Effects Of Intravenous Metoprolol Research Articles

Effects of intravenous metoprolol by two injection methods on atrial fibrillation and rapid ventricular rates complicated with heart failure

目的 探讨不同方式静脉注射美托洛尔对心房颤动(房颤)快速心室率(快室率)伴心力衰竭(心衰)的疗效及安全性.方法 90例房颤快室率伴心衰的患者经常规抗心衰药物治疗后,观察0.5 h,如心率仍＞100次/min、血压≥100/60 mm Hg(1 mm Hg=0.133 kPa)者,随机分3组:①美托洛尔注射液10 mg稀释后经微泵静脉滴注(微泵组)1 h;②美托洛尔注射液5 mg于10 min缓慢静脉推注(推注组),观察10 min,如心率仍大于100次/min,血压≥90/60 mm Hg,则再重复一次;③生理盐水对照组.当患者心率≤60 次/min、血压＜90/60 mm Hg时注射停止.各组静脉注射药物前及开始时给予美托洛尔注射液或生理盐水后1 h观察症状、体征、心率、血压、肺部啰音、无创血流动力学和血清脑钠肽、心钠肽等指标.结果 美托洛尔2种静脉注射方式给药后,大多数患者心衰症状、体征明显改善,心率、脑钠肽显著下降(F值分别为15.929、14.534,均P＜0.01)且比对照组明显(F值分别为5.011,4.559,均P＜0.05),收缩压、舒张压有所降低但与对照组差异无统计学意义;无创心功能参数中,微泵组心脏指数、心输出量、每搏指数、每搏输出量、左室射血时间增加且比对照组明显(F值分别为4.435、4.726、3.965、3.450、5.966,均P＜0.05),推注组无类似效应.结论 美托洛尔2种静脉注射方式治疗房颤快室率伴心衰均是有效和安全的,微泵方式给药有更好的血流动力学效应。

Effect of intravenous metoprolol before hospital admission on chest pain in suspected acute myocardial infarction: Gardtman M, Dellborg M, Brunnhage C, et al Am Heart J 137:821–829 May 1999

Effect of intravenous metoprolol before hospital admission on chest pain in suspected acute myocardial infarction: Gardtman M, Dellborg M, Brunnhage C, et al Am Heart J 137:821–829 May 1999

Failure of intravenous metoprolol to limit acute myocardial infarct size in a nonreperfused porcine model

The usefulness of intravenous β-adrenergic receptor blockade in limiting infarct size when neither reperfusion nor collateral flow occurs is unknown. The effect of intravenous metoprolol on limiting myocardial infarct size was therefore examined in a nonreperfused porcine model. Closed-chest techniques were used to occlude the left anterior descending coronary artery, after which animals were randomized at 20 minutes to receive intravenous metoprolol, 0.75 mg/kg, or placebo. Infarct size examined at 5 hours with Evans blue and triphenyltetrazolium ataining techniques was expressed as a percentage of total ventricular myocardium at ischemic risk. This percentage was not significantly different between the groups (84% ± 5% with metoprolol vs 90% ± 4% with placebo; p = 0.4). Myocardial infarct size was not significantly decreased at 5 hours by early administration of intravenous metoprolol when the infarct artery remained occluded and collateral flow was minimal.

Effects of acute cardioselective and non-selective beta-adrenergic blockade on left-ventricular volumes and vascular resistance at rest and during exercise

The effects of intravenous metoprolol and propranolol on left-ventricular performance were studied by radionuclide cardiography in eight healthy young men at rest and during exercise. At rest, a fall of 7 to 10 mmHg was recorded in systolic blood pressure after both drugs (p less than 0.05). The decrease in cardiac output entirely ascribed to relative bradycardia was 18% after propranolol (p less than 0.01) compared with 6% after metoprolol (p less than 0.05). Left-ventricular volumes did not change at rest. Systemic vascular resistance increased by 14% after metoprolol and by 28% after propranolol (both p less than 0.05). During submaximal bicycle exercise the systolic blood pressure fell by 15 mmHg after both drugs (p less than 0.05). The reduction in exercise heart rate was 17 beats min-1 and 18 beats min-1 (both p less than 0.01), but propranolol reduced cardiac output by 18% (p less than 0.01) compared with 5% (p less than 0.05) after metoprolol, reflecting a reduction in stroke volume induced only by non-selective blockade. A more pronounced left-ventricular end-diastolic dilatation during exercise was allowed by metoprolol and the fall in the exercise ejection fraction was, therefore, smaller after this drug. Concomitantly, the calculated systemic vascular resistance was increased only 6% by metoprolol (p less than 0.05) compared with a 29% increase by propranolol (p less than 0.01). These findings suggest that, at least in healthy subjects, metoprolol is superior to propranolol in the ability to limit adverse cardiovascular changes.

