Oshita M, Sato N, Yoshihara H, Takei Y, Kashio S, Hijioka T, Fukui H, Goto M, Matsunaga T, Okumura S
First Department of Medicine, Osaka University Medical School, Japan.
Alcohol Alcohol Suppl. 1991;1:317-20.
In the perfused rat liver, infusion of ethanol induced an initial increase in portal pressure which is an indicator of vasoconstriction and a subsequent increase in lactic dehydrogenase (LDH) release, which is an indicator of cell damage in a dose-dependent fashion. Simultaneous infusion of sodium nitroprusside, a potent vasodilator, (100 microM) inhibited the increases in portal pressure and LDH release. Focal hepatocellular necrosis evidenced by trypan-blue stained cell nuclei were localized in midzonal and pericentral area of the liver lobules at 60 min after ethanol load. These ethanol-induced microcirculatory disturbance might be involved in the pathogenesis of alcoholic liver disease.
在灌注大鼠肝脏中，输注乙醇会导致门静脉压力最初升高，这是血管收缩的一个指标，随后乳酸脱氢酶（LDH）释放增加，这是细胞损伤的一个指标，且呈剂量依赖性。同时输注强效血管扩张剂硝普钠（100微摩尔）可抑制门静脉压力升高和LDH释放增加。在乙醇负荷后60分钟，锥虫蓝染色细胞核所显示的局灶性肝细胞坏死定位于肝小叶的中区和中央周围区域。这些乙醇诱导的微循环紊乱可能参与了酒精性肝病的发病机制。
