The Possible Role of Gastric Acid Against Non-steroidal Anti-inflammatory Drugs-induced Gastric Microcirculatory Disturbance in Rats
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Accession number;04A0592330
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| Title;The Possible Role of Gastric Acid Against Non-steroidal Anti-inflammatory Drugs-induced Gastric Microcirculatory Disturbance in Rats |
| Author;
FUNATSU TOSHIYUKI
(Yamanouchi Pharmaceutical Co., Ltd., JPN)
CHONO KOJI
(Yamanouchi Pharmaceutical Co., Ltd., JPN)
HIRATA TAKUYA
(Yamanouchi Pharmaceutical Co., Ltd., JPN)
KETO YOSHIHIRO
(Yamanouchi Pharmaceutical Co., Ltd., JPN)
KIMOTO AISHI
(Yamanouchi Pharmaceutical Co., Ltd., JPN)
SASAMATA MASAO
(Yamanouchi Pharmaceutical Co., Ltd., JPN)
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Journal Title;Japanese Pharmacology & Therapeutics
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Journal Code:Z0947A
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ISSN:0386-3603
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VOL.32;NO.7;PAGE.429-434(2004)
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| Figure&Table&Reference;FIG.4, REF.19 |
| Pub. Country;Japan |
| Language;Japanese |
| Abstract;Non-steroidal anti-inflammatory drugs (NSAIDs) are well known to cause gastric microcirculatory disturbance. The mechanisms by which these agents suppress mucosal blood flow are not fully understood, although, the depletion of mucosal prostaglandins has been proposed as one possible way. The purpose of this study is to investigate the role of gastric acid and prostaglandins on gastric mucosal blood flow in diclofenac-treated rats. A rat stomach was mounted in an ex vivo chamber, instilled with 2 mL of saline, and injected diclofenac sodium (5mg/kg) subcutaneously under the ventrolateral skin. Gastric mucosal blood flow was measured sequentially using a laser Doppler perfusion image system. Diclofenac did not affect gastric mucosal blood flow although it strongly decreased mucosal PGE2 content. However, gastric mucosal blood flow was decreased after 0.1 N HCl was substituted for saline inside the gastric chamber. The decrease in gastric mucosal blood flow was recovered after replacement with saline. These results suggest that not only mucosal prostaglandins but also gastric acid may play an important role in NSAIDs-induced gastric microcirculatory disturbance. (author abst.) |
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