Dependency of myocardial reactive hyperemia on coronary artery pressure in the dog.
Dependency of myocardial reactive hyperemia on coronary artery pressure in the dog.
复制标题
狗心肌反应性充血对冠状动脉压力的依赖性。
DOI：
10.1152/ajpheart.1981.240.5.h709
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发表时间：
1981
期刊：
影响因子：
--
通讯作者：
Bishop,VS
中科院分区：
文献类型：
--
作者：
Dole,WP;Montville,WJ;Bishop,VS
我们研究了 20 只闭胸麻醉狗短暂血流停止后冠状动脉压力对心肌反应性充血的影响。通过右颈动脉插入套管，从加压动脉储库对回旋动脉进行灌注。将冠状动脉压力从 60 mmHg 增加至 160 mmHg 不会改变心率、体循环压力或左心室 dP/dtmax。对于10秒的流入阻塞，冠状动脉压力从40毫米汞柱增加20毫米汞柱，导致充血峰值流量[40+/-4至257+/-18（SE）ml/min]、总充血流量（2+/-1至42+/-4ml）和充血流量持续时间（9+/-2至37+/-3秒）成比例增加。当闭塞前压力保持恒定而闭塞后压力变化时，这些结果没有变化。闭塞时间较短后，冠状动脉压力对充血血流的影响逐渐减弱。这些数据表明，冠状动脉压力对短暂动脉血流停滞后心肌反应性充血的特征有重大影响。观察到的压力依赖性表明，冠状动脉反应性充血可能部分是一种被动血流反应，这可以通过正常血管对闭塞后压力的反应性的短暂抑制来解释。反应性充血的被动成分可以解释心脏中典型观察到的血流债务的过度偿还。
We studied the effects of coronary artery pressure on myocardial reactive hyperemia following brief flow arrests in 20 closed-chest anesthetized dogs. The circumflex artery was perfused from a pressurized arterial reservoir with a cannula inserted through the right carotid artery. Increasing coronary pressure from 60 to 160 mmHg did not alter heart rate, systemic pressure, or left ventricular dP/dtmax. For 10-s inflow occlusions, 20-mmHg increments in coronary pressure from 40 to 160 mmHg resulted in proportional increases in peak hyperemic flow [40 +/- 4 to 257 +/- 18 (SE) ml/min], total hyperemic flow (2 +/- 1 to 42 +/- 4 ml), and the duration of hyperemic flow (9 +/- 2 to 37 +/- 3 s). These results were unchanged when preocclusion pressure was held constant and postocclusion pressure varied. The influence of coronary artery pressure on hyperemic flow was progressively less pronounced after occlusions of shorter duration. These data indicate that coronary artery pressure has a major influence on the characteristics of myocardial reactive hyperemia after brief periods of arterial flow arrest. The observed pressure dependency suggests that coronary reactive hyperemia may be, in part, a passive flow response that could be explained by a transient depression of the normal vascular reactivity to postocclusion pressure. A passive component to reactive hyperemia could account for the overrepayment of bloow flow debt characteristically observed in the heart.