Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of acute beta-adrenoceptor blockage (Metoprolol) (M), 0.1 mg/kg i.v.) on left ventricular performance has been investigated at rest and during exercise in 15 patients with 2--3 months old transmural myocardial infarctions. Coronary venous and arterial norepinephrine (NE) concentrations were determined. There was no significant change in arterial and coronary venous NE concentrations (0.27 and 0.22 ng/ml, respectively) after blockage of beta-adrenoceptors (0.36 vs 0.26 ng/ml), which caused a fall of stroke volume from 79 to 68 ml, a reduction of ejection fraction from 62 to 55% and of circumferential fibre shortening form 1.2 to 0.9 circ/sec. During physical exercise the plasma NE concentration in the arterial (0.51 ng/ml) and coronary venous (0.6 ng/ml) blood increased significantly and increased even further to 0.65 and 0.76 ng/ml, respectively, following administration of Metoprolol. The arterio-coronary sinus difference in NE concentrations demonstrate a release of NE from the myocardium. As compared to control values, heart rate following Metoprolol was lower (116 vs 106/min), mean PCV pressure was slightly increased (from 21 to 23 mm Hg) and there was a fall of cardiac index from 6.3 to 5.2 l/min X m2. It is likely that the increased sympathetic activity after Metoprolol and during exercise is a compensatory reaction due to the hemodynamic effects of blockade of beta-adrenoceptors. Further studies are in preparation in order to find out if this is only a transient phenomenon during the early adaptation phase after blockade of beta-adrenoceptors.
 ...
PMID:[Effects of acute beta-adrenoceptor blockage (metoprolol i.v.) on plasma norepinephrine concentration and hemodynamics in postmyocardial infarction patients]. 47 45

Metoprolol, a cardioselective beta-receptor blocker, was administered to 12 patients three to ten hours after sustaining a transmural myocardial infarction, and the effect of the drug (10 mg i.v., followed by 50 mg orally every eight hours) was followed for 48 hours. Heart rate decreased by 16% and cardiac output by 27%, while blood pressure and stroke volume decreased little and pulmonary "wedge" pressure was not significantly changed. Even in patients with initially definitely elevated left-ventricular filling pressure (greater than 20 mm Hg) the drug was well tolerated without any further rise in pressure. Since left-ventricular work was significantly decreased (stroke work--15%, cardiac output--31%) and the duration of diastole, decisive for coronary perfusion, was prolonged, it is concluded that early administration of beta-receptor blockers has a favourable effect on myocardial oxygenation and possibly reduce ultimate infarct size.
 ...
PMID:[Treatment of acute myocardial infarction with metoprolol (author's transl)]. 63 87

In 19 patients with arterial hypertension the hemodynamics were determined with a Swan-Ganz-thermodilution catheter at rest and during supine ergometer exercise before and after 5 mg intravenous Propranolol (P) (10 pats.) respectively 10 mg of intravenous Metoprolol (9 pats.). During exercise, P caused a significantly higher increase in pulmonary capillary wedge pressure (PCP) (15.0 +/- 4.0 to 25.3 +/- 4.0 mm Hg), than M (10.9 +/- 4.8 to 17.4 +/- 5.5 mmHg) (p less than 0.025). There was a uniform reduction of the cardiac output (CO), after P and M. P caused a reduction of the CO by a decrease in heart rate and stroke volume, M through a significantly greater decrease in heart rate (p less than 0.0005), without a change in stroke volume (p less than 0.05). The changes in PCP and stroke volume give evidence of a more negative inotropic effect of P compared to M.
 ...
PMID:[Hemodynamic changes in patients with arterial hypertension after beta-receptor blockade with propranolol and metoprolol (author's transl)]. 73 94

The contribution of adrenergic receptors to the cardiovascular responses to cocaine (5 mg/kg i.v.) were examined in conscious, free-moving rats instrumented for continuous measurement of arterial pressure, heart rate and blood flows in the mesentery and hindquarters or ascending aorta. Cocaine elicits an immediate (peak) and sustained pressor response with a concomitant reduction in heart rate. Prazosin (0.1 mg/kg i.v.) pretreatment significantly reduced both the peak and sustained pressor responses by attenuating the increases in systemic, mesenteric and hindquarters vascular resistances. Idazoxan pretreatment (1 mg/kg i.v.) attenuated the peak increase in hindquarters vascular resistance. Whereas propranolol pretreatment (1 mg/kg i.v.) attenuated the peak pressor response, the sustained pressor response was enhanced due to increased hindquarters and systemic vascular resistances. Metoprolol pretreatment (1 mg/kg i.v.) enhanced the sustained pressor response to cocaine, in part due to increased heart rate and mesenteric vascular resistances. Upon examination of the cardiac effects of cocaine, a sustained bradycardic response was observed, whereas stroke volume and cardiac output were relatively unaffected. The bradycardic response to cocaine was attenuated by yohimbine (0.1 mg/kg i.v.), prevented by prazosin and converted to a tachycardia after idazoxan (1 mg/kg) pretreatment. After propranolol pretreatment, cocaine substantially decreased cardiac output and stroke volume. Our results demonstrate that cocaine produces a biphasic pressor response in conscious rats and that the mechanisms underlying the dual responses vary in intensity and mode of action in different vascular beds, but are primarily dependent upon alpha-1 adrenergic receptor-mediated vasoconstriction.
 ...
PMID:Adrenergic mechanisms underlying cardiac and vascular responses to cocaine in conscious rats. 135 13

