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1.
Summary The chronotropic response to a single oral dose of propranolol in 23 healthy subjects has been related to the plasma propranolol concentration and the density of -adrenoceptors on peripheral polymorphonuclear leucocytes. The percentage reduction in exercise-induced tachycardia was significantly correlated with the log plasma propranolol concentration within subjects but not between subjects. Taking the concentration of the active metabolite 4-hydroxypropranolol into account did not improve the interindividual correlation. The reduction in exercise-induced tachycardia was significantly correlated with the maximum binding density of (125I)-hydroxybenzylpindolol on polymorphonuclear leucocyte membrane fragments measured before medication. A response index (% reduction in exercise-induced tachycardia/plasma propranolol concentration) was correlated with the maximum binding density of (125I)-hydroxybenzylpindolol (predrug) at 2 h (rs=0.72), 4 h (rs=0.84) and 6 h (rs=0.73) after dosing. The data suggest that interindividual variation in the response to propranolol after a single oral dose is determined by interindividual differences both in plasma propranolol and adrenoceptor density.  相似文献   
2.
The effect on left ventricular function of a gradual withdrawalof chronic metoprolol treatment in postinfarction patients wasstudied. All patients were in a randomized double-blind post-infarctionstudy with metoprolol (M 100–200 mg daily; N=14) or placebo(P; N =18). After three years treatment the study medicationwas gradually withdrawn during one week. M-mode echocardiography,guided by concomitant cross-sectional recordings, were performedbefore, one and 12 weeks after the withdrawal. Treatment (i.e.M or P) had to be reinstituted in eight patients (5 M; 3P) becauseof the development of disabling symptoms during the follow-up.Heart rate was lower in patients treated with M (57±4)than with P (69±10) (p<0.01). One week after withdrawalof M, heart rate had increased to 77± 13(p<0.001),while patients on P showed no significant change. In order tominimize the influence of heart rate on the evaluation of timeintervals in the cardiac cycle, heart rate dependent correctionfactors were used. One week after M withdrawal there was a prolongationof the pre-ejection period (PEP) from 120±15 ms to 133±16ms (p< 0.01), mainly due to a prolongation of the intervalfor early isovolumetric contraction (Q Mc) from 87±10ms to 101±11 ms (N=11; p0.001). Simultaneously, valuesfor isovolumetric relaxation increased from 228±28msto 286±39 MS (n = 11; p0.001), starting from a somewhatlower value than P before withdrawal, reaching an insignificantlyhigher level and returning to the levels of P. During withdrawalof P stable values were encountered. Twelve weeks after withdrawal,there were no longer significant differences between M and Pgroups. In conclusion, after a one week gradual withdrawal ofM in patients with ischaemic heart disease, a transient increaseof both isovolumetric contraction and relaxation phases occur,suggesting depressed myocardial function, despite a transientrebound increase in heart rate.  相似文献   
3.
Summary Inhibition of adipose tissue lipolysis may be involved in the impairment of endurance capacity after administration of a -adrenoceptor blocker. During endurance exercise, no significant decrease in plasma glycerol and free fatty acid (NEFA) concentrations after -adrenoceptor blockade is found. However, the levels during recovery from exhaustion are lower after -adrenoceptor blockade. This study was designed to investigate whether the lower levels after exercise are due to -adrenoceptor blockade or to the shorter time to exhaustion after administration of a -adrenoceptor blocker.In a single-blind study, 11 well-trained male subjects (age 23 (0.9) y) performed a cycle ergometer test at 70% Wmax until exhaustion 2 h after intake of 80 mg propranolol. One week later, the test was repeated after intake of placebo and was stopped at the time of exhaustion in the previous test. Average exercise time was 24 min. During exercise plasma glucose was lower, whereas plasma lactate and the respiratory exchange ratio were significantly higher when the subjects were on propranolol. Glycerol and NEFA concentrations during exercise were not significantly different between the two conditions. Despite an identical exercise time, glycerol and NEFA concentrations during recovery were significantly lower after propranol treatment.In conclusion, lipolysis is inhibited during exercise after propranolol, probably causing a shift from fat to carbohydrate combustion.  相似文献   
4.
Summary Beta-blockers with less cardiodepressive effect than traditional nonselective beta1+2-blocking agents could be useful in the treatment of hypertension, provided the reduction in blood pressure was satisfactory. Epanolol, a selective beta1-receptor blocker with intrinsic sympathomimetic activity, induced a fall in intraarterial pressure of 8% at rest sitting and 11% during 100 W bicycle exercise after the first dose of 200 mg in 12 patients with essential hypertension. Heart rate, stroke index, and cardiac index initially fell by 14%, 11%, and 23%, respectively. The total peripheral resistance index increased by 21% after 2 hours, and then reverted towards the pretreatment level. After 10 months of epanolol treatment (mean 300 mg/day), the reduction in arterial pressure was 5% at rest and 10% during exercise. Cardiac index and heart rate were still reduced 14–21%, while total peripheral resistance was unchanged or slightly increased (2–10%). Twenty-four hour ambulatory blood pressure was higher on epanolol (300 mg/day) than on atenolol (150 mg/day) treatment (137/97 vs. 128/91 mmHg). Thus, the achieved blood pressure reduction induced by epanolol was moderate, while other characteristics of beta-receptor blockade, in particular, the reduction of heart rate and cardiac output, were maintained. This suggests that the compound may be useful for other cardioavascular disorders, e.g., angina pectoris in patients without hypertension or cardiac arrhythmia.  相似文献   
5.
