Pancreatic damage resulting from temporary portal triad interruption during partial hepatectomy: protective effect of a prostaglandin I2 analogue
Abstract
Hyperamylasemia often occurs after hepatectomy, but the detailed mechanism of this phenomenon remains unclear. This study was designed to examine the influence on the pancreas and other organs of temporary portal triad interruption during hepatectomy and to evaluate the protective effect of a prostaglandin I2 analogue. Sprague-Dawley rats were intravenously administered normal saline (NS group) or a prostaglandin I2 analogue (PG group) and underwent 70% hepatectomy with temporary portal triad interruption. The 7-day survival rate and the levels of plasma liver enzymes, portal pancreatic enzymes, and endotoxin were determined. Intestinal permeability was evaluated from the portal blood concentration of fluorescein isothiocyanate-labeled dextran administered into the small intestine. The liver, pancreas, small intestine, and lung were examined histologically. Apoptosis in the pancreas was observed by the terminal transferase-mediated dUTP-biotin nick end labeling method. The survival rate of the NS group was 50%, whereas that of the PG group was significantly higher at 100% (P < 0.05). Plasma liver enzymes increased in both groups and showed no significant difference. Portal amylase and lipase levels were significantly lower in t...Continue Reading
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Apoptosis
Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis