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

血管闭塞方法分析急慢性肝损伤中的肝脏血流动力学

基本信息

批准号：
10557138
负责人：
SHIBAMOTO Toshishige
金额：
$ 3.58万
依托单位：
Shinshu University School of Medicine
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B)
财政年份：
1998
资助国家：
日本
起止时间：
1998 至 1999
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-10557138/
关键词：
triple occlusion pressure portal pressure hepatic circulation portal hypertension liver cirrhosis isolated perfused rat liver carbon tetrachloride ischemia-reperfusion portal hypertension liver injury ischemia reperfusion

项目摘要

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.

我们通过使用三重血管闭塞压（Pto）方法测量肝窦压力来测定急性或慢性肝损伤大鼠的肝段血管阻力。急性肝损伤是通过门静脉缺血1小时然后再灌注1小时诱导的。肝动脉灌注肝脏Pto的测量显示，再灌注后肝血管阻力增加主要是由门脉血管阻力增加引起的。 (Rpv)虽然肝静脉(Rhv)和肝动脉(Rha)阻力增加，但再灌注引起双相肝脏重量增加，与初始峰值(3分钟)和第二峰值(60分钟)呈正相关。 Pto 增加，表明正弦压力增加对最初再灌注后体重增加的贡献可能是由于肝功能评估的肝细胞损伤所致。灌胃四氯化碳（CCD24D2）超过12周，导致肝纤维化，即慢性肝损伤，导致镜下微结节性纤维化、腹水和肝功能检测显示基础水平异常。 CCl4处理组大鼠的Rpv、Rhv和Rha均大于对照组然而，不含 CCl-D24-D2 的对照大鼠中，Rpv 的增加占主导地位，而 Rha 的增加很少。这一发现表明，肝纤维化中的门脉高压主要是由门脉血管阻力增加引起的。还在 CCL-D24 处理的肝脏中研究了对内皮素-1 (ET-1) 的肝血管收缩反应。 CClIID24D2大鼠的Rpv和Rhv与对照大鼠相比减弱，而Rha在两组之间没有观察到显着差异。