应用体视学及细胞化学对大鼠氟烷性肝炎发生机理的研究  

A Stereological and Cytochemical Study on the Pathogenesis of Hepatitis Induced by Halothane in Rats

作　　者：郑唯强[1] 詹鎔洲[1] 俞卫锋[2] 王景阳 

机构地区：[1]第二军医大学病理解剖学教研室,200433 [2]长海医院麻醉科,200433

出　　处：《第二军医大学学报》1993年第4期308-312,共5页Academic Journal of Second Military Medical University

摘　　要：采用Ca^(2+)细胞化学定位与EDX电镜微量元素分析,结合肝脏显微病理的体视学分析及肝脏超微病理的电子计算机图象处理,从生化及形态学角度探讨了肝细胞钙平衡的改变在氟烷性肝炎发生发展中的作用。结果表明,在酶诱导缺氧条件下,吸入氟烷可致肝细胞胞浆及线粒体钙负荷增加,其原因一方面是由于氟烷使肝细胞从细胞外摄取钙增加,而泵出Ca^(2+)减少;另一方面是由于氟烷使细胞内贮存Ca^(2+)释放增加。提示肝细胞Ca^(2+)平衡的改变在氟烷性肝炎的发生发展中起着重要作用。This study was designed to investigate the relationship between the hepatotoxicity of Halothane and altered hepatic calcium homeostasis in enzyme-induced hypoxic rats by means of Ca2+ cytochemistry location and EDX microanalysis combined with micropathological stereology of liver and ultrastructural analysis by computer. The results showed that more calcium precipitated the cytoplasm and mitochondria of liver following Halothane exposure than the controls. Based on the experiments, this alteration appeared to be contributed to the accelerated uptake of Ca2+ by the hepatocytes and lessened to pump out the decreased loaded Ca2+ on the other hand. The release of the reserved Ca2+ was increased by Halothane as compared with controls. These results suggest that a loss of regulation of cellular Ca2+ levels plays an important role in the mechanism of hepatotoxicity by Halothane exposure.

关 键 词：组织化学 肝炎 中毒性 氟烷 大鼠 

分 类 号：R575.1[医药卫生—消化系统]