16, 16 Dimethyl prostaglandin E sub(2) prevents the development of fulminant hepatitis and blocks the induction of monocyte/macrophage procoagulant activity after murine hepatitis virus strain 3 infection

• Published in: The Journal of clinical investigation Vol. 80; no. 3; pp. 881 - 889
• Main Authors: Abecassis, M, Falk, JA, Makowka, L, Dindzans, V J, Falk, R E, Levy, G A
• Format: Journal Article
• Language: English
• Published: 01-01-1987
• ISSN: 0021-9738

16, 16 Dimethyl prostaglandin E sub(2) (dmPGE sub(2)), a known cytoprotective agent, was examined for its ability to alter the course of fulminant hepatitis in an experimental model of fulminant viral hepatitis, murine hepatitis virus type 3 (MHV-3). Fully susceptible BALB/cJ mice, infected with 100 50% lethal doses (LD sub(50)) of MHV-3 developed histologic and biochemical evidence of fulminant hepatitis, as evidenced by massive hepatic necrosis with hypoglycemia, metabolic acidosis, and a markedly elevated serum alanine aminotransferase (ALT) (mean, 1,402 plus or minus 619 IU/liter). In contrast, animals treated with dmPGE sub(2) either before of after infection (up to 48 h) demonstrated a marked reduction in both histologic and biochemical evidence of liver damage as characterized by normal blood glucose, total CO sub(2), and ALT determinations (mean ALT, 63 plus or minus 40 IU/liter). Splenic macrophages recovered from infected and untreated BALB/cJ mice demonstrated a marked augmentation in procoagulant activity (PCA) from a basal 10 plus or minus 5 mU/10 super(6) splenic macrophages to a maximum of 615 plus or minus 102 mU/10 super(6) splenic macrophages, whereas no increase in macrophage PCA was detected in infected animals treated with dmPGE sub(2).