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Intragastric nicotine protection against 40% ethanol injury in rat stomach

Role of ganglionic stimulation or blockade

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Abstract

Intragastric nicotine (4 mg/kg) protects against 40% ethanol-induced gastric mucosal injury and raises mean blood pressure. We postulated that this protective effect was mediated by the ganglionic stimulatory property of nicotine and therefore could be abolished by ganglionic blockers. Rats were pretreated with intraperitoneal hexamethonium (10 mg/kg) or mecamylamine (2 mg/kg) to block peripheral or central autonomic ganglia, respectively. Intragastric vehicle or nicotine (4 mg/kg) was then administered. The total lengths of the linear gastric corpus mucosal lesions induced by intragastric 40% ethanol were measured by an unbiased observer using a caliper. The results showed that both intraperitoneal hexamethonium and mecamylamine pretreatments protected against 40% ethanol-induced gastric mucosal injury. Neither modified the protective effect of intragastric nicotine. The protective effect of hexamethonium and mecamylamine was associated with a significant increase in the volume of gastric mucus and gastric juice. The increase in the volume of gastric content (mucus and juice) was partially responsible for the protective effect of these ganglionic blockers. In a separate experiment, intraperitoneal nicotine (4 mg/kg) also protected against 40% ethanol-induced gastric mucosal injury and raised mean blood pressure. These data indicate that the protection against 40% ethanol-induced gastric mucosal injury is not unique to intragastric nicotine. Such protection can be induced by ganglionic blocking doses of hexamethonium and mecamylamine, or a ganglionic stimulatory dose of intraperitoneally administered nicotine. Whether ganglionic stimulation or blockade plays a role in the mechanism of intragastric nicotine protection, however, remains to be determined. Further studies of the regulation of gastric mucus production and gastric juice volume may shed light on the mechanism of protection afforded by intragastric nicotine.

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Authors and Affiliations

  1. Research and Medical Services, Sepulveda Veterans Administration Medical Center, Center for Ulcer Research and Education Division of Gastroenterology (111G), UCLA School of Medicine, 91343, Los Angeles, California

    Kazuo Endoh MD, John Kao BS, Margaret Baker BS &  Felix W. Leung MD

Authors
  1. Kazuo Endoh MD
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  2. John Kao BS
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  3. Margaret Baker BS
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  4. Felix W. Leung MD
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Additional information

Supported by Veterans Administration Medical Research Funds, and in part by research grants (0162-01, 0162-02 and 0291-01) from the Smokeless Tobacco Research Council, Inc., and by funds (IRT 80) provided by the Cigarette and Tobacco Surtax Fund of the State of California through the Tobacco-Related Disease Research Program of the University of California to F.W.L. Dr. Endoh is a recipient of the University of California Tobacco-Related Disease Research Program Research Fellowship Award (FT 37).

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Endoh, K., Kao, J., Baker, M. et al. Intragastric nicotine protection against 40% ethanol injury in rat stomach. Digest Dis Sci 37, 1840–1846 (1992). https://doi.org/10.1007/BF01308077

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  • DOI: https://doi.org/10.1007/BF01308077

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