Riess Matthias L, Camara Amadou K S, Chen Qun, Novalija Enis, Rhodes Samhita S, Stowe David F
Department of Anesthesiology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA.
Am J Physiol Heart Circ Physiol. 2002 Jul;283(1):H53-60. doi: 10.1152/ajpheart.01057.2001.
NADH increases during ischemia because O(2) shortage limits NADH oxidation at the electron transport chain. Ischemic (IPC) and anesthetic preconditioning (APC) attenuate cardiac reperfusion injury. We examined whether IPC and APC similarly alter NADH, i.e., mitochondrial metabolism. NADH fluorescence was measured at the left ventricular wall of 40 Langendorff-prepared guinea pig hearts. IPC was achieved by two 5-min periods of ischemia and APC by exposure to 0.5 or 1.3 mM sevoflurane for 15 min, each ending 30 min before 30 min of global ischemia. During ischemia, NADH initially increased in nonpreconditioned control hearts and then gradually declined below baseline levels. This increase in NADH was lower after APC but not after IPC. The subsequent decline was slower after IPC and APC. On reperfusion, NADH was less decreased after IPC or APC, mechanical and metabolic functions were improved, and infarct size was lower compared with controls. Our results indicate that IPC and APC cause distinctive changes in mitochondrial metabolism during ischemia and thus lead to improved function and tissue viability on reperfusion.
在缺血期间，烟酰胺腺嘌呤二核苷酸（NADH）会增加，因为氧气短缺限制了电子传递链上NADH的氧化。缺血预处理（IPC）和麻醉预处理（APC）可减轻心脏再灌注损伤。我们研究了IPC和APC是否同样改变NADH，即线粒体代谢。在40个用Langendorff法制备的豚鼠心脏的左心室壁上测量NADH荧光。通过两次5分钟的缺血期实现IPC，通过暴露于0.5或1.3 mM七氟醚15分钟实现APC，每次均在30分钟全心缺血前30分钟结束。在缺血期间，未预处理的对照心脏中NADH最初增加，然后逐渐下降至基线水平以下。APC后NADH的这种增加较低，但IPC后没有。IPC和APC后随后的下降较慢。在再灌注时，IPC或APC后NADH减少较少，机械和代谢功能得到改善，与对照组相比梗死面积较小。我们的结果表明，IPC和APC在缺血期间引起线粒体代谢的独特变化，从而导致再灌注时功能改善和组织活力提高。
