Surgically induced hepatic failure in animals

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Cirrhosis of the liver accounts for approximately 30,000 deaths annually in the United States. In addition, many patients die of acute hepatic failure. Approximately one third of all deaths from liver disease are directly related to hepatic insufficiency. Hepatic coma is frequently the end stage of progressive hepatic insufficiency. Despite abundant reports on clinical and experimental findings, the cause of hepatic coma is still only partially understood. The reason for this can be traced back to a lack of knowledge of the total scope of liver function, leading to a limited understanding of hepatic failure.

To develop effective hepatic support systems, the establishment of good animal models of hepatic failure has been the goal of many investigators. Various methods have been conceived, tried, and evaluated. These models can be classified into two main groups: drug induced or surgically induced.

One factor of critical importance in establishing animal models is that the pathologic situations must be well controlled and comparable to clinical disease states. The models must be critically reproducible to eliminate possible false-negative or false-positive results. Drug-induced hepatic necrosis by CCl4,1 anesthetic agents,2 dimethylnitrosamine,3,4 and yellow phosphorus5 has many disadvantages, such as low reproducibility and the possible involvement of other organs. For this reason, drug-induced hepatic insufficiency has been abandoned.

Surgical procedures used to induce hepatic failure should be as simple as possible, reproducible, and should produce varying types of liver cell damage and failure. Three surgical procedures have been selected for use in our studies of hepatic failure: (1) . .



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