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犬右冠状动脉急性闭塞诱发的代偿性心脏机制。

Compensatory cardiac mechanisms evoked by acute occlusion of the right coronary artery in dogs.

作者信息

Geiran O, Molaug M, Kiil F

出版信息

Acta Physiol Scand. 1984 Feb;120(2):185-95. doi: 10.1111/j.1748-1716.1984.tb00124.x.

DOI:10.1111/j.1748-1716.1984.tb00124.x
PMID:6711336
Abstract

The cardiac response to intermittent occlusion of the right coronary artery was examined in anesthetized open-chest dogs at different levels of blood volume. The reduction in stroke volume averaged 15 +/- 2% and was related to the extent of the ischemic area (r = 0.72), which comprised 45-70% of the free wall of the right ventricle. Ultrasonic recordings of segment lengths showed end-diastolic distention and activation of the Frank-Starling mechanism in the uninjured parts of the free wall. The transseptal end-diastolic pressure difference was abolished, suggesting movement of the interventricular septum to the left. Nevertheless, the relationship between stroke volume and left ventricular end-diastolic pressure (left ventricular function curve) as well as the relationship between stroke volume and the end-diastolic segment length of the left ventricular free wall were unaltered. Comparisons of data obtained at similar stroke volume showed activation of the Frank-Starling mechanism in the interventricular septum which may compensate for the negative effect of a change in its position.

摘要

在麻醉开胸犬处于不同血容量水平时,研究了右冠状动脉间歇性闭塞时的心脏反应。每搏输出量平均减少15±2%,且与缺血区域范围相关(r = 0.72),该缺血区域占右心室游离壁的45 - 70%。节段长度的超声记录显示舒张末期扩张以及游离壁未损伤部分的Frank-Starling机制激活。室间隔舒张末期压差消失,提示室间隔向左移动。然而,每搏输出量与左心室舒张末期压力之间的关系(左心室功能曲线)以及每搏输出量与左心室游离壁舒张末期节段长度之间的关系未改变。对相似每搏输出量时获得的数据进行比较显示,室间隔中Frank-Starling机制激活,这可能补偿了其位置改变的负面影响。

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