缺血后适应脑保护的耗散结构基础与脑缺血损伤的非线性特征

脑缺血损伤的机制十分复杂，主要内容涉及谷氨酸兴奋毒性、Ca2＋毒性、自由基损伤、一氧化氮损伤、炎性反应以及内质网和线粒体功能障碍等，这些复杂的机制网络具有耗散结构的非线性特征。近年发现缺血后适应可能通过P13K、Akt、MAPK、PKC等通路，KATP通道，抗凋亡等方式阻止或减轻损伤，从而实现脑保护，而形成一个复杂的信号转导体系。而对复杂的生命系统的研究起着指导作用的耗散结构理论是从更高水平层次研究复杂系统的系统科学，文中将从哲学的角度阐释缺血后适应产生大脑保护的耗散结构基础。

Dissipative Structure Foundation of Cerebral Protection with Postconditioning and Brain Ischemia Mechanisms with Nonlinear Characteristics

Glutamate excitotoxicity, calcium toxicity, free radical damage, nitric oxide damage, inflammatory response, dysfunction of the endoplasmic reticulum and mitochondria are the known mechanisms of cerebral ischemia injury. The complex networks of the known mechanisms come along with nonlinear characteristics of dissipative structure. Undergoing postconditioning, pathways of PI3K, Akt, MAPK and PKC, KATP channel and anti--apoptosis take on brain protection, as a complex system. The dissipative structure theory, a higher level of system--level study of complex systematic science, plays a key role in the complex life science system. In perspective of philosophy, this article reviews the dissipative structure foundation of ischemic postconditioning which contributes to cerebral protection.