Vascular occlusion methods analyze hepatic hemodynamics in acute and chronic liver injury

We determined hepatic segmental vascular resistances of rats with the acute or chronic liver injury by measuring the sinusoidal pressure using the triple vascular occlusion pressure(Pto)method。The acute hepatic injury was induced by 1 hr-ischemia followed by 1 hr-reperfusion in portally and hepatic arterially perfused livers.The measurement of Pto revealed that the increased hepatic vascular resistance after reperfusion is mainly caused by an increase in the portal vascular resistance(Rpv)although the hepatic venous(Rhv)and hepatic arterial(Rha)resistances are increased。Reperfusion caused biphasic liver weight gain with the initial peak(3min)and the second peak(60min)。The initial increase was positively correlated with an increase in Pto，suggesting the contribution of the increased sinusoidal pressure to the initial post-reperfusion weight gain。The late liver weight gain may be due to the hepatocelular damages assessed by liver function test and bile flow rate。The hepatic fibrosis that served as the chronic liver injury was induced by intragastric administration of carbon tetrachloride(CCl I D24西耶D2)over 12weeks，which caused microscopically micronodular fibrosis，ascites and abnormal liver function test.Pto measurement showed that basal levels of Rpv，Rhv，and Rha of the CCl4-treated rats were all greater than that of the CCl I D24锡D2-free control rats.However，the increase in Rpv was predominant over that in Rhv，and Rha was minimally increased。This finding suggests that portal hypertension in liver fibrosis is caused by mainly an increase in vascular resistance of the portal side。The hepatic vasoconstrictive reactivity to endothelin-1(ET-1)was also studied in CCl I D24 I D2-treated livers.The response to ET-1 of Rpv and Rhv in the CCl I D24西耶D2 rats was attenuated compared with that in the control rats，whereas no significant difference in the Rha was observed between two groups.

We determined hepatic segmental vascular resistances of rats with the acute or chronic liver injury by measuring the sinusoidal pressure using the triple vascular occlusion pressure (Pto) method. The acute hepatic injury was induced by 1 hr-ischemia followed by 1 hr-reperfusion in portally and hepatic arterially perfused livers. The measurement of Pto revealed that the increased hepatic vascular resistance after reperfusion is mainly caused by an increase in the portal vascular resistance (Rpv)although the hepatic venous (Rhv) and hepatic arterial (Rha) resistances are increased. Reperfusion caused biphasic liver weight gain with the initial peak (3 min)and the second peak (60 min). The initial increase was positively correlated with an increase in Pto, suggesting the contribution of the increased sinusoidal pressure to the initial post-reperfusion weight gain. The late liver weight gain may be due to the hepatocelular damages assessed by liver function test and bile flow rate. The hepatic fibrosis that served as the chronic liver injury was induced by intragastric administration of carbon tetrachloride (CClィイD24ィエD2) over 12 weeks, which caused microscopically micronodular fibrosis, ascites and abnormal liver function test. Pto measurement showed that basal levels of Rpv, Rhv, and Rha of the CCl4-treated rats were all greater than that of the CClィイD24ィエD2-free control rats. However, the increase in Rpv was predominant over that in Rhv, and Rha was minimally increased. This finding suggests that portal hypertension in liver fibrosis is caused by mainly an increase in vascular resistance of the portal side. The hepatic vasoconstrictive reactivity to endothelin-1 (ET-1) was also studied in CClィイD24ィエD2-treated livers. The response to ET-1 of Rpv and Rhv in the CClィイD24ィエD2 rats was attenuated compared with that in the control rats, whereas no significant difference in the Rha was observed between two groups.