Effects of experimental cirrhosis on splanchnic microvascular fluid and solute exchange in the rat.
In human cirrhosis, there is evidence that there are considerable alterations in fluid and solute exchange in the hepatic and intestinal microcirculations . Experimental cirrhosis was induced in rats by using oral phenobarbitone and carbon tetrachloride inhalation over an 8-wk period. Portal venous pressure, hepatic and intestinal lymph flows, and lymph and plasma protein concentrations were measured. Liver samples were obtained for histologic examination. Portal venous pressure increased from a normal value (control animals) of 9.0 (6.3-13.1) cmH2O to 17.9 (9.0-29.0) cmH2O in cirrhotic rats. There was a strong correlation between the degree of fibrotic change on histology and portal venous pressure. Lymph flows from the intestine and liver in cirrhotic animals were increased threefold and 30-fold, respectively, over values obtained from control animals. There was a good correlation between intestinal and liver lymph flows and portal venous pressure. Analysis of lymph/plasma protein concentration ratios at various lymph flow suggests that capillary permeability in the small intestine during sustained portal hypertension is comparable to that in normal animals. However, the highly permeable blood-lymph barrier of the normal liver becomes markedly restrictive in cirrhotic animals.[1]References
- Effects of experimental cirrhosis on splanchnic microvascular fluid and solute exchange in the rat. Barrowman, J.A., Granger, D.N. Gastroenterology (1984) [Pubmed]
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