Schwartz G G, McHale P A, Greenfield J C
Circ Res. 1982 Jan;50(1):28-37. doi: 10.1161/01.res.50.1.28.
This study was undertaken to determine whether coronary blood flow can be regulated in response to coronary arterial occlusions briefer than a single diastole. The possible involvement of metabolic vs. myogenic mechanisms in such regulation was investigated. Eleven conscious dogs with experimentally produced complete heart block, chronically implanted electromagnetic flow probes, and pneumatic occluders on the left circumflex coronary artery were studied. Diastolic coronary occlusions lasting 100 to 400 msec were performed at paced heart rates of 40, 60, and 120 beats/min. At a heart rate of 60 beats/min, a 200-msec occlusion was sufficiently long to produce a significant reactive hyperemic response; 400-mec occlusions resulted in larger responses, while 100-msec occlusions did not generate a discernible response. The onset of reactive hyperemia was delayed from the end of the occlusion until the first post-occlusion systole. The length of this delay could be altered by changing the heart rate or occlusion duration, but no significant response was detected before the first post-occlusion systole. This characteristic of the data is more consistent with a metabolic than with a myogenic mechanism. If the response is metabolic, the data demonstrate that autoregulation of coronary flow by such a mechanism is very rapid, occurring during the first systole in which a flow deficit is detected by the myocardium.
本研究旨在确定冠状动脉血流是否能够针对短于单个舒张期的冠状动脉闭塞做出调节反应。研究了代谢机制与肌源性机制在这种调节中可能的参与情况。对11只清醒犬进行了研究,这些犬通过实验制造了完全性心脏传导阻滞,长期植入了电磁血流探头,并在左旋冠状动脉上安装了气动闭塞器。在起搏心率为40、60和120次/分钟时,进行了持续100至400毫秒的舒张期冠状动脉闭塞。在心率为60次/分钟时,200毫秒的闭塞时间足够长,可产生显著的反应性充血反应;400毫秒的闭塞导致更大的反应,而100毫秒的闭塞未产生可察觉的反应。反应性充血的起始从闭塞结束延迟至闭塞后第一个收缩期。这种延迟的时长可通过改变心率或闭塞持续时间来改变,但在闭塞后第一个收缩期之前未检测到显著反应。数据的这一特征与代谢机制而非肌源性机制更为一致。如果该反应是代谢性的,数据表明通过这种机制对冠状动脉血流的自动调节非常迅速,发生在心肌检测到血流不足的第一个收缩期。