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脑缺血预处理即给予短暂亚致死量缺血可对随后的长时间致死性缺血损伤产生耐受。各国学者就其机制进行了广泛研究并发现这与受体激活和一系列信号转导有关,涉及阿片受体、一氧化氮、腺苷、丝裂原活化蛋白激酶等信号途径、N-甲基-D-天冬氨酸受体、生长因子、线粒体和核生存蛋白、Toll样受体等。但具体机制尚未完全阐明且还处于动物实验阶段,如何把实验结果应用于临床是今后将要解决的问题。
Short-term ischemic preconditioning of ischemic preconditioning is tolerated by subsequent prolonged ischemic insult. Scholars around the world conducted a comprehensive study of its mechanism and found that this is related to receptor activation and a series of signal transduction, involving opioid receptors, nitric oxide, adenosine, mitogen-activated protein kinase and other signaling pathways, N-methyl D-aspartate receptors, growth factors, mitochondria and nuclear survivin, Toll-like receptors and the like. However, the specific mechanism has not yet been fully elucidated and still in the experimental stage of animals. Therefore, how to apply the experimental results to clinical practice is a problem to be solved in the future.