Apstein C S, Deckelbaum L, Hagopian L, Hood W B
Am J Physiol. 1978 Dec;235(6):H637-48. doi: 10.1152/ajpheart.1978.235.6.H637.
The mechanical and metabolic effects of 3 min of complete global ischemia and 25 min of reperfusion were studied in the isolated rat heart. The decrease in contracile function was biphasic; a rapid 50% decline occurred in the first 10 s of ischemia, after which contractile function transiently stabilized and then fell at a slower rate. During reperfusion, recovery of relaxation was impaired relative to recovery of contractile function. A second period of ischemia and reflow produced changes in contractility, relaxation, and lactate production virtually identical to the initial one. In the absence of glycolytic blockade, tissue lactate accumulation developed, no contracture occurred, the pacing threshold did not increase, and reperfusion after 3 min of ischemia resulted in complete recovery of contractile function. Glycolytic blockade with 0.1 mM iodoacetate (IAA) prevented ischemic lactate production, accelerated the fall in contractility, caused irreversible contracture after 30 s of ischemia, an irreversible increase in pacing threshold within 3 min of ischemia, and poor recovery of contractile function with reperfusion. Thus during the first 3 min of severe ischemia, glycolysis exerted a net beneficial effect on myocardial function despite significant tissue lactate accumulation.
在离体大鼠心脏中研究了3分钟完全性全心缺血和25分钟再灌注的机械和代谢效应。收缩功能的降低呈双相性;在缺血的最初10秒内迅速下降50%,此后收缩功能短暂稳定,然后以较慢的速度下降。在再灌注期间,相对于收缩功能的恢复,舒张功能的恢复受损。第二次缺血和再灌注期引起的收缩性、舒张性和乳酸生成变化与最初的情况几乎相同。在没有糖酵解阻断的情况下,组织乳酸积累增加,未发生挛缩,起搏阈值未升高,缺血3分钟后再灌注导致收缩功能完全恢复。用0.1 mM碘乙酸(IAA)进行糖酵解阻断可防止缺血性乳酸生成,加速收缩性下降,在缺血30秒后引起不可逆挛缩,在缺血3分钟内使起搏阈值不可逆升高,再灌注时收缩功能恢复不良。因此,在严重缺血的最初3分钟内,尽管组织乳酸大量积累,糖酵解对心肌功能仍产生了净有益作用。