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六十年代至七十年代前期,从临床观察及部分实验材料认为654-2的抗休克作用主要是通过其扩血管作用改善微循环。七十年代后期以未,大量实验研究结果说明,654-2抗休克作用的机制主要不是通过扩张血管增加器官血流量,而在于它能在细胞水平上保护细胞、提高细胞对缺血缺氧的耐受性,从而稳定溶酶体和线粒体等亚细胞结构,减少溶酶体酶的释放和休克因子的产生,因而减轻或防止休克过程向不可逆发展的倾向。
From the 1960s to the early 1970s, from the clinical observation and some experimental materials, it is considered that the anti-shock effect of 654-2 mainly improves microcirculation through its vasodilator effect. In the late 1970s, a large number of experimental studies have shown that 654-2 anti-shock mechanism is not mainly through the dilation of blood vessels to increase organ blood flow, but rather it can protect cells at the cellular level and improve cell hypoxia-ischemia Tolerance to stabilize lysosomes and mitochondria and other subcellular structures, reduce the release of lysosomal enzymes and the production of shock factors, thus reducing or preventing the tendency of shock process to irreversible development.