Yabe K, Takeo S
Department of Pharmacology, Tokyo University of Pharmacy and Life Science, Japan.
Heart Vessels. 1997;12(3):136-42. doi: 10.1007/BF02767131.
The present study was undertaken to determine whether or not tissue glycogen depletion prior to ischemia, and subsequent attenuation of tissue lactate accumulation during ischemia, correlates with postischemic functional recovery of the preconditioned heart. Isolated rat hearts were subjected to 40-min ischemia and 30-min reperfusion. Preconditioning with 5-min ischemia and 5-min reperfusion reduced the preischemic glycogen and postischemic lactate levels of the heart to 60.5 +/- 5.6% and 66.9 +/- 7.7% respectively, of values in non-preconditioned hearts (n = 6), and improved the recovery of the rate-pressure product (RPP) of the ischemic/reperfused heart (87.0 +/- 5.8% versus 25.2 +/- 4.5% of the initial value for the non-preconditioned group, n = 8). Treatment with polymyxin B (50 microM) abolished the preconditioning-induced postischemic recovery of the RPP. Treatment of the non-preconditioned heart with phorbol 12-myristate 13-acetate (15 pmol/5 min) resulted in an improvement in the postischemic recovery of RPP. Neither of these treatments affected the preischemic glycogen and postischemic lactate levels. The results suggest that preischemic glycogen depletion and subsequent attenuation of ischemic lactate accumulation do not play a major role in the preconditioning-induced protection against postischemic contractile dysfunction in perfused rat hearts.
本研究旨在确定缺血前组织糖原耗竭以及随后缺血期间组织乳酸积累的减弱是否与预处理心脏的缺血后功能恢复相关。将离体大鼠心脏进行40分钟缺血和30分钟再灌注。用5分钟缺血和5分钟再灌注进行预处理，使心脏缺血前糖原水平和缺血后乳酸水平分别降至未预处理心脏（n = 6）的60.5±5.6%和66.9±7.7%，并改善了缺血/再灌注心脏的心率-血压乘积（RPP）恢复情况（预处理组为初始值的87.0±5.8%，未预处理组为25.2±4.5%，n = 8）。用多粘菌素B（50μM）处理可消除预处理诱导的RPP缺血后恢复。用佛波醇12-肉豆蔻酸酯13-乙酸酯（15 pmol/5分钟）处理未预处理的心脏可改善RPP的缺血后恢复。这两种处理均未影响缺血前糖原水平和缺血后乳酸水平。结果表明，缺血前糖原耗竭以及随后缺血乳酸积累的减弱在预处理诱导的对灌注大鼠心脏缺血后收缩功能障碍的保护中不发挥主要作用。
