Studies on the effect of acute doses of indomethacin (prostaglandins inhibitor) during induced liver failure.

Fifty four male mice were divided into 3 main groups. Control group (6 mice), Schistosoma mansoni infected group (24 mice) and carbon tetrachloride (CC14) treated group (24 mice). The last two groups were further subdivided into (4) subgroups (6 mice/each). One of them served as a control while the other 3 subgroups received (0.75, 1.25 & 2.5 mg/100g B.W.) of indomethacin respectively. CC14 treated mice were severely live 2 damaged than those infected by S. mansoni. Indomethacin made the liver functions deteriorate. Schistosomiasis did not affect kidney functions while urea & creatinine were elevated in CC14 treated group. Indomethacin led to more elevation of both. Histological studies of liver treated by CC14 revealed portal venous congestion, granular cytoplasm and cellular infiltration while schistosomiasis produced the classic granulomatous reaction. Indomethacin treatment led to distortion of hepatic cell arrangement as well as marked cellular infiltration and congestion. On the other hand, kidney treated with CC14 showed cellular infiltration around glomeruli, indomethacin caused marked congestion and cellular infiltration. Schistosoma infection did not produce any histological changes. All recorded changes could be attributed to the toxic effect of indomethacin, inhibition of prostaglandins and weakness of the immunological cells of the liver.