大鼠肝血窦内皮细胞缺血再灌注损伤机理及防护的研究  

Mechanism and prevention of hepatic sinusoid epithelial cell injuried by ischemia and reperfusion in rats

作　　者：赵永福[1] 秦保明[1] 叶学祥[1] 

机构地区：[1]河南医科大学第一附属医院普外科,450052

出　　处：《中国普通外科杂志》1999年第5期368-371,共4页China Journal of General Surgery

摘　　要：目的　研究肝血窦内皮细胞（ＳＥＣ） 缺血再灌注损伤机理及防护方法。方法　采用大鼠肝部分热缺血再灌注模型，并用丹参和异搏定作为实验组，观察缺血４５ ｍｉｎ 及再灌注３０ ｍｉｎ 后ＳＥＣ 超微结构的变化，及其与氧自由基（ＯＦＲ） 和钙离子拮抗剂的关系，并测定血清谷丙转氨酶（ＡＬＴ） ，谷草转氨酶（ＡＳＴ） 值。结果　缺血再灌注后ＳＥＣ 有损伤，但与ＯＦＲ和细胞内钙超载无关；丹参可防护其损伤，而异搏定不能，但二者均可使肝功能损害减轻。结论　ＯＦＲ 和细胞内钙超载不是ＳＥＣ 缺血再灌注损伤的原因；丹参可防护ＳＥＣ 及肝细胞的缺血再灌注损伤；异搏定不能防护ＳＥＣ 缺血再灌注损伤，但可防护肝细胞损伤，保护肝功能。Objective To study the mechanism and prevention of hepatic sinusoid epithelial cell(HSEC) injury caused by ischemia and reperfusion in rats. Methods In the group treated with Dan Shen and group treated with Isoptin, HSEC ultrastructural changes and its relation with both oxygen free radical(OFR) and intracellular calcium overload as well as serum ALT and AST were observed 45?min after ischemia and 30?min after reperfusion respectively in the rat model of partial normothermic ischemia and reperfusion. Results HSEC displayed injury after ischemia and reperfusion, but showed no relation with OFR or intracellular calcium overload. Dan Shen was able to prevent HSEC from injury, but Isoptin was unable. However both of the medicines could reduce liver damage. Conclusions Neither OFR nor intracellular calcium overflow is the cause of the injury in ischemia and referfusion; Dan Shen can prevent HSEC and hepatocytes in ischemia and reperfusion of injury; Isoptin is unable to prevent HSEC from injury, while it is able to prevent hepatocytes injury so as to protect liver function in ischemia and reperfusion.

关 键 词：再灌注损伤/预防和控制 上皮细胞/超微结构 肝/血液供给 丹参/药理学 异搏定/药理学 细胞低氧/药物作用 

分 类 号：R364.12[医药卫生—病理学] R285.5[医药卫生—基础医学]