ETHANOL-INDUCED ISCHEMIA IN PANCREAS AND A MECHANISM OF INTRALOBULAR FIBROSIS

DOI
  • SETO Akira
    The First Department of Pathology, School of Medicine, Showa University

Bibliographic Information

Other Title
  • アルコールによる膵虚血と小葉内線維化機序について
  • —Especially the pathophysiological influence on active oxygens generating during recirculation in the post-ischemic stage—
  • ―特に血行再開時に産生される活性酸素の病理生理学的影響―

Search this article

Description

Ethanol-induced alterations in pancreatic blood flow have been investigated in relation to pathomorphological and biochemical aspects. Twenty-seven rabbits free from any anesthetic influences were studied at two levels of 40% ethanol infusion. Higher and lower doses were 15 ml/kg (n= 21) and 2.5m1/kg (n=6), respectively. The ethanol was administered directly into each rabbit's stomach. Experimental period provided three groups, consisting of one time infusion, up to 4 weeks, and 8 weeks. Following one time administration, pancreatic blood flow (measured by hydrogen gas technique with Height-Area Method on computer), tissue amylase, lipase and the ratio of RNA/DNA were all increasing after the lower ethanol dosage. Contrary to this, after the higher dosage, all of those were decreasing. As to ethanol dosage, the pancreatic alterations indicated a biphasic reaction. Administering higher dosage ethanol caused marked ischemia in pancreas after 30 to 45 minutes. In the ischemic stage, the pancreas provided swelling of rER and mitochondria. In the recirculating stage, those damages were much more aggravating, and a part of swelling mitochondria were turned into vacuoles at the vicinity of the basement membrane. In the same stage, active oxygen and hydroperoxide increased with an decrease in vitamin E and T-cholesterol. The results indicate that radical production has occurred in the post-ischemic stage during recirculation. In a long term up to 8 weeks, the ratio of RNA/DNA decreased with time, reversely hydroperoxide increased. Histologically, the collagen fibrils in the surrounding acinar cells were thickening with time. After 8 weeks, those were determined as mature collagen fiber under an electromicroscope. This fibrosis provide an active fibrosis without caused through any necrosis. It is concluded that since active oxygens can promote the polymerization of collagen fibril, the experimental ethanol-induced fibrosis and the active fibrosis can be affected by the active oxygen.

Journal

Details 詳細情報について

Report a problem

Back to top