Brain ischemic anoxia. Mechanisms of injury.
Brain ischemic anoxia. Mechanisms of injury.
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脑缺血缺氧。
DOI：
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发表时间：
1984
期刊：
影响因子：
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通讯作者：
C. D. Winegar
中科院分区：
文献类型：
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作者：
B. White;J. Wiegenstein;C. D. Winegar
发展有效的治疗方法以保护心脏骤停患者的正常神经功能取决于我们对缺血性缺氧的病理生理学的日益加深的理解。因此，有必要回顾我们对这些机制的新理解，以及实验室对保护因心脏骤停而受损的神经元的治疗方法的研究。早期的学说认为，4到6分钟的缺血缺氧会导致不可逆的脑损伤，这是基于20世纪40年代对呼吸100%氮气的狗所做的工作。1，2然而，从Ames和Guarian3以及Hossman和Kleihues4的工作中可以明显看出，神经元本身对完全缺血缺氧具有实质性的内在抵抗力。证据表明，中枢神经系统神经元可以耐受20到60分钟的完全缺血缺氧，而不会造成不可逆转的损伤。在这些严重的侮辱之后，神经元重新获得合成蛋白质、产生三磷酸腺苷(ATP)的能力，以及
THE DEVELOPMENT of effective therapy to preserve normal neurological function in patients surviving a cardiac arrest hinges on our growing understanding of the pathophysiology of ischemic anoxia. It is worthwhile, then, to review our new understanding of these mechanisms, as well as the laboratory search for therapies to protect neurons injured by cardiac arrest. The early doctrine that four to six minutes of ischemic anoxia leads to irreversible brain injury was based on work done in the 1940s with dogs subjected to breathing 100% nitrogen.1,2However, it became apparent from work by Ames and Guarian3and Hossman and Kleihues4that the neurons themselves have substantial intrinsic resistance to complete ischemic anoxia. The evidence suggests that CNS neurons can tolerate between 20 and 60 minutes of complete ischemic anoxia without irreversible injury. Following these severe insults, neurons regain the ability to synthesize protein, produce adenosine triphosphate (ATP), and