论文部分内容阅读
为探讨654-2抗休克的细胞机制,本工作在家兔晚期失血性休克模型上,观察654-2对休克动物肝细胞线粒体镁含量改变的影响,结果发现,失血性休克动物血浆镁浓度进行性升高与动物血压的降低呈负相关关系;休克动物肝线粒体镁含量明显减少;而用654-2治疗时,显著抑制失血性休克时血浆镁和肝线粒体镁含量的改变,明显改善休克动物的预后。实验结果提示654-2可能具有稳定休克动物肝线粒体的作用。
In order to investigate the cellular mechanism of 654-2 anti-shock, we investigated the effect of 654-2 on the change of mitochondrial magnesium content in liver cells of shock animals. We found that the plasma magnesium concentration of hemorrhagic shock animals Sexual increase and animal blood pressure was negatively correlated; shock animals, liver mitochondrial magnesium content decreased significantly; while treatment with 654-2, significantly inhibited hemorrhagic shock in plasma magnesium and liver mitochondrial magnesium content changes, significantly improved shock animals The prognosis. The experimental results suggest that 654-2 may have the effect of stabilizing the animal liver mitochondria.