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在近廿年中,一些实验研究资料表明,脑神经细胞的死亡,并不是在缺血-缺氧期间或之后立即发生的,而可能是心肺复苏后另有其它机制参与的后果。近来,钙离子(Ca~(2+))在细胞及内脏发生病理改变过程所起的作用受到了广泛的重视。Ca~(2+)可能是休克、脓毒血症、创伤及缺氧导致组织损害的触发因素。损害的发生与Ca~(2+)向细胞内转移有密切的关系。故而,若能阻滞Ca~(2+)的转移或许能改变上述病理过程的发生和发展。
In the past 20 years, some experimental studies have shown that the death of brain nerve cells does not occur immediately after or during ischemia-hypoxia and may be the result of other mechanisms after CPR. Recently, the role of calcium ion (Ca 2+) in the process of pathological changes in cells and viscera has been widely recognized. Ca ~ (2+) may be the trigger factor of shock, sepsis, trauma and hypoxia leading to tissue damage. The occurrence of damage and Ca ~ (2+) to the intracellular metastasis are closely related. Therefore, if the block Ca 2+ transfer may change the occurrence and development of the pathological process.