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

We determined hepatic segmental vascular ressistances of rats with the acute or chronic liver injury by measuring the sinusoidal pressure using the triple vascular occlusion pressure （Pto） method。急性肝炎损伤是由1小时的分裂引起的，由1小时的反复灌注在门户和肝炎的局部灌注的人中引起的。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。重复融合导致双重liver的权重增加，初始峰值（3分钟）和第二峰值（60分钟）。初始增加与Pto中的增加有积极的相关性，并提出了增加的突触压力对初始后再灌注权重增益的贡献。Late Liver Weight Gain可能会得到由Liver功能测试和Bile Flow Rate评估的Hepatocelular Damage。由慢性肝脏损伤引起的慢性纤维是由四氯碳管理局（CClyy D24 ye D2）诱导的，超过12周，导致微观纤维、皮层和非正常肝脏功能测试。Pto测量显示了CCl 4处理的Rpv、Rhv和Rha的基本水平比CCl 4处理的Rpv、Rhv和Rha的所有老鼠都要大。However，Rpv的增加预示着Rhv的增加，而Rha的增加也很小。这篇文章发现了一个建议，即Liver Fibrosis中的门户高血压主要是由门户侧面的血管抵抗力引起的。对endothelin-1（ET-1）的混合气相反应也在CCly-D24-D2处理的livers中研究过。对Rpv和Rhv在CCLIY D24 Y D2老鼠的反应是由对照老鼠进行比较的，Rha在两组之间观察到没有明显的差异。

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.