Role of blood flow in acute gastric lesion after hepatectomy and effect of prostaglandin I2 and H2-receptor antagonist

In order to investigate the cause of gastric mucosal lesion following hepatectomy, changes of gastric, pancreatic and femoral arterial blood flow were measured in 70% hepatectomized rabbits. Following administration of 0.5 microgram/kg of GRP, gastric blood flow increased to 120% of the basal level in the controls, but reached to only 107% of the basal level in the hepatectomized rabbits. Following hemorrhage of 10% of the total blood volume seven days after hepatectomy, blood flow decreased to 55% of the basal level in the stomach, 57% in the pancreas and 76% in the femoral artery. Although pancreatic blood flow recovered to 81% of the basal level, gastric blood flow remained low, 59% of the basal level, suggesting poor recovery of gastric blood flow as compared to pancreatic blood flow. Administration of PGI2 and ranitidine in hepatectomized rabbits with hemorrhage conferred a considerable degree of recovery of gastric blood flow in the PGI2 group (from 56% to 80%) and in the ranitidine group (from 52% to 72%). Thus, disturbance of reaction and poor recovery of gastric blood flow following hemorrhage were indicated as important causes of acute gastric mucosal lesion associated with hepatectomy. Both PGI2 and ranitidine appeared to be effective for the maintenance of gastric blood flow after hepatectomy.