Hess M L, Kukreja R C
Division of Cardiology, Medical College of Virginia, Richmond 23298, USA.
Ann Thorac Surg. 1995 Sep;60(3):760-6. doi: 10.1016/0003-4975(95)00574-5.
Repeated brief ischemic episodes result in prolonged depression of contractile function despite the absence of irreversible damage, a phenomenon called myocardial stunning. Considerable evidence exists to suggest that oxygen radicals, particularly the hydroxyl radical formed as a result of Fenton reaction or nitric oxide-peroxynitrite pathway, may contribute to the pathogenesis of myocardial stunning. The generation of free radicals may cause sarcoplasmic reticulum dysfunction, and both of these mechanisms may lead to calcium overload, which in turn could exacerbate the damage initiated by oxygen radicals. Antioxidant therapy has been shown to effectively attenuate or even prevent the development of prolonged depression of contractility in many studies. In addition, preconditioning with brief ischemic insults is able to trigger protection, which appears to attenuate stunning 24 to 48 hours later. The mechanism of this protection is not known, although one or more members of the heat shock protein family may have a role in protection against stunning.
尽管没有不可逆损伤，但反复短暂的缺血发作会导致收缩功能长期抑制，这一现象称为心肌顿抑。有大量证据表明，氧自由基，特别是通过芬顿反应或一氧化氮-过氧亚硝酸盐途径形成的羟基自由基，可能参与心肌顿抑的发病机制。自由基的产生可能导致肌浆网功能障碍，这两种机制都可能导致钙超载，进而加剧由氧自由基引发的损伤。在许多研究中，抗氧化治疗已被证明能有效减轻甚至预防收缩力长期抑制的发生。此外，短暂缺血预处理能够触发保护作用，这种保护作用似乎在24至48小时后减轻顿抑。虽然热休克蛋白家族的一个或多个成员可能在预防顿抑中发挥作用，但这种保护机制尚不清楚。
