Ovize M, Aupetit J F, Rioufol G, Loufoua J, André-Fouët X, Minaire Y, Faucon G
Hôpital Cardiovasculaire et Pneumologique Louis Pradel, Hôpital Saint Joseph et Saint Luc, France.
Am J Physiol. 1995 Jul;269(1 Pt 2):H72-9. doi: 10.1152/ajpheart.1995.269.1.H72.
Preconditioning protects the rat heart from ventricular arrhythmias. However, the mechanism of this beneficial effect and its existence in large animal models remain unknown. We submitted 49 pigs to 40 min of left anterior descending coronary occlusion and 2 h of reperfusion and assessed the incidence of ventricular fibrillation (VF) and time to VF. Monophasic action potential duration (MAPD) and ventricular fibrillation threshold (VFT) were measured throughout the experiment. Preconditioning significantly reduced infarct size but failed to reduce the incidence of VF either during the 40-min ischemic insult or the following reperfusion. Moreover, preconditioning accelerated the onset of VF during the prolonged ischemia; time to VF averaged 8 +/- 2 min in the preconditioned group vs. 18 +/- 2 min in the control group (P < 0.05). This premature peak of VF in preconditioned hearts was associated with a significant decrease of VFT and shortening of MAPD. This suggests that preconditioning does not limit the incidence of VF in the pig model. Rather, preconditioning decreases the time to VF in this species, likely through lowering of the VFT and shortening of the action potential duration.
预处理可保护大鼠心脏免受室性心律失常的影响。然而，这种有益作用的机制及其在大型动物模型中的存在情况仍不清楚。我们将49头猪进行40分钟的左前降支冠状动脉闭塞和2小时的再灌注，并评估室颤（VF）的发生率和发生室颤的时间。在整个实验过程中测量单相动作电位持续时间（MAPD）和室颤阈值（VFT）。预处理显著减小了梗死面积，但在40分钟的缺血损伤期间或随后的再灌注期间未能降低VF的发生率。此外，预处理加速了长时间缺血期间VF的发作；预处理组发生室颤的平均时间为8±2分钟，而对照组为18±2分钟（P<0.05）。预处理心脏中VF的这种过早峰值与VFT的显著降低和MAPD的缩短有关。这表明预处理在猪模型中并不能限制VF的发生率。相反，预处理可能通过降低VFT和缩短动作电位持续时间来缩短该物种发生室颤的时间。
