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An high intrathoracic vagotomy results in loss of vagal tone and a greater rate of tachycardia during thoracoscopy and esophagectomy. There were no differences, however, in cardiac dynamics between the esophagectomy groups. Thus, vagal injury is not the sole reason for cardiac dysfunction after esophagectomy.
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Neither the kinetics of the hydrophilic beta-adrenoceptor blocker atenolol nor those of the lipophilic metoprolol were influenced by the concurrent administration of amitriptyline. Compared with placebo, chronic administration (14 days) of atenolol and metoprolol (each as monotherapy) did not significantly reduce oxidative liver metabolism as measured by antipyrine half-life and by 6-beta-hydroxycortisol excretion. Compared with atenolol and metoprolol monotherapy, chronic administration of amitriptyline concurrently with each of the beta-adrenoceptor blockers produced an insignificant decrease (circa 10-20%) in antipyrine half-life and 6-beta-hydroxycortisol excretion. Amitriptyline appears therefore to have little enzyme-inducing activity.
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This prespecified secondary analysis of the GEMINI study (n=1106) evaluated change in body weight after 5 months.
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In the present study, therefore, the effect of isoprenaline (ISO), activators and inhibitors of the protein kinase A (PKA) pathway on I(Kr) and I(Ks) was studied in canine ventricular myocytes using the whole cell patch clamp technique.
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The effects of beta-blockade on glucose metabolism are complex. Some patients with impaired glucose tolerance while taking a non-selective beta-blocker, showed some improvement in glucose tolerance when therapy was changed to a beta1-blocker (metoprolol). Serum K+ values tend to rise slightly on beta-blocking therapy; small increases in serum urea and creatinine also occur. A rise in plasma triglycerides was noted in patients starting beta-blocking therapy; this effect seemed to be more marked on metoprolol than on non-selective beta-blockers.
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Metoprolol, a beta 1-adrenergic blocking agent, has been found effective in the treatment of hypertension. A death due to deliberate ingestion of metoprolol is described, including the case history, postmortem toxicologic findings, and identification and quantitation of the drug by high pressure liquid chromatography and gas chromatography/mass spectrometry. Metoprolol levels were found to be 4.7 mg/L in blood, 194 mg/L in urine, 3.3 mg/L in vitreous humor, 3.9 mg/L in pleural fluid, 254 mg/L in bile, 7.1 mg/kg in kidney, and 6.3 mg/kg in liver.
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Beta-blockers are an established treatment for chronic heart failure. However, the relationship between their benefit and the severity of the disease remains to be determined.
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In the Thrombolysis in Myocardial Infarction (TIMI) Phase II trial, patients received intravenous recombinant tissue-type plasminogen activator (rt-PA) and were randomized to either a conservative or an invasive strategy. Within this study, the effects of immediate versus deferred beta-blocker therapy were also assessed in patients eligible for beta-blocker therapy, a group of 1,434 patients of which 720 were randomized to the immediate intravenous group and 714 to the deferred group. In the immediate intravenous group, within 2 hours of initiating rt-PA metoprolol was given (5 mg intravenously at 2-minute intervals over 6 minutes, for a total intravenous dose of 15 mg, followed by 50 mg orally every 12 hours in the first 24 hours and 100 mg orally every 12 hours thereafter). The patients assigned to the deferred group received metoprolol, 50 mg orally twice on day 6, followed by 100 mg orally twice a day thereafter. The therapy was tolerated well in both groups and the primary end point, resting global ejection fraction at hospital discharge, averaged 50.5% and was virtually identical in the two groups. The regional ventricular function was also similar in the two groups. Overall, there was no difference in mortality between the immediate intravenous and deferred groups, but in the subgroup defined as low risk there were no deaths at 6 weeks among those receiving immediate beta-blocker therapy in contrast to seven deaths among those in whom beta-blocker therapy was deferred. These findings for a secondary end point in a subgroup were not considered sufficient to warrant a recommendation regarding clinical use. There was a lower incidence of reinfarction (2.7% versus 5.1%, p = 0.02) and recurrent chest pain (18.8% versus 24.1%, p less than 0.02) at 6 days in the immediate intravenous group. Thus, in appropriate postinfarction patients, beta-blockers are safe when given early after thrombolytic therapy and are associated with decreased myocardial ischemia and reinfarction in the first week but offer no benefit over late administration in improving ventricular function or reducing mortality.
