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目的:进一步探讨脑肿消围攻缺血性中风急性期脑水肿的作用机制。方法:建立大鼠大脑中动脉阻塞(MCAO)脑缺血动物模型,采用单因素方差分析,检测不同时间点大鼠脑组织含水量、脑细胞Ca2+浓度、脑组织中磷脂酶A(2PLA2)活性表达的变化,并与Ca2+通道阻断剂(尼莫地平)进行对比性研究。结果:脑肿消可使缺血后脑组织中PLA2活性表达水平、Ca2+含量、脑含水量降低,进而减轻脑水肿。其保护作用与钙离子拮抗剂(尼莫地平)相似。结论:脑肿消抑制PLA2活性、降低细胞Ca2+、减轻脑水含量,最终减轻脑水肿的病理改变。
OBJECTIVE: To further explore the mechanism of cerebral edema on brain edema in the acute phase of ischemic stroke. METHODS: An animal model of middle cerebral artery occlusion (MCAO) cerebral ischemia in rats was established. The brain water content, brain cell Ca2+ concentration, and brain tissue phospholipase A (2PLA2) activity at different time points were measured by one-way analysis of variance. Changes in expression and comparative studies with Ca2+ channel blockers (nimodipine). RESULTS: Brain edema can reduce the level of PLA2 activity, Ca2+ content and brain water content in the brain tissue after ischemia, and then reduce cerebral edema. Its protective effect is similar to the calcium antagonist (nimodipine). Conclusion: Brain vasopressor inhibits the activity of PLA2, decreases the cellular Ca2+, and reduces the brain water content, and finally reduces the pathological changes of brain edema.