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力（PTO）方法测量正弦压，确定了大鼠急性或慢性肝损伤的大鼠肝节分性血管抗性。急性肝损伤是由1小时的偶然造成的，然后在门户和肝动脉灌注的生命中进行1小时重新灌注。 PTO的测量表明，尽管肝静脉（RHV）和肝脏伪像增加了肝血管耐药性（RPV），但再灌注后肝血管耐药的增加主要是由于门户血管耐药性（RPV）引起的。再灌注导致双相肝脏体重增加，而初始峰（3分钟）和第二个峰（60分钟）。初始增加与PTO的增加正相关，表明正弦压力增加对初始重新灌注后体重增加的贡献。晚期肝脏的体重增加可能是由于肝功能评估的肝细胞损伤肝纤维化是慢性肝损伤的肝纤维化，该肝纤维化是由胃内胃内四氯化碳（CCLI D24E D2）诱导的，在12周内引起了微观微纤维纤维纤维纤维化，腹部纤维化，腹腔纤维化，腹部和递Abnormanalmoral liver liver sests test test。 PTO测量表明，经CCL4处理的大鼠的RPV，RHV和RHA的基本水平都大于CCLI D24E D2-d2无对照大鼠的基本水平。但是，RPV的增加与RHV相比是主要的，而RHA的增加最少增加。这一发现表明，肝纤维化中的门静脉高血压主要是由于门户方面的血管耐药性增加引起的。对内皮素-1（ET-1）的肝血管收缩反应性也在CCLII D24 D2处理的生活中研究。与对照大鼠相比，CCLII D24 D2大鼠中RPV和RHV对ET-1的反应被减弱，而在两组之间，RHA没有显着差异。