Sasaki Hideki, Shimizu Mitsuyuki, Ogawa Kazuhiko, Okazaki Fumiko, Taniguchi Masayuki, Taniguchi Ikuo, Mochizuki Seibu
Division of Cardiology, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo, Japan.
Int Heart J. 2007 Mar;48(2):205-13. doi: 10.1536/ihj.48.205.
Recently, it has been reported that ischemic postconditioning, a brief episode of ischemia-reperfusion performed after prolonged ischemia, can reduce ischemic myocardial injury. However, the effects of ischemic postconditioning on ischemia/reperfusion injury remain unclear. We investigated the effects of brief ischemia-reperfusion before (ischemic preconditioning) and after (ischemic postconditioning) prolonged ischemia on myocardial ischemia/reperfusion injury, especially reperfusion arrhythmias.
Adult male Sprague-Dawley rats weighing about 400-500 g were used. The isolated heart was perfused using a working heart method (Krebs-Henseleit bicarbonate buffer). In the control group, after stabilization, diastolic global ischemia for 15 minutes was produced by a one-way ball valve with electrical pacing (330 bpm, 2.0 V). After ischemia, the heart was reperfused for 20 minutes. In the preconditioning and postconditioning groups, 5-minute global ischemia was produced before and after ischemia for 15 minutes with a 1 minute interval. An electrocardiogram was performed and left ventricular pressure (LVP, +dP/dt, -dP/dt) and CK activity in coronary effluent were measured during the protocol.
Ischemic preconditioning did not affect the incidence or duration of reperfusion ventricular arrhythmias. Ischemic postconditioning could terminate reperfusion ventricular arrhythmias completely and reduced the duration of reperfusion ventricular arrhythmias significantly (P < 0.01). Furthermore, the recovery ratio of +dP/dt at 20 minutes after initial reperfusion was significantly higher in the postconditioning group than in the other groups.
These results suggest that ischemic postconditioning can terminate reperfusion arrhythmias with no reduction of cardiac function, and may be useful for correcting stunned myocardium.
最近有报道称，缺血后处理，即在长时间缺血后进行的短暂缺血再灌注，可减轻缺血性心肌损伤。然而，缺血后处理对缺血/再灌注损伤的影响仍不明确。我们研究了长时间缺血之前（缺血预处理）和之后（缺血后处理）的短暂缺血再灌注对心肌缺血/再灌注损伤的影响，尤其是对再灌注心律失常的影响。
使用体重约400 - 500克的成年雄性Sprague-Dawley大鼠。采用工作心脏法（Krebs-Henseleit碳酸氢盐缓冲液）对离体心脏进行灌注。在对照组中，稳定后，通过单向球阀和电起搏（330次/分钟，2.0伏）产生15分钟的舒张期全心缺血。缺血后，心脏再灌注20分钟。在预处理组和后处理组中，在15分钟缺血之前和之后以1分钟的间隔产生5分钟的全心缺血。在实验过程中进行心电图检查，并测量左心室压力（LVP、+dP/dt、-dP/dt）和冠状动脉流出液中的CK活性。
缺血预处理不影响再灌注室性心律失常的发生率或持续时间。缺血后处理可完全终止再灌注室性心律失常，并显著缩短再灌注室性心律失常的持续时间（P < 0.01）。此外，再灌注初始20分钟时后处理组的 +dP/dt恢复率明显高于其他组。
这些结果表明，缺血后处理可终止再灌注心律失常且不降低心功能，可能有助于纠正心肌顿抑。