Effects of acute cardioselective and non-selective beta-adrenergic blockade on left-ventricular volumes and vascular resistance at rest and during exercise

The effects of intravenous metoprolol and propranolol on left-ventricular performance were studied by radionuclide cardiography in eight healthy young men at rest and during exercise. At rest, a fall of 7 to 10 mmHg was recorded in systolic blood pressure after both drugs (p less than 0.05). The decrease in cardiac output entirely ascribed to relative bradycardia was 18% after propranolol (p less than 0.01) compared with 6% after metoprolol (p less than 0.05). Left-ventricular volumes did not change at rest. Systemic vascular resistance increased by 14% after metoprolol and by 28% after propranolol (both p less than 0.05). During submaximal bicycle exercise the systolic blood pressure fell by 15 mmHg after both drugs (p less than 0.05). The reduction in exercise heart rate was 17 beats min-1 and 18 beats min-1 (both p less than 0.01), but propranolol reduced cardiac output by 18% (p less than 0.01) compared with 5% (p less than 0.05) after metoprolol, reflecting a reduction in stroke volume induced only by non-selective blockade. A more pronounced left-ventricular end-diastolic dilatation during exercise was allowed by metoprolol and the fall in the exercise ejection fraction was, therefore, smaller after this drug. Concomitantly, the calculated systemic vascular resistance was increased only 6% by metoprolol (p less than 0.05) compared with a 29% increase by propranolol (p less than 0.01). These findings suggest that, at least in healthy subjects, metoprolol is superior to propranolol in the ability to limit adverse cardiovascular changes.

Effects of intravenous metoprolol on global and regional left ventricular function after coronary arterial reperfusion in acute myocardial infarction

Coronary reperfusion in myocardial infarction improves infarct zone motion, but its effect on the global ejection fraction has been less consistent. The directional movement of the ejection fraction is determined by the opposing influences of improved infarct zone motion and diminishing hyperkinesia in the noninfarct zone. Noninfarct zone hyperkinesia has been attributed to catecholamine stimulation, the Frank-Starling mechanism or intraventricular interactions that unload noninfarcted segments. To investigate the influence of catecholamine stimulation, 9 men presenting with a first myocardial infarction (mean age 53 ± 13 years) were studied. Coronary reperfusion was accomplished <4 hours after the onset of myocardial infarction. Radionuclide ventriculography was then performed before and immediately after the intravenous administration of 15 mg of metoprolol. End-diastolic volume did not change, but end-systolic volume increased 28% after metoprolol (p = 0.041). The ejection fraction decreased from 55 ± 13% before metoprolol to 45 ± 14% after its administration (p = 0.002). There was no effect of intravenous metoprolol on infarct zone motion, whereas motion in the noninfarcted segment decreased (p = 0.002). The patients underwent repeat ventriculography after receiving metoprolol, 100 mg orally twice a day for 9 days. Infarct zone motion improved (p < 0.002) and the ejection fraction increased to 55 ± 12% (p < 0.02). Normal zone motion did not change. Thus, compensatory hyperkinesia is at least in part caused by catecholamine stimulation. Conclusions regarding the effects of reperfusion on global ventricular performance can be influenced by the timing of ejection fraction determinations relative to metoprolol therapy.

Effect of intravenous metoprolol on reversible obstructive airways disease.

We gave increasing doses of metoprolol intravenously to seven subjects with stable chronic obstructive pulmonary disease (COPD) who were also receiving their usual bronchodilators. Six of the seven tolerated up to 0.2mg/kg metoprolol without adverse effects, although there were declines in forced expiratory volume in 1 sec (FEV1). At 0.15 mg/kg mean FEV1 fell 12% (p less than 0.025), and at 0.2 mg/kg mean decline in FEV1 was 15% (p less than 0.01). These findings suggest that 0.2 mg/kg metoprolol may be given intravenously to most patients with COPD in addition to previously administered bronchodilators without precipitating clinically significant adverse effects. Any side effects that develop can be reversed by beta agonists.

Haemodynamic dose-response effects of i.v. metoprolol in coronary heart disease.

The haemodynamic effects of intravenous metoprolol, over the dose-range 2.5--20 mg, were studied in 12 patients with coronary heart disease. The pharmacodynamic activity of the drug was confirmed by the suppression of exercise systolic pressure and tachycardia. There were statistically significant dose-response reductions in systolic and diastolic pressures, heart rate and cardiac output together with a dose-related increase in pulmonary wedge pressure. In patients with coronary heart disease intravenous metoprolol should probably not exceed the doses used in this study and should be administered with caution in patients with impairment of pumping function.

Haemodynamic effects of intravenous metoprolol

Haemodynamic effects of intravenous metoprolol