[
Abstract]
[
Full Text PDF] (in Japanese / 5329KB)
[Members Only And Two Factor Auth.]
J.Jpn. Surg. Soc.. 87(2): 180-188, 1986
Original article
EXPERIMENTAL STUDY ON THE PATHOGENESIS OF ACUTE ULCERATION IN OBSTRUCTIVE JAUNDICE
-WITH REFERENCE TO GASTRIC MUCOSAL BLOOD FLOW-
We prepared obstructive jaundice models in rats in order to study the mechanism of acute ulceration in obstructive jaundice centering on impediments to gastric wall blood flow and changes in gastric mucosal NA and PGE
2 when the rats were subjected to water immersion restraint stress. The results were:
1. In the obstructive jaundice 2 weeks group, when subjected to water immersion restraint stress, gastric mucosal NA reached a dried up stage from the incipient stage, causing gastric mucosal impediments at the same time, showing a significant decrease of gastric mucosal PGE
2. Intragastric pH was at a similar level of excessive acidity in all groups ; gastric acid is believed to be a secondary factor promoting ulceration.
2. Gastric mucosal PGE
2 showed a significant decrease coinciding with the increase in ulceration index, being a possible factor of ulceration;it is also presumed to regulate gastric wall blood flow alternatively with gastric mucosal NA.
3. Pre-treatment with PGE
2 prior to loading stress resulted in a decrease in gastric wall blood flow being significantly controlled. The administration of PGE
2 brought about an improvement in gastric wall blood flow and a consequent increase in gastric mucosal NA, being judged effective for acute ulceration in obstructive jaundice.
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