|
KMID : 0378019660090010055
|
|
New Medical Journal
1966 Volume.9 No. 1 p.55 ~ p.68
|
|
|
Studies on Experimental Pancreatitis
|
|
|
|
|
Abstract
|
|
|
Although the pathogenesis of acute pancreatitis remains obscure, it is widely held that autodigestion of thepancreas by prematurely activated pancreatic trypsin is an important factor. A number of studies on the treatment of induced pancreatitis using various trypsin inhibitors was attempted (Coffey et al., 1950, Forell et al., 1955). The results were inconsistent (Hoffman et al., 1953, Rush and Cliffton, 1952). A new product, Trasylol. (Bayer), has received wide acclaim for its effectiveness in the treatment of acute pancreatitis in human(Frey, 1953, Bernard et al. 1959, Bedacht, 1960, Maurer, 1962).
Propylthiouracil was claimed to decrease enzyme production at the cellular level by reduction in cellular metabolism. Reid et al. (1958) have offered experimental evidence that the administration of huge doses of this agent is capable of preventing hemorrhagic necrosis in the experimental duodenal-closed-loop pancreatitis by Pfeffer, but as yet there has been no conclusive report concerning the efficacy of this drug in either human or experimental pancreatitis.
Hexamethonium and atropine or their congeners appear to be drugs of choice in the relief of pain in acute pancreatitis since their additional pharmacologic effects, which include suppressions of gastric acidity(Davies et al., 1953, Annis and Hallenbeck, 1951), relaxation of the sphincter(Hong et al., 1956), and inhibition of pancreatic secretion by means of preventing release of secretin or pancreozymin from duodenal mucosa(Hong et al.,. 1961, Hur, 1962, Elmslie et al., 1964).
The present study was undertaken to evaluate the effects of atropine, hexamethonium, propylthiouracil as well as Trasylol in rabbits with bile-induced experimental pancreatitis, obtaining serial measurement of the serum. and the tissue pancreatic enzyme levels and histopathologic study of pancreas.
|
|
|
KEYWORD
|
|
|
|
|
|
FullTexts / Linksout information
|
|
|
|
|
|
Listed journal information
|
|
|
|
|