| dc.contributor | Rinc�n, A.R., Inst. of Molec. Biology in Medicine, Hospital Civil de Bel�n, University of Guadalajara, Jalisco, Mexico, Inst. of Molec. Biology in Medicine, University of Guadalajara, P.O. Box: 2-500, Jalisco M�xico, C.P. 44281, Mexico; Covarrubias, A., Inst. of Molec. Biology in Medicine, Hospital Civil de Bel�n, University of Guadalajara, Jalisco, Mexico; Pedraza-Chaverr�, J.; Poo, J.L.; Armend�riz-Borunda, J., Inst. of Molec. Biology in Medicine, Hospital Civil de Bel�n, University of Guadalajara, Jalisco, Mexico; Panduro, A., Inst. of Molec. Biology in Medicine, Hospital Civil de Bel�n, University of Guadalajara, Jalisco, Mexico | |
| dc.description.abstract | The pathogenesis of renal function alteration associated with liver disease remains to be elucidated. Although different experimental animal models have been utilized in order to explain such pathophysiological state, none of them have completely explained the mechanisms involved. In this study we performed differential hemodynamic, hepatic and renal function alteration studies after induction of acute liver damage via intragastric administration of a single dose of CCl4 to cirrhotic and non-cirrhotic rats. Cirrhotic rats with acute liver damage exhibited a significant decrease in mean arterial pressure followed by a decreased glomerular filtration rate, urinary sodium concentration and an induction of plasma renin concentration and activity. At the same time, a significant association between oliguria and mortality was observed. The renal histopathological studies revealed glomeruli with mesangial hypercellularity and thickening of capillary wall, but not tubular epithelial injury. All these alterations were not detected in the control group, i.e. by non-cirrhotic rats with acute liver damage. This study suggests that the effect of CCl4 on kidney structure and function depends on the functional state of the liver. Since this experimental model of acute liver damage in cirrhotic rats presents hemodynamics and renal function alterations similar to those observed in the hepatorenal syndrome in man, it could be utilized to study the pathogenesis of renal function alterations associated with liver damage. | |
