| Objectives1 To establish the hepatic ischemia-reperfusion models of blocked the portal vein for different time, the porta hepatis for 30min and the hepatic artery with the common bile duct for 30min in rats. The relevant biochemical indicators and cytokines were detected, the rate of bacterial translocation in the liver and the intestinal mesenteric lymph nodes was evaluated and the pathological changes of the liver tissue and the intestinal mucosa were observed.2 To investigate the effect and the mechanism of intestinal congestion in hepatic ischemia-reperfusion injury in rats.MethodsFifty-six male Sprague-Dawley rats were randomly divided into seven groups(n=8): the portal vein blocked for 0min group(P0), 15min group( P15), 30min group(P30)and 45min group(P45), sham-operated group(SO), the porta hepatis blocked for 30min group(H30)and the hepatic artery with the common bile duct blocked for 30min group(A30).Then the samples were collected after reperfusion for 60min. All rats were observed in macropathology, Alanine aminotransferase(ALT) levels in the serum were detected by the method of Reitman-Frankel and tumor necrosis factor-α(TNF-α) by ELISA, malondialdehyde(MDA) content in liver tissue were detected by thiobarbituric acid (TBA) reaction and superoxide dismutase(SOD) by hydroxylamine assay-developed from xanthine oxidase assay , the rate of bacterial translocation in the liver and the intestinal mesenteric lymph nodes was evaluated, the pathological changes of the liver tissue and the intestinal mucosa were observed by light microscopy, the ultrastructural changes of the hepatic cells were observed by electron microscope.Results1 Animals in macropathology, the red color of the liver in A30 deepened with a paucity of petechiae after reperfusion for 60 min. P30 and H30 had varying degrees of pathological changes, such as intestinal congestion and edema, expansion of intestinal tract and hepatic degeneration in inequality of size with gloomy color. The pathological changes, such as intestinal congestion and edema, expansion of intestinal tract and the size of hepatic degeneration, aggravated with the portal vein occlusion time in the groups of blocked the portal vein.2 The serum levels of ALT and TNF-αin P30 were higher than that in SO and A30 (P <0.05), as well as the levels that in H30 higher than that in SO and A30. ALT and TNF-αlevels in the serum increased with the portal vein occlusion time in the groups of blocked the portal vein after reperfusion for 60 min (all P <0.05).3 There was no statistically significant difference in the content of MDA and SOD between that in SO and A30 (P>0.05), SOD content in P30 were lower than that in SO and A30 (P<0.05), but MDA content higher (P<0.05), as well as the content that in H30 higher than that in SO and A30. SOD content in liver tissue descended and MDA content escalated with the portal vein occlusion time in the groups of blocked the portal vein (all P <0.05).4 The rate of bacterial translocation in the liver and the intestinal mesenteric lymph nodes in SO and A30 were low, but increased in P30 and H30. The rate of bacterial translocation from intestine increased with the portal vein occlusion time in the groups of blocked the portal vein (all P<0.05).5 Histological examination of the liver tissue showed the pathological changes, such as hepatic sinusoid existing congestion, inflammatory cell infiltration, cellular swelling and necrosis in P30 and H30. According to the pathological injury grade scores of liver, the injury scores in P30 was higher than that in SO and A30 (P <0.05), as well as the scores in H30 higher than that in SO and A30. The pathological changes of the liver tissue, such as hepatic sinusoid existing congestion, inflammatory cell infiltration, cellular swelling and necrosis, aggravated with the portal vein occlusion time in the groups of blocked the portal vein. According to the pathological injury grade scores of liver, There were statistically significant difference between the injury scores in each group (P<0.05).6 Histological examination of the intestinal mucosa showed the pathological changes, such as congestion, inflammatory cell infiltration, epithelial cells necrosis and exfoliation in P30 and H30. According to the histological injury grade scores of the intestinal mucosa defined by Chiu, the injury scores in P30 was higher than that in SO and A30 (P <0.05), as well as the scores in H30 higher than that in SO and A30. The pathological changes of intestinal villus structure, such as congestion, inflammatory cell infiltration, epithelial cells necrosis and exfoliation, aggravated with the portal vein occlusion time in the groups of blocked the portal vein. According to the histological injury grade scores of the intestinal mucosa defined by Chiu, There were statistically significant difference between the injury scores in each group (P<0.05).7 Under electron microscope the ultrastructure of hepatic cells were normal in SO, there was tiny chromatin margination in endonuclear in A30. The pathological changes, such as obvious chromatin margination, morphologic abnormality of nucleus, mitochondrial swelling with irregular arrangement were showed in P30, such as interruption of nuclear membrane, chromatin pycnosis and conglobation, obvious mitochondrial swelling, crista mitochondriales porosity and deliquescence with irregular arrangement were showed in H30. The pathological change, such as morphologic abnormality of nucleus, chromatin margination and abnormal mitochondrion, aggravated with the portal vein occlusion time in the groups of blocked the portal vein. Conclusions1 Hepatic ischemia-reperfusion injury has intimate relationship with intestinal congestion. The degree of hepatic ischemia-reperfusion injury and intestinal injury aggravate with the portal vein occlusion time.2 The mechanisms of hepatic ischemia-reperfusion injury could have been due to endotoxemia and bacterial translocation from intestine induced by the intestinal congestion after blocking the porta hepatic and TNF-αsecreted by activated Kupffer cells.
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