|Budget Amount *help
¥2,100,000 (Direct Cost : ¥2,100,000)
Fiscal Year 1991 : ¥500,000 (Direct Cost : ¥500,000)
Fiscal Year 1990 : ¥1,600,000 (Direct Cost : ¥1,600,000)
To elucidate the pathogenesis of acute acalculaous cholecystitis, the gallbladder was subjected to ischemia-reperfusion by simultaneously occlusing the middle hepatic artery and the superior mesenteric vein in dogs, and the degree of inflammation and biochemcal changes in the gallbladder mucosa were studied by yarying the duration of ischemia or reperfusion. Cholecystitis was produced in all animals by 45-min ischemia followed by 90-min reperfusion as the shortest ischemia and reperfusion times. In this model, prologation of the ischemic time increased the area of mucosal inflammation horizontally with in-creases of the PLA_2 activity. content of lipoid peroxide, whereas by prolonging the reperfusion time the inflammation area spread deeper vertically toward the serosal side with significant increase in the mucosal PLA_2 activity, content of lipid peroxide and SOD activity. Moreover, the present study revealed that free radicals were eliminated efficiently by the intraarterial infusion of a mixuture of SOD and CAT, clearly suppressing the development of cholecystitis.
The levels of PGE_2, PGF_2alpha, 6KF, and TXB_2 in the gallbladder lavage fluid increased significantly after ischemia-reperfusion, and especially PGE_2 level was correlated well with inflammation area of the gallbladder mucosa. Infusion of a mixture of SOD, CAT and quinacrine into the cystic artery during the reperfusion time causd the reduction in the levels of PGE_2 and PGF_2 alpha in the gallbladder lavage fluid and inflammation area in the gallbladder.
The repeating ischemia-reperfusion of the gallbladder caused cholesterosis, reducation of pH, a decrease in the concentration of bile acid and lecithin in the gallbladder bile, and an increase in the cholesterol saturation index.