Canty J M
Department of Medicine, State University of New York, Buffalo.
Circ Res. 1988 Oct;63(4):821-36. doi: 10.1161/01.res.63.4.821.
The present study was intended to define the interrelation among endocardial flow, endocardial function, and coronary arterial pressure during spontaneous autoregulation in the left ventricle of chronically instrumented unanesthetized dogs. Steady-state sonomicrometric measurements of regional function and epicardial coronary artery pressure were used to determine the lower pressure limit of endocardial autoregulation while global indexes of myocardial demand remained constant. Transmural wall thickening in the circumflex bed remained unchanged (+/- 5% of control values) until coronary pressure fell below 39 +/- 5.6 (SD) mm Hg. Endocardial segment shortening was similarly constant until coronary pressure fell below 42 +/- 7.4 mm Hg. There was no significant change in endocardial flow as coronary pressure was reduced over the autoregulatory plateau from 84 to 49 mm Hg (1.05-0.99 ml/min/g, p = NS). Below the critical pressure limits, small additional reductions in pressure were associated with marked reductions in both endocardial flow and function. The coronary pressure-function relation was linear as well as steep in this range for both wall thickening (r = 0.94 +/- 0.05) and segment shortening (r = 0.96 +/- 0.03). Although the relation between endocardial flow and function showed more variability than pressure-function relations at low pressures, wall thickening reductions and endocardial flow reductions related on a nearly one-to-one basis. The present study establishes that the coronary pressure-function relation can be used to define the lower limit of endocardial autoregulation. It also indicates that the lower pressure limit of endocardial autoregulation is considerably less than in anesthetized animals (40 vs. 70 mm Hg) and that steady-state flow above this limit is controlled more tightly. Although these differences may relate to systemic hemodynamics, it seems likely that general anesthesia and/or acute surgical instrumentation alter coronary autoregulation under at least some experimental circumstances.
本研究旨在确定在长期植入仪器的未麻醉犬左心室自发自动调节过程中，心内膜血流、心内膜功能和冠状动脉压力之间的相互关系。在心肌需求的整体指标保持恒定的情况下，使用区域功能和心外膜冠状动脉压力的稳态超声心动图测量来确定心内膜自动调节的下限压力。直到冠状动脉压力降至39±5.6（标准差）mmHg以下，回旋支床的透壁壁增厚保持不变（±对照值的5%）。直到冠状动脉压力降至42±7.4 mmHg以下，心内膜节段缩短同样保持恒定。当冠状动脉压力在自动调节平台期从84 mmHg降至49 mmHg时（1.05 - 0.99 ml/min/g，p = 无显著性差异），心内膜血流没有显著变化。在临界压力下限以下，压力的小幅额外降低与心内膜血流和功能的显著降低相关。在此范围内，冠状动脉压力 - 功能关系对于壁增厚（r = 0.94±0.05）和节段缩短（r = 0.96±0.03）而言既是线性的也是陡峭的。尽管在低压下心内膜血流与功能之间的关系比压力 - 功能关系表现出更多变异性，但壁增厚减少和心内膜血流减少几乎呈一对一相关。本研究证实冠状动脉压力 - 功能关系可用于定义心内膜自动调节的下限。它还表明心内膜自动调节的下限压力远低于麻醉动物（40 mmHg对70 mmHg），并且高于此限的稳态血流受到更严格的控制。尽管这些差异可能与全身血流动力学有关，但在至少某些实验情况下，全身麻醉和/或急性手术植入似乎会改变冠状动脉自动调节。
