ArticleDigestive diseases and sciences1999
Potentiating effect of passive cigarette smoking on gastrointestinal damage induced by indomethacin in rats.
Article in Digestive diseases and sciences, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 9 citations in OpenAlex.
- Smoking-gene interaction and disease development: relevance to pancreatic cancer and atherosclerosis.World journal of surgery · 2005Review
- Effect of smoking on serum pepsinogen I level depends on serological status of Helicobacter pylori.Japanese journal of cancer research : Gann · 2001Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cigarette smoking and nonsteroidal antiinflammatory drugs (NSAIDs) have been associated with gastroduodenal ulcers. The present study aimed to clarify the ulcerogenic mechanisms of passive cigarette smoking on gastrointestinal damage induced by indomethacin in fasted or in fasted and refed rats. Rats were exposed to cigarette smoke (0%, 1%, 2%, or 4%, v/v) before and/or after indomethacin administration. Cigarette smoke dose-dependently potentiated indomethacin-induced gastric mucosal lesions in the fasted animals and further lowered gastric blood flow. The gastric myeloperoxidase activity (a marker enzyme for neutrophils) was also potentiated. In addition, passive cigarette smoking increased the mortality and aggravated duodenal ulceration and also the reduction of duodenal blood flow in the fasted and refed rats after indomethacin treatment. The results indicated that the potentiating effect of passive cigarette smoking on indomethacin-induced gastroduodenal lesions is probably due to the depression of blood flow in the gastroduodenal mucosa and to the aggravation of neutrophil infiltration in the gastric mucosa.
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