Cholinoceptor Blockers Protect against Ethanol-Induced Gastric Mucosal Damage in Rats

Cho, C.H.; Ogle, C. W.

doi:10.1159/000138860

Cited by 8 publications

(2 citation statements)

References 4 publications

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“…The atropine dose we used was similar to previous studies,25,26 and was half the dose reported to have a full blocking effect in studies of heart rate variability 27. Immobilization and gavage tended to be associated with longer emptying times, although significance was never reached in the breath test, possibly due to the relatively low number of animals studied, especially in the gavage group.…”

Section: Discussionmentioning

confidence: 70%

Validation of Octanoate Breath Test for Measuring Gastric Emptying in Rats

Demedts

Vanormelingen

Billoen

et al. 2013

J Neurogastroenterol Motil

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Background/AimsLack of simple and repeatable tests hampers gastric emptying studies in rats. The aim of this study was to adapt the 14C-octanoate solid gastric emptying breath test for application in rats, and to validate it against radioscintigraphic method.MethodsAfter ingestion of a meal containing 3 mCi 99mTc and 2 µCi 14C-octanoate, 23 male Wistar rats were placed on a gamma camera in a airflow container. Scintigraphic images were taken at regular intervals. The amount of 14CO2 in a regularly replaced hyamine hydroxide solution, capturing CO2 in the outflow air, was counted using liquid scintillation spectrometry. 99mTc gastric retention curves and 14CO2-excretion curves were fitted to their respective data. Three rats underwent the same procedures after administration of atropine.ResultsOverall Tr10% (time at which 10% of the original amount of 99mTc remained in the stomach) was 355 ± 64 minutes; Te90% (time at which 90% of total amount of 14CO2 was excreted) was 325 ± 106 minutes. Their correlation coefficient was 0.71, R-square 0.50 and P < 0.005. Tr1/2 (50% of original amount of 99mTc remained) was 124 ± 28 minutes; Te1/2 (50% of total amount of 14CO2 excreted) 114 ± 32 minutes. Their correlation coefficient was 0.83 with R-square of 0.69 and P < 0.00005. In 12 immobilized animals correlation was even better: correlation coefficient 0.84; R-square 0.71 and P < 0.001 (Tr10% was 388 ± 117 minutes; Te90% 532 ± 219 minutes; Tr1/2 of 165 ± 54 minutes; Te1/2 of 175 ± 67 minutes). Atropine significantly lengthened all emptying times: 904 ± 307 and 1461 ± 684 minutes for Tr10% and Te90%, respectively; and 432 ± 117 minutes for Tr1/2 and 473 ± 190 minutes for Te1/2.ConclusionsWe adapted and validated the 14C-octanoate gastric emptying breath test for application in rats.

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Section: Discussionmentioning

confidence: 70%

Validation of Octanoate Breath Test for Measuring Gastric Emptying in Rats

Demedts

Vanormelingen

Billoen

et al. 2013

J Neurogastroenterol Motil

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“…Even in cases with successful healing, the high relapse rate as well as other unexpected severe sideeffects (including mortality) after vagotomy suggest that it should not be recommended as a treatment of choice for gastric ulcers (Weinberg & McLenathen 1963;Stabile & Passaro 1983); antimuscarinic drugs have, therefore, been a more suitable alternative form of therapy. Atropine, an antimuscarinic drug, reduces the severity of gastric lesion formation (Foschi et a1 1986;Cho & Ogle 1991). However, contrasting results have been reported in another study using intragastric treatment with antisecretory doses of atropine (Martinotti et al 1984).…”

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confidence: 99%

The Vagus Nerve and its Non-cholinergic Mechanism in the Modulation of Ethanol-induced Gastric Mucosal Damage in Rats

Cho

Ogle

1994

Journal of Pharmacy and Pharmacology

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The role of the cholinergic pathway in the vagus nerve in modulating gastric lesion formation by ethanol was examined, using an ex-vivo stomach chamber preparation. Subdiaphragmatic vagotomy significantly increased the lesion areas but lowered acid secretion and gastric mucosal blood flow (GMBF). Atropine had no effect, whereas pirenzepine antagonized ethanol-induced mucosal damage. All three procedures showed similar potencies in depressing acid secretion, but only pirenzepine reversed the fall in the GMBF produced by ethanol. These differential effects of vagotomy, atropine and pirenzepine on gastric function suggest that the cholinergic component in the vagus nerve may not be important in the formation of ethanol-induced gastric damage. The persistent protective action as well as the restoration of ethanol-induced GMBF drop by pirenzepine in vagotomized animals further support this hypothesis. The worsening effect of vagotomy is probably modulated by a non-cholinergic mechanism, the abolition of which makes the gastric mucosa more susceptible to damage by ethanol. The acid-independent protective action of pirenzepine and its influence on the GMBF, which were not exhibited by atropine, are indeed unique and perhaps may be attributed to this non-cholinergic pathway.

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Intragastric nicotine protection against 40% ethanol injury in rat stomach

Endoh¹,

Kao²,

Baker³

et al. 1992

Digest Dis Sci

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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.(ABSTRACT TRUNCATED AT 250 WORDS)

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Cholinoceptor Blockers Protect against Ethanol-Induced Gastric Mucosal Damage in Rats

Cited by 8 publications

References 4 publications

Validation of Octanoate Breath Test for Measuring Gastric Emptying in Rats

Validation of Octanoate Breath Test for Measuring Gastric Emptying in Rats

The Vagus Nerve and its Non-cholinergic Mechanism in the Modulation of Ethanol-induced Gastric Mucosal Damage in Rats

Intragastric nicotine protection against 40% ethanol injury in rat stomach

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