Zuurbier C J, van Beek J H
Laboratory for Physiology, Vrije Universiteit (ICaR-VU), Amsterdam, The Netherlands.
Cardiovasc Res. 1997 Jul;35(1):113-9. doi: 10.1016/s0008-6363(97)00104-1.
To investigate effect of brief ischemia on mitochondrial function in intact myocardium, rather than in isolated mitochondria.
The mitochondrial response was characterized by the mean response time (tmito) of cardiac mitochondrial O2 consumption to steps in heart rate. Isolated isovolumic rabbit hearts were perfused at 28 degrees C with a constant flow of Tyrode solution containing 11 mM glucose. O2 consumption and tmito were determined before ischemia and after 25 min of no-flow global ischemia during which hearts were either paced (I + P, n = 8) or unpaced (I - P, n = 8). A non-ischemic control group (N = 8) was also examined.
At 20 min reperfusion, developed left ventricular pressure (DLVP) after I + P was decreased to 47 +/- 3% (mean +/- s.e.m.; P < 0.05) of control DLVP without significant changes in venous creatine kinase efflux, indicating contractile stunning. In contrast complete contractile recovery was observed after I - P. Before ischemia, tmito was 11.2 +/- 0.6 and 14.9 +/- 0.7 s for heart rate steps from 60 to 70 and from 60 to 120 beats/min, respectively. The tmito was lower (P < 0.05) for the corresponding downward steps (10.5 +/- 0.6 and 12.4 +/- 0.6 s, respectively). An increase (P < 0.05) in tmito was observed in the course of the experiment for upward (1.2 +/- 0.3 s) and downward steps (1.4 +/- 0.3 s), but the change was similar after ischemia to that in time-matched controls (P > 0.05, both for I - P and I + P vs. control). Oxygen consumption, compared at fixed levels of the rate x pressure product, was unchanged after ischemia (P > 0.05, for both I - P and I + P vs. controls), suggesting undiminished efficiency of mitochondrial ATP production.
Twenty-five minutes ischemia does not affect mitochondrial function in rabbit hearts at 28 degrees C, even when contractile stunning resulted.
研究短暂缺血对完整心肌而非分离线粒体中线粒体功能的影响。
线粒体反应通过心脏线粒体氧消耗对心率阶跃变化的平均反应时间（tmito）来表征。将离体等容兔心在28℃下用含11 mM葡萄糖的泰罗德溶液以恒定流量灌注。在缺血前以及无血流全心缺血25分钟后（期间心脏要么起搏（I + P，n = 8）要么不起搏（I - P，n = 8））测定氧消耗和tmito。还检查了一个非缺血对照组（N = 8）。
在再灌注20分钟时，I + P组左心室舒张末压（DLVP）降至对照组DLVP的47±3%（平均值±标准误；P < 0.05），静脉肌酸激酶流出无显著变化，表明存在收缩功能障碍。相比之下，I - P组观察到完全的收缩功能恢复。缺血前，心率从60次/分钟升至70次/分钟以及从60次/分钟升至120次/分钟时，tmito分别为11.2±0.6秒和14.9±0.7秒。相应的向下心率阶跃变化时tmito较低（P < 0.05）（分别为10.5±0.6秒和12.4±0.6秒）。在实验过程中，向上（1.2±0.3秒）和向下（1.4±0.3秒）心率阶跃变化时观察到tmito增加（P < 0.05），但缺血后的变化与时间匹配的对照组相似（I - P和I + P与对照组相比，P均> 0.05）。在固定的心率×压力乘积水平下比较氧消耗，缺血后无变化（I - P和I + P与对照组相比，P均> 0.05），表明线粒体ATP生成效率未降低。
25分钟缺血不影响28℃下兔心的线粒体功能，即使出现了收缩功能障碍。
