ABSTRACT
The acute pathophysiological response of the liver to the various microbial, viral, chemical, and hypoxic insults is remarkably consistent with respect to the activation of leukocytes and platelets and the production of various inflammatory molecules and cytokines. The failure of 16,16-dimethyl prostaglandin E to prolong survival, despite the absence of biochemical and histological evidence of liver failure, underscores the complexity of fulminant systemic viral infection. In the case of fulminant hepatitis due to viral infection, histopathological studies have revealed severe and extensive hepatocyte necrosis resembling that seen experimentally in the rabbit by a Schwartzman reaction using Escherichia coli endotoxin. In an experimental murine model of viral hepatitis, murine hepatitis virus strain 3 (MHV) infection produces a strain-dependent spectrum of disease. The proliferative response of splenic mononuclear cells from resistant and susceptible mice differs significantly in response to MHV infection. The induction of procoagulant activity in the susceptible animals corresponds to disturbances seen within the microcirculation of the liver.
