Sepsis and cholestasis: basic findings in the sinusoid and bile canaliculus

It is well known that the liver plays a major role in the clearance of systemic toxemia and is postulated as a regulational organ in the host-defense system. The well-controlled interaction between hepatic parenchymal cells and sinusoidal lining cells including macrophages and Kupffer cells can systematically regulate even critical infections. However, when patients are under the overload condition caused by severe infection, rejection of a transplanted liver and other hapatic dysfunction often are experienced following surgery. Among various signs and symptoms of hepatic dysfunction, progressive cholestasis is recognized as a polarized representation of the irreversible changes in hepatic constitutional cellular functions, especially in hepatic parenchymal cells. Bile canaliculi, the smallest components of the biliary tree, lie between the apical surfaces of adjacent hepatocytes. Septic cholestasis might be a result of disturbance of the total bile canalicular system, i.e., bile secretion, canalicular contraction, and so on. Recently, the molecular biology of the hepatocellular transport system has become better understood, and the pathophysiological condition of cholestasis can be explained as a representation of the intracellular molecular transcriptional system. Cellular changes in surgical cholestasis and molecular findings concerning the bile canaliculus are introduced in this article.