Bolli R, Zhu W X, Thornby J I, O'Neill P G, Roberts R
Department of Medicine, Baylor College of Medicine, Houston, Texas 77030.
Am J Physiol. 1988 Jan;254(1 Pt 2):H102-14. doi: 10.1152/ajpheart.1988.254.1.H102.
The postischemic recovery of contractile function [measured as systolic wall thickening (WT)] was analyzed in 21 conscious dogs undergoing a 15-min coronary occlusion followed by 7 days of reperfusion (REP). Average WT was still depressed 24 h after REP (85% of base line, P less than 0.001) and returned to base line by 48 h. Analysis of individual dogs, however, revealed marked variability, whereby some recovered completely by 1 h of REP and others required up to 48 h. WT recovered completely within 30 min in dogs with collateral blood flow (CBF) greater than 50% of nonischemic zone flow (NZF) but was still impaired at 24 h (P less than 0.05) in those with CBF less than 25% of NZF. There was a close, curvilinear relation between WT during the first 4 h of REP and transmural CBF, which was described best by an exponential equation WT (as percent of base line) = P0-P1e-P2.CBF(as % of NZF) (r2 = 0.92 at 1 h, 0.76 at 2 h, 0.71 at 3 h, and 0.72 at 4 h), where P0, P1, and P2 are regression coefficients. Importantly, the slope of the regression line was very steep at low CBF, implying that even small differences in CBF produce large differences in postischemic function. Heart rate, systolic pressure, and rate-pressure product during ischemia were also related to WT after REP, but when the effect of CBF was taken into account, the influence of these variables became insignificant. The size of the occluded vascular bed did not correlate with postischemic WT. The presence of hypokinesis or akinesis during ischemia was associated with rapid recovery after REP, but there was no relation between ischemic and postischemic dysfunction when dyskinesis was present during occlusion. Thus, on the average, regional function remains depressed for 24 h after a 15-min ischemic episode, but there is considerable individual variability. This variable rate of recovery is determined primarily by the severity of blood flow reduction during ischemia. Systemic hemodynamics may modulate recovery of function indirectly via their effects on ischemic blood flow.
在21只清醒犬中分析了缺血后收缩功能的恢复情况[以收缩期室壁增厚（WT）来衡量]，这些犬经历了15分钟的冠状动脉闭塞，随后进行7天的再灌注（REP）。再灌注24小时后平均WT仍低于基线水平（为基线的85%，P<0.001），48小时后恢复至基线水平。然而，对个体犬的分析显示存在显著差异，一些犬在再灌注1小时后完全恢复，而另一些犬则需要长达48小时。侧支血流（CBF）大于非缺血区血流（NZF）50%的犬，WT在30分钟内完全恢复，但CBF小于NZF 25%的犬在24小时时仍存在功能受损（P<0.05）。再灌注最初4小时内的WT与透壁CBF之间存在密切的曲线关系，用指数方程WT（作为基线的百分比）=P0 - P1e - P2·CBF（作为NZF的百分比）能最好地描述这种关系（1小时时r2 = 0.92，2小时时r2 = 0.76，3小时时r2 = 0.71，4小时时r2 = 0.72），其中P0、P1和P2为回归系数。重要的是，在低CBF时回归线的斜率非常陡峭，这意味着即使CBF的微小差异也会导致缺血后功能的巨大差异。缺血期间的心率、收缩压和心率 - 压力乘积也与再灌注后的WT相关，但在考虑CBF的影响后，这些变量的影响变得不显著。闭塞血管床的大小与缺血后WT无关。缺血期间存在运动减弱或运动不能与再灌注后快速恢复相关，但在闭塞期间存在运动障碍时，缺血和缺血后功能障碍之间无相关性。因此，平均而言，15分钟缺血发作后局部功能在24小时内仍低于正常水平，但个体差异很大。这种恢复速度的差异主要由缺血期间血流减少的严重程度决定。全身血流动力学可能通过对缺血血流的影响间接调节功能恢复。
