豚鼠心房心肌完全收缩性舒张恢复的延迟。

H Reichel, K Baumann
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引用次数: 0

摘要

在豚鼠离体灌注左心房中,在37℃和240/min的刺激速率下记录压力振幅,并插入可变静息暂停。经过较长时间间隔后,制剂产生最大压力,这与灌注时间或任何正性肌力干预无关。发现后者可缩短恢复完全收缩性所需的时间。硝苯地平(5 × 10(-7)M)主要通过延迟恢复时间发挥负性肌力作用;乙酰胆碱(2 × 10(-7)M),通过在整个刺激间隔范围内同时降低所有压力振幅。后一种效果与降低[Ca2+]o的效果相似。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Delay in diastolic restitution of full myocardial contractility in guinea pig atrium.

In an isolated perfused left atrium of guinea pig, pressure amplitudes were recorded at 37 degrees C and a stimulation rate of 240/min with interposed variable resting pauses. After prolonged intervals the preparation develops maximum pressure, which does not depend on perfusion time or on any positive inotropic intervention. The latter is found to shorten the time needed for restitution of full contractility. Nifedipine (5 X 10(-7)M) exerts its negative inotropic effect mainly by a delay in restitution time; acetylcholine (2 X 10(-7)M), by a concomitant reduction of all pressure amplitudes over the whole range of stimulus intervals. The latter effect is similar to that of lowering [Ca2+]o.

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