A sensitive and efficient method was developed for the determination of atenolol in human urine by gas chromatography-mass spectrometry (GC-MS). Atenolol and metoprolol (internal standard, IS) were extracted from human urine with a mixture of chloroform and butanol at basic pH with liquid-liquid extraction. The extracts were derivatized with N-Methyl-N-(trimethylsilyl)trifluoroacetamide (MSTFA) and analyzed by GC-MS using a capillary column. The standard curve was linear (r = 0.99) over the concentration range of 50-750 ng/mL. Intra- and inter-day precision, expressed as the relative standard deviation were less than 5.0%, and accuracy (relative error) was better than 7.0%. The analytical recovery of atenolol from human urine has averaged 91%. The limit of quantification was 50 ng/mL. Also, the method was successfully applied to a patient with hypertension who had been given an oral tablet of 50 mg atenolol.
Hypertension, a major complication in kidney transplant recipients, is associated with premature death and graft loss. However, an optimal antihypertensive therapy for these patients has not been established [Chinese Clinical Trial Registry No. ChiCTR-TRC-10001071].
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β(1)-Adrenergic blockade with metoprolol attenuated the regadenoson-induced increase in HR more than the increase in CBF.
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Established hypertension is associated with enhanced susceptibility to life-threatening arrhythmias. However, little is known about the effects of the development of hypertension on the electro-physiological properties of the heart. To study this relationship, dogs were chronically instrumented for recording mean arterial pressure and conducting cardiac electrical testing during right ventricular pacing using an intracavitary bipolar catheter. In normotension, ventricular fibrillation threshold was determined under alpha-chloralose anesthesia, after which perinephritic hypertension was induced by wrapping one kidney in silk followed by contralateral nephrectomy. During serial testing of the same animals, ventricular fibrillation threshold was significantly increased early in the development of hypertension (2 to 3 weeks after renal wrapping), but found to be significantly reduced at 6 to 7 weeks after renal wrapping. The increase in ventricular fibrillation threshold was eliminated by cholinergic blockade.
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Carvedilol treatment in experimental myocarditis leads to reduced expression of proinflammatory cytokines and MMPs, which contributes to reduced matrix degradation and ultimately to improved structural integrity of the heart. Besides the antiadrenergic potential, carvedilol is beneficial due to a wide range of biological activities (antiinflammatory, antifibrotic, antioxidative and immunomodulatory).
The benefits of b-blockers in HF patients were sex-related different.
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beta-Blocker use improves outcomes even more for the patient with diabetes mellitus than for the patient without diabetes with a history of acute myocardial infarction or coronary artery disease. beta-Blockers facilitate shifting the metabolism of the myocardium away from free fatty acid toward glucose utilization, thereby reducing the cardiac workload and myocardial ischemia. beta-Blockers are also able to reverse the fetal gene induction program to reverse myocardial remodeling and improve ventricular function. Side effects of beta-blockers in the patient with diabetes include increased insulin resistance with worsening glycemic control, elevated triglyceride levels, and lowered levels of high-density lipoprotein cholesterol. Increased frequency of hypoglycemia and its lack of recognition can also be a problem in the insulin-deficient patient but is a minimal problem with the patient with type 2 diabetes. In addition, vasoconstriction, caused by unopposed alpha-activity, can worsen peripheral vascular disease. However, carvedilol, a nonselective beta-blocker with vasodilating and insulin-sensitizing properties, can largely circumvent these problems and is the ideal beta-blocker for the patient with diabetes.
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The tremor of a patient with debilitating essential tremor who could not take propranolol (because of severe asthma) was dramatically reduced when metoprolol tartrate was administered in standard doses. Metoprolol appears to be an excellent alternative antitremor drug to propranolol in such patients.
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The influence of acute beta 1-receptor blockade using 50 mg metoprolol or beta 1/beta 2-blockade using 40 mg propranolol resulted in an equipotent reduction of cardiac frequency and systolic blood pressure without influencing diastolic pressure in ten healthy probands. There was no reduction of maximal bicycle ergometric exercise by either beta-receptor blocking agent. Serum glucose levels did not change during metoprolol in comparison to pre-test values. In contrast, propranolol resulted in a significant decrease of glucose levels during maximal exercise and 5 minutes after end of exercise. Plasma lactate was moderately lowered by both beta-receptor blockers after 20 min constant exercising when compared to pre-medication. Both substances reduced the insulin level in a comparable way during the exercise test. Serum triglyceride concentrations did not alter significantly during exercise tests. Serum free fatty acid levels showed a decreasing tendency until maximal exercise; however, there was no significant difference between values obtained with metoprolol or propranolol and drug-free pre-test.
