Nanji A A, Jui L T, French S W
Department of Pathology, New England Deaconess Hospital, Boston, MA 02215.
Life Sci. 1989;45(10):885-90. doi: 10.1016/0024-3205(89)90202-6.
Two groups of experimental animals with pair-fed controls were studied to evaluate the effect of chronic carbon monoxide (CO) exposure on progression of experimental alcoholic liver injury. Eight pairs of male Wistar rats were continuously infused liquid diet and ethanol or isocaloric dextrose for four months. Four pairs were also exposed to CO. Liver damage was followed monthly by serum ALT and morphologic assessment of liver biopsy. Serum levels of ALT were significantly higher in the CO-ethanol group compared to other groups. Electron microscopy revealed a greater degree of cell necrosis in the CO exposed group which explained the significantly higher ALT activity in these animals. Both experimental groups (CO-ethanol and air-ethanol) had significantly greater liver damage than controls. Carboxyhemoglobin levels were not different in the ethanol-fed and control group. Our results show that chronic CO exposure enhances liver cell necrosis in ethanol-fed rats thereby lending support to the hypothesis that ethanol and hypoxia enhance cellular disruption in the liver which could be important in the pathogenesis of alcoholic liver disease in rats.
研究了两组配有成对喂养对照的实验动物，以评估长期暴露于一氧化碳（CO）对实验性酒精性肝损伤进展的影响。八对雄性Wistar大鼠连续四个月接受液体饮食和乙醇或等热量葡萄糖输注。四对大鼠还暴露于CO中。每月通过血清ALT和肝活检的形态学评估来跟踪肝损伤情况。与其他组相比，CO-乙醇组的血清ALT水平显著更高。电子显微镜检查显示，CO暴露组的细胞坏死程度更高，这解释了这些动物中ALT活性显著更高的原因。两个实验组（CO-乙醇组和空气-乙醇组）的肝损伤均明显大于对照组。乙醇喂养组和对照组的羧基血红蛋白水平没有差异。我们的结果表明，长期暴露于CO会增强乙醇喂养大鼠的肝细胞坏死，从而支持以下假设：乙醇和缺氧会增强肝脏中的细胞破坏，这可能在大鼠酒精性肝病的发病机制中起重要作用。
