Pancreatic damage resulting from temporary portal triad interruption during partial hepatectomy: protective effect of a prostaglandin I2 analogue.

BACKGROUND

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.

METHODS

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.

RESULTS

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 the PG group than in the NS group at 12 and 24 h after hepatectomy. Tissue damage in the pancreas and other organs was observed histologically along with the elevation of pancreatic enzymes. Although there were no significant differences between the two groups on hematoxylin and eosin staining, apoptotic acinar cells were only seen in the NS group. The portal endotoxin level (at 3 and 6 h after hepatectomy) and small intestinal permeability (at 1 and 3 h after hepatectomy) were significantly lower in the PG group compared to the NS group.

CONCLUSIONS

Temporary portal triad interruption induced hyperamylasemia, congestive damage to the pancreas, and portal endotoxemia due to increased small intestinal permeability. A prostaglandin I2 analogue was able to protect the pancreas and small intestine from such damage.