Jain U
Department of Anesthesia, University of California, San Francisco 94121.
J Card Surg. 1993 Mar;8(2 Suppl):238-41. doi: 10.1111/j.1540-8191.1993.tb01315.x.
Myocardial stunning commonly occurs after cardiopulmonary bypass (CPB). Myocardial stunning can be cardioprotective under some conditions, but in other situations may actually contribute to myocardial infarction (MI). Vascular endothelial stunning may be one of the mechanisms by which myocardial stunning can cause MI. It has been found that 15 minutes of reversible ischemia is enough to cause elevations in vascular resistance and impairment of vasodilator responsiveness. However, no correlation between contractile dysfunction and microvascular stunning has been observed. Transduction defects (increased oxygen extraction and consumption despite normal regional oxygen blood flow and delivery) may be another mechanism by which stunning predisposes to MI, indicating uncoupling of substrate utilization from energy production. In addition, abnormalities in wall motion, oxygen free radical toxicity, hypotension, use of inotropic agents (leading to increased oxygen consumption, high heart rates, and arrhythmias) increase the risk of cellular necrosis. Following CPB, flow limitations due to diffuse atherosclerosis in some areas may result in poor contractility, and newly grafted areas have a high probability of becoming ischemic and stunned. These areas are likely to contribute to MI.
心肌顿抑常见于体外循环(CPB)后。在某些情况下,心肌顿抑可能具有心脏保护作用,但在其他情况下实际上可能导致心肌梗死(MI)。血管内皮顿抑可能是心肌顿抑导致MI的机制之一。已发现15分钟的可逆性缺血足以导致血管阻力升高和血管舒张反应受损。然而,未观察到收缩功能障碍与微血管顿抑之间存在相关性。转导缺陷(尽管局部氧血流和输送正常,但氧摄取和消耗增加)可能是顿抑易导致MI的另一种机制,表明底物利用与能量产生解偶联。此外,壁运动异常、氧自由基毒性、低血压、使用正性肌力药物(导致氧消耗增加、心率加快和心律失常)会增加细胞坏死的风险。CPB后,某些区域由于弥漫性动脉粥样硬化导致的血流受限可能会导致收缩功能不良,新移植区域很可能发生缺血和顿抑。这些区域可能会导致MI。