Tani M, Hasegawa H, Suganuma Y, Shinmura K, Kayashi Y, Nakamura Y
Department of Geriatric Medicine, Keio University School of Medicine, Tokyo, Japan.
Am J Physiol. 1996 Dec;271(6 Pt 2):H2515-9. doi: 10.1152/ajpheart.1996.271.6.H2515.
Protection of the ischemic myocardium by pretreatment with a high dose of 2,3-butanedione monoxime (BDM) is attributed to the enhancement of glycolytic ATP production rather than to the inhibition of contracture during mild ischemia. Our objective was to investigate whether the inhibition of contracture would protect the arrested heart during prolonged ischemia. Isolated perfused rat hearts were subjected to 30 min of low-flow ischemia followed by reperfusion. Ischemic hearts were treated with BDM (5 mmol/l) after beating stopped. BDM ameliorated the increase in intraventricular pressure after ischemia without significant changes in ATP levels and with a decreased accumulation of lactate. BDM treatment accelerated the recovery of function and high-energy phosphates with reduced myocardial Ca2+ overload. The results of this study suggested that inhibition of contracture can protect the heart from ischemia-reperfusion injury.
高剂量的2,3 - 丁二酮单肟（BDM）预处理对缺血心肌的保护作用归因于糖酵解ATP生成的增强，而非轻度缺血期间挛缩的抑制。我们的目的是研究挛缩的抑制是否会在长时间缺血期间保护停搏的心脏。将离体灌注的大鼠心脏进行30分钟的低流量缺血，然后再灌注。心跳停止后，对缺血心脏用BDM（5 mmol/l）进行处理。BDM改善了缺血后心室内压的升高，ATP水平无显著变化，乳酸积累减少。BDM处理加速了功能和高能磷酸盐的恢复，心肌Ca2+超载减少。本研究结果表明，挛缩的抑制可保护心脏免受缺血 - 再灌注损伤。