Summary Metoprolol and carvedilol are widely used in the treatment of hypertension, but no randomized comparison of their hemodynamic activity has been previously reported. Their comparative effects on heart rate, systemic blood pressure, and echocardiographically determined aortic and femoral artery blood flow were measured at rest and at 2 and 24 hours after the first dose of each drug, and again after 4 weeks of sustained monotherapy in 12 male and 12 female patients, aged 36–68 years with uncomplicated sustained hypertension according to a randomized single-blind protocol. Nine patients in each drug group achieved the target diastolic blood pressure of <90 mmHg on the initial doses of each drug; this was achieved in the remainder following doubling of each dose. Neither drug occasioned withdrawal of any patient due to adverse reactions. Both drugs significantly reduced heart rate, although the reduction at 2 hours was significantly greater after metoprolol than after carvedilol. Both drugs reducd systolic pressure throughout the study; the reduction at 2 hours was significantly greater after carvedilol than after metoprolol. In contrast, the diastolic blood pressure was persistently reduced only by carvedilol. The cardiac output, determined as the aortic systolic blood flow, after carvedilol was not significantly different from pretreatment values throughout the study but was significantly reduced in the metoprolol-treated patients at each point of measurement. After metoprolol the systemic and femoral vascular resistances derived from conventional formulae were consistently and significantly increased over pretreatment values throughout the study and were significantly greater than in the carvedilol group at all measurement points. The hemodynamic differences between these two beta-blocking drugs may be explained by the additional vasodilator activity of carvedilol associated with its alpha1-adrenoceptor blocking activity. The long-term clinical and prognostic implications of these pharmacodynamic differences between beta-adrenoceptor antagonists with and without additional vasodilator activity in the treatment of hypertensive patients remain to be determined.  相似文献   
6.
Summary Plasma concentrations of alprenolol during one inter-dose interval and steady-state plasma concentrations have been determined in 30 patients treated for a prolonged period. The latter varied 25-fold between patients who received identical doses. Peak plasma concentrations were achieved at similar times in different patients, but only the level 5–7 h after administration was well correlated (r=0.997) with the steady-state concentration. The type of pharmacokinetic analysis described here is recommended for studies of the relationships between plasma concentration and effects of drugs with short half-lives.  相似文献   
7.
Summary In a placebo controlled double-blind study in six healthy male volunteers the effects of single oral doses of 100 mg and 200 mg of tolamolol on plasma concentrations of prolactin, growth hormone and luteinising hormone were investigated. In a second placebo controlled single-blind study in a further six healthy male volunteers the effects of single oral doses of 200 mg tolamolol and 160 mg propranolol on the same plasma hormone concentrations were compared. A dose dependent increase in plasma prolactin concentration was demonstrated after tolamolol. The increase in plasma prolactin concentration was not evident after propranolol. Plasma growth hormone and luteinising hormone concentrations were not significantly changed by either propranolol or tolamolol.Report prepared by Pfizer Central Research, Europe  相似文献   
8.
Summary In order to compare the effects of acute and chronic beta-blockade on infact size, the left circumflex coronary artery was occluded for 6 hours in 33 anesthetized dogs. The dogs (18 to 22 kg) were divided in to three groups; group 1 (N=10) served as controls, group 2 received intravenous nadolol (average dose 1.25 mg/kg) just prior to coronary occlusion, and group 3 received oral nadolol (80 mg) twice daily for 16 days prior to coronary occlusion. To ensure equivalent degrees of beta-blockade at the time of occlusion, group 2 and 3 dogs were given incremental doses of intravenous nadolol to abolish the chronotropic response to isoproterenol (2 /kg IV). Left ventricular pressure, its first derivative (dP/dt), and heart rate were monitored. The anatomic risk region was determined antemortem by Evan's blue staining while the infarct zone was delineated postmortem by tetrazoleum staining. Compared to Group 1, heart rate was 22% lower in group 2 and 15% lower in group 3 dogs 6 hours after occlusion (p<0.05). There were no differences among groups in peak left ventricular systolic pressure or mean arterial pressure. Infarct size as a function of the area at risk was 68±3% in group 1, 52±7% in group 2, and 44±8% in group 3. A significant difference was found only between groups 3 and 1. The data suggest that chronic beta-blockade provides greater protection against ischemic-induced necrosis than does acute beta-blockade. The greater protective effect of chronic beta-blockade may be due to chronic adaptive changes in either blood flow or metabolism.  相似文献   
9.
