Experimental Study On Hepatic Damage Caused By Pagumogonimus Skrjabini In Rats

[ Objective ] To study the structural and functional hepatic damage caused by Pagumogonimus skrjabini in rats; To explore the mechanism of hepatic damage; To evaluate the action of liver functional examination on early diagnosis of hepatic damage caused by Pagumogonimus skrjabin.[Methods] 35 rats were randomly divided into three groups: 8 in control group, 11 in experimental group A, 16 in experimental group B. The 27 experimental rats were each injected through abdominal cavity with 15 metacercariaes of Pagumogonimus skrjabini. 1, 2, 4, 6, 8 and 52 weeks after infection, automatic biochemical analyzer was employed for the determination of serum levels of total protein, albumin, globulin, alanine aminotransferase (ALT), aspartate aminotransferase (AST), total bilirubin, conjugated bilirubin and unbound bilirubin of rats in both control group and experimental group A respectively. Data were analyzed with SPSS 11.5 statistic software. 1, 2, 8 and 52 weeks after infection, a part of rats in experimental group B were killed to obtain livers and the histopathologic changes of liver tissues were observed under both light microscope and transmission electron microscope.[Results] Hepatic damage in rats could be found during the infection. As to liver function: 4, 6 and 8 weeks after infection, serum levels of albumin were significantly lower in the experimental group A than those in the control group. 4, 6, 8, 52 weeks after infection, serum levels of globulin in the experimental group A were markedly increased. 6 and 8 weeks after infection, serum levels of ALT and AST in experimental group A were increased. There had no obvious changes in serum total protein, total bilirubin, conjugated bilirubin and unbound bilirubin in the course of infection. The changes in liver function of the rats in experimental group A were not significant in the first two weeks post-infection. As to liver structure: 1week after infection, liver cells became swelling, a part of liver cells became fatty degeneration. 2 weeks after infection, the most prominent pathologic change was acute suppurative inflammation, small abscess could be seen in liver tissues. 8 weeks after infection, fibroplastic proliferation could be seen in liver tissues, a part of hepatic lobules were destroyed and remodeled. 52 weeks after infection, liver tissues fibrosis was obvious, a lot of false hepatic lobules formed. Under transmission electron microscope, it was found that all the livers showed different degrees of fibrosis from two weeks after infection and fibrosis was obviously aggravated eight weeks after infection. In the course of infection, degeneration, necrosis and hemorrhage could also be seen in the liver tissues. Liver tissues of rats in control group showed no histopathologic changes.[Conclusions] Pagumogonimus skrjabini can cause the injury of liver function in rats. Pagumogonimus skrjabini infection mainly affects the metabolism of protein, the most prominent changes in liver function are the decrease of albumin and the increase of globulin, the activity of AST and ALT could change, there have no obvious changes in bilirubin in the course of infection. The decrease of albumin and the increase of globulin can be regarded as specific indicator of diagnosis of hepatic damage caused by Pagumogonimus skrjabin. Pagumogonimus skrjabini can also cause structural damage to livers of rats. The most prominent histopathologic changes of livers of rats infected with Pagumogonimus skrjabini are progressive fibrosis. At the same time, degeneration, necrosis and hemorrhage can also be seen in the liver tissues in the course of infection. The mechanism of hepatic damage is related to the mechanical and immune damage caused by Pagumogonimus skrjabini, fat storing cells play an important role in liver fibrosis. Liver functional examination is useful to early diagnosis of hepatic damage caused by Pagumogonimus skrjabin.