Early Propranolol Administration Does Not Prevent Development of Esophageal Varices in Cirrhotic Rats

Abstract

Background and Aims: Variceal bleeding is the most serious complication of portal hypertension associated with high mortality. This study was conducted to investigate any protective effect of early propranolol administration in the development and degree of esophageal varices in cirrhotic rats with portal hypertension. This topic is controversial in the literature. Methods: For the development of liver cirrhosis and esophageal varices, 60 rats underwent ligation of the left adrenal vein and complete devascularization of the left renal vein, followed by phenobarbital and carbon tetrachloride (CCl₄) administration. This operation enhances the development of cephalad collaterals, responsible for the induction of esophageal varices. After 2 weeks of CCl₄ administration, the rats were randomly separated into 2 groups. In group I, propranolol was continuously administered intragastrically throughout the study, whereas in group II normal saline (placebo) was administered instead. Cirrhosis was detected clinically by ascites development. Hemodynamic studies and morphometric analysis of the lower esophagus were performed after complete induction of cirrhosis, measuring the following parameters: portal pressure, total number of submucosal veins, total submucosal vessel area, mean cross-sectional submucosal vessel area, relative submucosal area (percentage) occupied by vessels and area of the single most dilated submucosal vein. Results: The statistical analysis revealed no statistically important difference between the 2 groups for the morphometrically studied parameters. However, portal venous pressure was lower in group I. Conclusion: Early propranolol administration did not protect rats from developing esophageal varices, despite the fact that a significant decrease in portal pressure was detected.

Phytochemical Constituents of Carrot (Daucus carota) Fruit Juice and its Hepatoprotective Property in CCl4-Induced Liver Cirrhotic Rats

“…Severe centrilobular necrosis occurs from highly reactive free radical metabolites and is also formed by the mixed function oxidase system in hepatocytes via CYP2E [15,16]. CCl4 augments lipid peroxidation and protein oxidation in hepatic cells, induces hepatic damage as well as apoptosis [17], induces necrosis, stimulates inflammation response, and causes fibrosis, which spreads to link the vascular structures that feed into and drain the hepatic sinusoid [18,19]. It activates the hepatic stellate cell (HSC) inducing hepatocyte apoptosis and necrosis [20].…”