A double-blind, randomized, placebo-controlled comparison of metoprolol (50 mg) and celiprolol (200 mg) was undertaken in nine normal volunteers. Rest and exercise (supine bicycle) hemodynamics were assessed at 0, 2, 4, 6, and 8 hours following single oral doses of medication administered at weekly intervals. The influence of the ancillary pharmacological properties of metoprolol and celiprolol on cardiac pumping indices was assessed from heart rate and peak aortic acceleration (pkA – Exerdop). Following placebo, the heart rate and pkA increased progressively with exercise duration and workload. Following metoprolol 50 mg, the heart rate (–9.7 beat/min at 75 watts exercise) and pkA decreased. The blunting of acceleration was greater at higher exercise workloads (–6.7 m/sec2 at 75 watts exercise). Celiprolol reduced heart rate (–6.9 beat/min at 75 watts exercise) without a change in pkA. The heart rate/pkA relationship showed significant parallel displacement, downwards after metoprolol but upwards after celiprolol. Thus, for a given heart rate increment there was a greater decrease in pkA after metoprolol compared with celiprolol. The different ancillary pharmacological profiles of metoprolol and celiprolol resulted in contrasting hemodynamic profiles. The observed differences in the heart rate/pkA relationships may be attributable to the peripheral actions of these agents. The therapeutic relevance of the better maintained cardiac pumping indices on celiprolol for ischemic patients with impaired cardiac function warrants further investigation.  相似文献   
10.
CONTEXT: The Metoprolol CR/XL Randomized Intervention Trial in Chronic Heart Failure (MERIT-HF), the Cardiac Insufficiency Bisoprolol Study II (CIBIS-II), and the Carvedilol Prospective Randomized Cumulative Survival Study (COPERNICUS) have all demonstrated highly significant positive effects on total mortality as well as total mortality plus all-cause hospitalization in patients with heart failure. While none of these trials are large enough to provide definitive results in any particular subgroup, it is of interest for physicians to examine the consistency of results as regards efficacy and safety for various subgroups or risk groups. OBJECTIVE: To summarize results from both predefined as well as post-hoc subgroup analyses performed in the MERIT-HF trial, and to provide guidance as to whether any subgroup is at increased risk, despite an overall strongly positive effect, and to discuss the difficulties and limitations in conducting such subgroup analyses. For some subgroups we performed metaanalyses with data from the CIBIS II and COPERNICUS trials in order to obtain more robust data on mortality in subgroups with a small number of deaths (e.g. for women). SETTING: MERIT-HF was run in 14 countries, and randomized a total of 3,991 patients with symptomatic systolic heart failure (NYHA class II to IV with ejection fraction < or =0.40). Treatment was initiated with a very low dose with careful titration to a maximum target dose of 200 mg metoprolol succinate controlled release/extended release (CR/XL), or highest tolerated dose. MAIN OUTCOME MEASURES: Total mortality (first primary endpoint), total mortality plus all-cause hospitalization (second primary endpoint), and total mortality plus hospitalization for heart failure (first secondary endpoint) analyzed on a time to first event basis. RESULTS: Overall, MERIT-HF demonstrated a 34% reduction in total mortality ( p = 0.00009 nominal) and a 19% reduction for mortality plus all-cause hospitalization ( p = 0.00012). The first secondary endpoint of mortality plus hospitalization for heart failure was reduced by 31% ( p = 0.0000008). The results were remarkably consistent for both primary outcomes and the first secondary outcome across all predefined subgroups as well as nearly all post-hoc subgroups. Metoprolol CR/XL has been very well tolerated, overall as well as in all subgroups analyzed. Overall 87% of the patients reached a dose of 100 mg or more of metoprolol CR/XL once daily, and 64% reached the target dose of 200 mg once daily. CONCLUSION: Our results show that when carefully titrated, metoprolol CR/XL can safely be instituted for the overwhelming majority of outpatients with clinically stable systolic heart failure, with minimal side effects or deterioration. The time has come to overcome the barriers that physicians perceive to beta-blocker treatment, and to provide it to the large number of patients with heart failure in need of this therapy, including also high risk patients like elderly patients, patients with severe heart failure, and patients with diabetes. Because of the increased risk, these are the patients in whom treatment will have the greatest impact as shown by number of lives saved and number of hospitalizations avoided. The target dose should be strived for in all patients who tolerate this dose. We should expect some variation of the treatment effect around the overall estimate as we examine a large number of subgroups due to small sample size in subgroups and due to chance. However, we believe that the best estimate of treatment effect for any particular subgroup should be the overall effect observed in the trial.  相似文献   
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