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d-索他洛尔对犬急性缺血性心力衰竭的血流动力学影响。

Hemodynamic effects of d-sotalol in acute ischemic heart failure in dogs.

作者信息

Mortensen E, Tande P M, Kløw N E, Refsum H

机构信息

Department of Medical Physiology, University of Tromsø, Norway.

出版信息

Am Heart J. 1992 Apr;123(4 Pt 1):970-7. doi: 10.1016/0002-8703(92)90705-z.

Abstract

This study was designed to determine the hemodynamic effects of the class III antiarrhythmic agent d-sotalol in acute ischemic heart failure at concentrations that prolong ventricular repolarization. In pentobarbital-anesthetized open-chest dogs, heart failure was induced by microembolization of the area supplied by the main left coronary artery until a stable left ventricular (LV) end-diastolic pressure of 25 +/- 2 mm Hg was achieved. Embolization shortened the QT interval by 30 +/- 11 msec, while 1 and 2 mg/kg d-sotalol intravenously after embolization lengthened the QT interval by 23 +/- 7 and 39 +/- 7 msec, respectively (n = 7). Heart rate increased after embolization by 19 +/- 7 beats/min, while it decreased by 12 +/- 6 beats/min and by 21 +/- 5 beats/min after d-sotalol. The depressed LV function after embolization assessed by LV pressures, stroke volume, cardiac output, ultrasonometrically estimated LV volume, the pressure-volume relationship, and the time for isovolumic relaxation was not changed following infusion of 1 or 2 mg/kg d-sotalol. Plasma concentrations of d-sotalol were 1.55 +/- 0.33 and 2.58 +/- 0.50 micrograms/ml, respectively. In conclusion, d-sotalol at concentrations prolonging repolarization was devoid of cardiodepressive effects in acute ischemic heart failure in dogs.

摘要

本研究旨在确定Ⅲ类抗心律失常药物d-索他洛尔在急性缺血性心力衰竭中,于延长心室复极的浓度下所产生的血流动力学效应。在戊巴比妥麻醉的开胸犬中,通过对左冠状动脉主要供血区域进行微栓塞诱导心力衰竭,直至左心室舒张末期压力稳定在25±2 mmHg。栓塞使QT间期缩短30±11毫秒,而栓塞后静脉注射1 mg/kg和2 mg/kg的d-索他洛尔分别使QT间期延长23±7毫秒和39±7毫秒(n = 7)。栓塞后心率增加19±7次/分钟,而给予d-索他洛尔后心率分别降低12±6次/分钟和21±5次/分钟。栓塞后通过左心室压力、每搏量、心输出量、超声心动图估计的左心室容积、压力-容积关系以及等容舒张时间评估的左心室功能抑制,在输注1 mg/kg或2 mg/kg的d-索他洛尔后未发生改变。d-索他洛尔的血浆浓度分别为1.55±0.33微克/毫升和2.58±0.50微克/毫升。总之,在犬急性缺血性心力衰竭中,延长复极的d-索他洛尔浓度未产生心脏抑制作用。

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