-blockers, these drugs reduce TPRI acutely and the reductions they produce in heart rate (HR) and CI are considerably lower. Our long-term data on labetalol (n = 15), prizidilol (n = 15) and dilevalol (n = 17) indicate a persistent reduction in TPRI and little or no decrease in exercise CI. Long-term data on carvedilol are not yet available. Approximately 70% of patients with mild to moderately severe essential hypertension achieved normal blood pressure during chronic treatment on beta-blockers with vasodilating activity.
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Urgent hypertension is defined by severe elevations of blood pressure without associated end-organ damage. The use of parenteral agents for this entity entails intensive monitoring and the potential for significant hemodynamic complications. Therefore, various oral regimens have been studied. Herein described are mechanisms of action, pharmacokinetics, clinical efficacy, and side effects of oral agents used in the treatment of urgent hypertension.
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Three case reports and 2 placebo-controlled trials were identified that used 4 beta-blockers (atenolol, labetalol, metoprolol, propranolol). Three national guidelines addressed beta-blocker use. Although published data are limited, propranolol and labetalol exert minimal to no effect on alleviating cocaine-induced coronary vasoconstriction. None of the evaluated national guidelines recommends beta-blockers as first-line agents in CIACS management.
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We investigated the profiles of sudden death and hemoconcentration induced by endothelin-1 (ET-1) and big endothelin-1 (big ET-1) in mice using various compounds as pharmacological tools. In ET-1-induced sudden death (5 nmol/kg, i.v.), pretreatment with the Ca(2+)-channel blockers, diltiazem, nifedipine or verapamil at a dose of 2 mg/kg, i.v. significantly inhibited the mortality and prolonged the latency to death. These Ca(2+)-channel blockers, however, failed to inhibit the rise in hematocrit (Ht), namely hemoconcentration, induced by ET-1 (2.5 nmol/kg). A beta-adrenoceptor agonist, isoproterenol (1 mg/kg) tended to prolong the latency, whereas, a beta-adrenoceptor blocker, propranolol (2 mg/kg), and an alpha- and beta-adrenoceptor blocker, labetalol (5 mg/kg), aggravated the sudden death. Esculetin (10 mg/kg) and fenbufen (10 mg/kg), which are enzyme inhibitors in the arachidonate cascade, prevented only the hemoconcentration. Anti-arrhythmic drugs, lidocaine (1 mg/kg) and disopyramide (20 mg/kg) did not improve any parameters. Big ET-1 also caused sudden death (20 and 25 nmol/kg, i.v.) and hemoconcentration (10 nmol/kg, i.v.). Of several proteinase inhibitors, only a metalloproteinase inhibitor, phosphoramidon (2 mg/kg i.v.), prevented the sudden death and the hemoconcentration induced by big ET-1 but not by ET-1. Ca(2+)-channel blockers exerted their protective effects only when a lower dose of big ET-1 was employed. These results indicate that the sudden death caused by both peptide is mainly due to myocardial ischemia and respiratory disorder, and that hemoconcentration caused by them is due to their vasoconstrictor action but to their effects on the vascular permeability via secondary endogenous factors.
Thirteen beta-blocking agents with different pharmacological properties were administered orally to 161 outpatients with essential hypertension for 5 weeks to assess their hemodynamic effects. Cardioselective ones, such as atenolol, metoprolol and acebutolol, reduced mean blood pressure (MBP) and the cardiac index. (CI) without any changes of the total peripheral resistance index. (TPRI). In the total 44 patients treated with these drugs, a positive correlation (r = 0.529, p less than 0.005) was found between the decrease in MBP and that of TPRI, but the decrease in MBP did not correlate with that of CI. Effects of non-cardioselective ones were classified arbitrarily into the following 3 patterns: 1) reduction of CI of more than 0.50 L/min/m2 and a slight increase of TPRI by more than 150 dyne . sec . cm-5 . m2 (nadolol, propranolol, o.prenolol and penbutolol), 2) reduction of TPRI by more than 150 dyne . sec . cm-5 . m2 (pindolol, bunitrolol and labetalol) and 3) the intermediate hemodynamic responses between the two patterns described above (carteolol, bupranolol and bufetolol). In all these 3 groups, the decrease in MBP correlated with that of TPRI (the first group, n = 45, r = 0.557, p less than 0.005; the second, n = 37, r = 0.525, p less than 0.005; the third, n = 35, r = 0.612, p less than 0.005), but did not correlate with the decrease of CI. These results suggest that the antihypertensive effects of beta-blocking agents mainly depend on the reduction of peripheral resistance, although their pharmacological properties are not uniform and their cardiodepressant effects are variable. Reduction of cardiac performance with these beta-blocking agents seemed to be a consequence of overall pharmacological actions including beta-receptor blockade, central effects and membrane stabilizing effects, and it may be antagonized by intrinsic sympathomimetic activity and the reduction in afterload for the heart. Vascular beta-receptor blocking action may play a part in decreasing the degree of reduction of the total peripheral resistance index, while their intrinsic sympathomimetic action on the vascular site may induce vasodilating effects.
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