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Pathophysiology of acute obstructive cholangitis
Author(s) -
Kawada N.,
Takemura S.,
Minamiyama Y.,
Inoue M.
Publication year - 1996
Publication title -
journal of hepato‐biliary‐pancreatic surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.63
H-Index - 60
eISSN - 1868-6982
pISSN - 0944-1166
DOI - 10.1007/bf01212771
Subject(s) - pathophysiology , nitric oxide , medicine , ligation , bile duct , gastroenterology , mediator , common bile duct , pathology
Because acute obstructive cholangitis is life‐threatening, understanding of the pathophysiology of this disease is required to establish a medical treatment. Experimental results indicate that obstruction of the bile duct itself does not induce acute cholangitis, but infection of gut‐derived bacteria such as Escherichia coli into the bile triggers fatal septicemia, which leads to liver injury and renal failure. In obstructive cholangitis, functional changes in sinusoidal lining cells are often seen. Mediators produced by Kupffer cells, endothelial cells, and stellate cells may modulate inflammatory reactions especially in the periportal area of bile duct ligated animals. In addition, proliferation of bile duct epithelial cells is induced by bile duct ligation. Recently, nitric oxide has been recognized as an important mediator of multiple organ failure. Actually, when bile duct ligated animals are treated with endotoxin, metabolites of nitric oxide in blood and plasma increase, indicating that nitric oxide may take part in the pathophysiology of acute obstructive cholangitis.