Pathophysiological aspect of the liver in acute obstructive suppurative cholangitis.
This study is prompted in order to clarify the pathophysiological aspect of the liver in acute obstructive suppurative cholangitis (AOSC). An experimental model of AOSC, was prepared by intracholedochal infusion of endotoxin in dogs with and without obstructive jaundice. In the patients with AOSC, liver function was aggravated remarkably compared with that in the stage of non suppurative cholangitis. A rapid fall of platelet count occurred. Experimentally, after intracholedochal infusion of endotoxin, liver function revealed significant hepatic cellular damage. A considerable increase in the S-OCT level was accompanied by a marked rise in blood ammonia concentration. Liver damage due to obstructive jaundice was further aggravated by endotoxin infusion. The level of serotonin in the liver tissue increased markedly after endotoxin infusion. This was accompanied by a rapid fall of platelet counts. Serotonin is considered to be a factor which may cause an impairment of hepatic microcirculation and then hepatic cellular damages. It may be concluded that AOSC is induced by cholangio-venous reflux of endotoxin. Liver function is impaired remarkably due to increased bile canalicular pressure, to the direct affect of endotoxin on liver cells during the process of cholangio-venous reflux, and to impairment of hepatic microcirculation in endotoxin shock. Liver dysfunction contributes to develop this clinical entity and play an important role to make its outcome fatal.
D000208:Acute Disease; D000641:Ammonia / Q000378:metabolism; D000818:Animals; D002761:Cholangitis / Q000097:blood / Q000378:metabolism / Q000503:physiopathology*; D004285:Dogs; D004731:Endotoxins / Q000494:pharmacology; D004926:Escherichia coli; D008099:Liver / Q000378:metabolism / Q000503:physiopathology*; D008111:Liver Function Tests; D012701:Serotonin / Q000378:metabolism; D013492:Suppuration
D004731:Endotoxins; D012701:Serotonin; D000641:Ammonia