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The two combination regimens were similarly effective in lowering blood pressure. After 48 weeks, in felodipine-irbesartan group, total scores of FSFI improved (P < 0.001). Items showing improvement in scores corresponded to desire, arousal and orgasm (P < 0.001; P = 0.002; P = 0.049, respectively). Levels of estradiol increased under treatment with felodipine-irbesartan (P = 0.003) and decreased under felodipine-metoprolol treatment (P < 0.001). The concentration of testosterone declined after felodipine-irbesartan therapy (P < 0.001) and increased under felodipine-metoprolol treatment (P < 0.001). In the felodipine-irbesartan group, decreases of 8-OHdG, 4-HNE (P < 0.001) and MDA (P < 0.001) were observed. The felodipine-irbesartan combination resulted in less oxidative stress. The differences in changes in 8-OHdG, 4-HNE and MDA between the two groups were significant (P < 0.05).
To identify the frequency of atrioventricular (AV) conduction improvement after discontinuation of the culprit drug in patients with AV block.
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The hemodynamic responses to 3 different therapeutical regimens: beta-adrenoceptor blockade, calcium inflow inhibition and combined alpha-beta-blockade were evaluated in 3 matched randomized groups of patients with ischemic heart disease and typical exercise-induced angina. The groups consisted of 22, 16 and 15 men, mean age 55-59 years. They were studied at rest and during ischemia-inducing exercise, before and after single oral doses of 100 mg metoprolol, 10 mg nifedipine and 200 mg labetalol. Pressures in the brachial artery and the pulmonary circulation were recorded by means of percutaneously introduced catheters. Cardiac output was determined according to the Fick principle. Metoprolol reduced mean arterial pressures, heart rate and cardiac output. Systemic vascular resistance and left ventricular filling pressure increased. Nifedipine resulted under all conditions in a distinct reduction of systemic vascular resistance and arterial pressures and a slight increase in heart rate and cardiac output. Left ventricular filling pressure was significantly lowered, the more the higher the initial level. The effect of labetalol was similar to that of nifedipine; however, cardiac output was unchanged and heart rate was slightly reduced. Left ventricular filling pressure was significantly lower. It is apparent that suppression of adrenergic stimulation by beta-receptor blockade alone may have adverse hemodynamic effects in ischemic heart disease and prompt further functional deterioration. Conversely, both calcium and combined alpha-beta-receptor blockade tend to improve left ventricular function by lowering both left ventricular preload and total systemic vascular resistance. The results strongly suggest that in patients in whom beta-receptor blockers appear indicated, their adverse hemodynamic effects can be offset by concomitant alpha1-receptor blockade or vasodilation without losing symptomatic efficacy. Combined alpha-beta-receptor blockade has the advantage over calcium antagonists alone to prevent any increase in adrenergic activity and related hyperkinetic response.
In a double-blind, cross-over multicentre trial, the prophylactic antimigraine effect of the beta 1-selective beta-blocker metoprolol was evaluated and compared with that of the non-selective beta-blocker propranolol. Metoprolol was used in a dosage of 50 mg b.i.d. and propranolol in 40 mg b.i.d. 56 patients with classical or common migraine were included in the double-blind part of the investigation. 3 patients withdrew, but none because of side-effects. The data suggest that metoprolol is clinically equivalent in effectiveness to propranolol in migraine prophylaxis regarding parameters such as attack frequency, improvement in sum of severity score and subjective evaluation. Both drugs were generally well tolerated and the number of reported side-effects was similar to those reported during the run-in period (placebo).
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ICA cells respond to irregular electrical activation with an increase in catecholamine-synthesizing enzymes. Drugs commonly used in clinical routine significantly influence the expression of TH and DBH by ICA cells via different signaling routes.
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To evaluate the effect of combined use of Chinese herbal medicine, Captopril and Metoprolol in treating mild-middle degree congestive heart failure.
Patients with catheterization-proven coronary artery disease (CAD) were enrolled in this prospective, double-blind, placebo-controlled study and randomly assigned to DMPI after placebo, low-dose metoprolol (up to 10 mg), and high-dose metoprolol (up to 20 mg). Patients underwent one Tc-99m sestamibi study at rest on a separate day. The interval between DMPI studies was