The cardiovascular effects of (+/-)-nebivolol, a potent beta 1-adrenoceptor antagonist, and its enantiomers, (+)-nebivolol (SRRR) and (-)-nebivolol (RSSS) in normotensive anaesthetized rats, have been investigated using metoprolol as a reference substance. The drugs decreased blood pressure and heart rate immediately after i.c.v. injection. These effects paralleled the beta-blocking potencies ((+)- greater than (+/-)-greater than (-)-nebivolol). Metoprolol induced a weaker hypotension than (+/-)-nebivolol, and a long-lasting reduction in stroke volume. As reported after i.v. administration, (+/-)-nebivolol and isomers by the i.c.v. route decreased peripheral vascular resistance following i.c.v. administration while metoprolol increased it. These effects are centrally mediated since cardiovascular responses to isoprenaline i.v. remained unchanged.
 ...
PMID:Cardiovascular effects of intracerebroventricular injections of (+/-)-nebivolol and its enantiomers--a comparison with those of metoprolol in the rat. 168 65

Several major studies investigated the possibility of a primary preventive effect of beta-blockers. The International Prospective Primary Prevention Study in Hypertension (IPPPSH) compared a beta-blocker-containing vs. a non-beta-blocker-containing antihypertensive regimen in 6,357 moderate-severe hypertensive men and women treated over 3-5 years. Blood pressure (BP) control was comparable with either regimen. beta-Blocker treatment was associated with less hypokalemia, earlier electrocardiogram normalization, and fewer withdrawals for uncontrolled hypertension. In agreement with the Medical Research Council (MRC) trial on mild hypertension and the Heart Attack Primary Prevention in Hypertension (HAPPHY) trial, but at variance with the Primary Prevention Metoprolol in Patients with Hypertension (MAPHY) study, cardiac event rates were similar in beta-blocker- and non-beta-blocker-treated patients. With either regimen, in-study BP reduction was associated with a lower rate of stroke as well as of cardiac events. In a subgroup analysis, nonsmokers appeared to derive beta-blocker benefit, the results being similar to those of the MRC. Smokers required higher doses of drugs to achieve diastolic target pressure, had a higher heart rate and hematocrit, and a higher cardiac event rate than nonsmokers at any given level of diastolic pressure. Except for the MAPHY trial, these primary prevention studies do not support the concept of a cardiac primary preventive effect of antihypertensive beta-blockade but stress the importance of good BP control and a comprehensive risk factor prevention approach in the management of hypertensive patients.
 ...
PMID:Smoking, antihypertensive treatment benefit, and comprehensive antihypertensive treatment approach: some thoughts on the results of the International Prospective Primary Prevention Study in Hypertension. 170 33

Using ultrasound techniques, parameters of left ventricular systolic and diastolic function were assessed in 23 patients with degree I-II essential hypertension treated with metoprolol. Metoprolol administration was followed by increases in ejection fraction (p less than 0.01) and stroke volume (p less than 0.05), a decrease in heart rate (p less than 0.01) while cardiac output remained unchanged. Left ventricular filling was abnormal in 12 patients (52.2%). After metoprolol, the ratio of early diastolic to late diastolic transmitral velocity (E/A) rose; the increase indirectly correlated both with the baseline value of E/A (r = -0.59, p less than 0.01), and the change in heart rate (t = -0.65, p less than 0.01). Improved left ventricular diastolic filling was significant only in patients showing abnormal baseline diastolic function, and may be due to the decrease in heart rate rather than a direct effect exerted by metoprolol on the myocardium.
 ...
PMID:The effect of metoprolol on left ventricular systolic and diastolic function in essential hypertension. 183 84

