We studied the effects of a series of vasodilators on intrahepatic vascular resistance of isolated perfused cirrhotic rat livers in basal conditions and during norepinephrine-induced vasoconstriction. Cirrhosis was induced by repeated intraperitoneal injections of carbon tetrachloride. The vasodilat
Morphological changes of hepatic microcirculation in experimental rat cirrhosis: A scanning electron microscopic study
β Scribed by Joji Haratake; Masanori Hisaoka; Osamu Yamamoto; Akio Horie
- Publisher
- John Wiley and Sons
- Year
- 1991
- Tongue
- English
- Weight
- 867 KB
- Volume
- 13
- Category
- Article
- ISSN
- 0270-9139
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β¦ Synopsis
Morphological changes of hepatic microcirculation, especially peribiliary plexus, in experimental rat cirrhosis that resulted from the repeated intraperitoneal injections of N-diethylnitrosamine, 100 mg/kg body weight/one shot/week, were examined by scanning electron microscope. Control rats were treated with saline. Whole blood vessels of the rats were perfused by saline and stuffed with methylmethacrylated resin. Multiple nodular changes were seen in the livers after the five injections (5 wk) of N-diethylnitrosamine, and diffuse nodular transformations mimicking human cirrhosis after six injections (6 wk) were also seen. Overall changes in experimental rats were numerous vascular channels mainly composed of venous branches around the parenchymal nodules, increased arterioportal anastomoses and flattening of veins, especially hepatic vein branches. Peribiliary plexuses of the experimental rats were much richer in the vessels than those of the controls, and many dilated veins, ramified from portal vein branches, were present in the former. Direct connections between peribiliary plexuses and sinusoids or between peribiliary plexuses and portal veins increased in the experimental rats. Studies concerning microcirculatory changes of peribiliary plexuses in experimental rat cirrhosis are rare. It was concluded that the abnormal peribiliary plexuses in this experimental series might participate in a collateral circulation under a state of portal hypertension.
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