Doenst T, Guthrie P H, Taegtmeyer H
Department of Internal Medicine, University of Texas-Houston Medical School, 77030, USA.
Mol Cell Biochem. 1998 Mar;180(1-2):153-61.
We tested the hypothesis that glycogen levels at the beginning of ischemia affect lactate production during ischemia and postischemic contractile function. Isolated working rat hearts were perfused at physiological workload with bicarbonate buffer containing glucose (10 mmol/L). Hearts were subjected to four different preconditioning protocols, and cardiac function was assessed on reperfusion. Ischemic preconditioning was induced by either one cycle of 5 min ischemia followed by 5, 10, or 20 min of reperfusion (PC5/5, PC5/10, PC5/20), or three cycles of 5 min ischemia followed by 5 min of reperfusion (PC3 x 5/5). All hearts were subjected to 15 min total, global ischemia, followed by 30 min of reperfusion. We measured lactate release, timed the return of aortic flow, compared postischemic to preischemic power, and determined tissue metabolites at selected time points. Compared with preischemic function, cardiac power during reperfusion improved in groups PC5/10 and PC5/20, but was not different from control in groups PC5/5 and PC3 x 5/5. There was no correlation between preischemic glycogen levels and recovery of function during reperfusion. There was also no correlation between glycogen breakdown (or resynthesis) and recovery of function. Lactate accumulation during ischemia was lowest in group PC5/20 and highest in the group with three cycles of preconditioning (PC3 x 5/5). Lactate release during reperfusion was significantly higher in the groups with low recovery of power than in the groups with high recovery of power. In glucose-perfused rat heart recovery of function is independent from both pre- and postischemic myocardial glycogen content over a wide range of glycogen levels. The ability to utilize lactate during reperfusion is an indicator for postischemic return of contractile function.
缺血开始时的糖原水平会影响缺血期间的乳酸生成以及缺血后收缩功能。将离体工作的大鼠心脏在生理负荷下用含葡萄糖（10 mmol/L）的碳酸氢盐缓冲液灌注。心脏接受四种不同的预处理方案，并在再灌注时评估心脏功能。缺血预处理通过以下方式诱导：5分钟缺血 followed by 5、10或20分钟再灌注的一个周期（PC5/5、PC5/10、PC5/20），或5分钟缺血 followed by 5分钟再灌注的三个周期（PC3 x 5/5）。所有心脏均经历15分钟的全心缺血，随后再灌注30分钟。我们测量了乳酸释放，记录主动脉血流恢复的时间，比较缺血后与缺血前的功率，并在选定时间点测定组织代谢物。与缺血前功能相比，PC5/10和PC5/20组再灌注期间的心脏功率有所改善，但PC5/5和PC3 x 5/5组与对照组无差异。缺血前糖原水平与再灌注期间功能恢复之间无相关性。糖原分解（或再合成）与功能恢复之间也无相关性。缺血期间乳酸积累在PC5/20组最低，在三个预处理周期组（PC3 x 5/5）最高。功率恢复低的组再灌注期间的乳酸释放明显高于功率恢复高的组。在葡萄糖灌注的大鼠心脏中，在广泛的糖原水平范围内，功能恢复与缺血前后心肌糖原含量均无关。再灌注期间利用乳酸的能力是缺血后收缩功能恢复的一个指标。
