de Toledo C F, Loureiro-Silva M R, Molina H M, Lanzoni V P, Kouyoumdjian M, Borges D R
Laboratório de Hepatologia Experimental, Universidade Federal de São Paulo.
Rev Assoc Med Bras (1992). 1995 Nov-Dec;41(6):367-72.
To study the hepatic clearance of a glycoprotein (rat plasma kallikrein) by the liver of rats with experimental decompensated cirrhosis.
Cirrhosis was induced by intragastrically administration of carbon tetrachloride 520 mg/kg/week, during 16-19 weeks. After this period, each liver was isolated, exsanguinated and perfused at 37 degrees C with 10nM rat plasma kallikrein (RPK).
58% of the animals died during the treatment and the remaining developed prostration, ascites, jaundice and bleeding; at the end of the treatment period serum aminotransferases were not altered and serum albumin decreased. The liver histology showed cirrhosis. RPK clearance rate of the cirrhosis group (5.4 +/- 0.9 pmol/g liver/10 min) was significantly lower (p < 0.05) than that of the control group (13.5 +/- 2.7 pmol/g liver/10 min).
The development of cirrhosis is associated with a decreased hepatic clearance of a glycoprotein which endocytosis is mediated by a receptor.
研究实验性失代偿期肝硬化大鼠肝脏对一种糖蛋白（大鼠血浆激肽释放酶）的清除情况。
通过每周经胃内给予520mg/kg四氯化碳，持续16 - 19周诱导肝硬化。在此期间结束后，分离每只大鼠的肝脏，放血并在37℃用10nM大鼠血浆激肽释放酶（RPK）进行灌注。
58%的动物在治疗期间死亡，其余动物出现虚脱、腹水、黄疸和出血；治疗期末血清转氨酶未改变但血清白蛋白降低。肝脏组织学显示为肝硬化。肝硬化组的RPK清除率（5.4±0.9pmol/g肝脏/10分钟）显著低于对照组（13.5±2.7pmol/g肝脏/10分钟）（p<0.05）。
肝硬化的发展与一种由受体介导内吞作用的糖蛋白的肝脏清除率降低有关。