In a randomized primary prevention trial including 3,234 men with mild to moderate uncomplicated hypertension, the effect of the beta-blocker metoprolol or a thiazide diuretic as an initial antihypertensive therapy was compared regarding the risk of sudden cardiovascular death during a follow-up ranging from 2.3 to 10.8 years (median of 4.2 years). Only men aged 40 to 64 years were included in the study. The randomization of patients into the metoprolol (n = 1,609) or diuretic group (n = 1,625) was performed after stratification for age, smoking habits, serum cholesterol, and systolic blood pressure. At baseline the two treatment groups were well matched. Metoprolol was given in a mean dose of 174 mg daily and the mean dose of thiazide diuretic was either 46 mg hydrochlorothiazide daily or 4.4 mg bendroflumethiazide daily. Identical blood pressure control was achieved using the fixed therapeutic schedule. Total and cardiovascular mortality were significantly lower for metoprolol than for diuretics, owing to fewer deaths from coronary heart disease and stroke. Of the cardiovascular deaths, 78% were classified as sudden cardiovascular deaths (occurred within 24 h after the onset of symptoms). There were significantly fewer sudden cardiovascular deaths in the metoprolol group compared to the diuretic group (32 v 45, P = .017). The present results suggest that initial antihypertensive therapy with metoprolol is associated with a lesser incidence of sudden cardiovascular deaths than initial diuretic treatment in uncomplicated hypertension.
 ...
PMID:Primary prevention of sudden cardiovascular death in hypertensive patients. Mortality results from the MAPHY Study. 202 46

The study aimed to compare the effects of thoracic epidural anaesthesia (TEA) with those of the beta-adrenoceptor blocker, metoprolol, on central haemodynamics in conscious rats with acute myocardial infarction. During methohexital anaesthesia, appropriate vascular catheters were inserted, a thoracic epidural catheter was implanted and the left coronary artery was ligated. A recovery period of 1-2 h elapsed after termination of surgery and anaesthesia. Experiments were performed on four separate groups of animals (A-D). In Group A (n = 10) mean arterial pressure (MAP), heart rate (HR), and cardiac output (CO) were measured, and stroke volume (SV) and systemic vascular resistance (SVR) were calculated before and 10-15 min after the induction of TEA (bupivacaine 5 mg.ml-1). In Group B (n = 6) left ventricular end-diastolic pressure (LVEDP) and maximal dP/dt were recorded as in Group A. In Group C (n = 10) central haemodynamics were measured 10 min after i.v. metoprolol (0.5 mg.kg-1) and again 10-15 min after the addition of TEA. In Group D (n = 6) LVEDP and max dP/dt were measured as in Group C. The reduction in CO, SV, HR and max dP/dt was of the same magnitude with TEA and metoprolol. TEA lowered MAP by 17%, while metoprolol did not change MAP. Metoprolol caused an increase in LVEDP from 20.8 +/- 1.8 to 27.5 +/- 2.7 mmHg (2.8 +/- 0.2 to 3.7 +/- 0.4 kPa) (P less than 0.01), while TEA induced a decrease in LVEDP from 24.2 +/- 1.4 to 17.8 +/- 1.6 mmHg (3.2 +/- 0.2 to 2.4 +/- 0.2 kPa) (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Effects of thoracic epidural anaesthesia on central haemodynamics compared to cardiac beta adrenoceptor blockade in conscious rats with acute myocardial infarction. 230 37

Severe heart failure is associated with a reduction in myocardial beta-adrenergic receptor density and an impaired contractile response to catecholamine stimulation. Metoprolol was administered during a 6-month period to 14 patients with dilated cardiomyopathy to examine its effects on these abnormalities. The mean daily dose of metoprolol for the group was 105 mg (range, 75-150 mg). Myocardial beta-receptor density, resting hemodynamic output, and peak left ventricular dP/dt response to dobutamine infusions were compared in 9, 14, and 7 patients, respectively, before and after 6 months of metoprolol therapy while the patients were on therapy. The second hemodynamic study was performed 1-2 hours after the morning dose of metoprolol had been given. Myocardial beta-receptor density increased from 39 +/- 7 to 80 +/- 12 fmol/mg (p less than 0.05). Resting hemodynamic output showed a rise in stroke work index from 27 +/- 4 to 43 +/- 3 g/m/m2, p less than 0.05, and ejection fraction rose from 0.26 +/- 0.03 to 0.39 +/- 0.03 after 6 months of metoprolol therapy, p less than 0.05. Before metoprolol therapy, dobutamine caused a 21 +/- 4% increase in peak positive left ventricular dP/dt; during metoprolol therapy, the same dobutamine infusion rate increased peak positive dP/dt by 74 +/- 18% (p less than 0.05). Thus, long-term metoprolol therapy is associated with an increase in myocardial beta-receptor density, significant improvement in resting hemodynamic output, and improved contractile response to catecholamine stimulation. These changes indicate a restoration of beta-adrenergic sensitivity associated with metoprolol therapy, possibly related to the observed up-regulation of beta-adrenergic receptors.
 ...
PMID:Increased beta-receptor density and improved hemodynamic response to catecholamine stimulation during long-term metoprolol therapy in heart failure from dilated cardiomyopathy. 253 58


1 2 3 4 Next >>