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. 2003 Sep 10:3:26.
doi: 10.1186/1471-230X-3-26.

Botulinum toxin in gastric submucosa reduces stimulated HCl production in rats

Matteo Runfola  1 , Simone Rossi, Simona Panunzi, Pier Luigi Spada, Daniele Gui
Affiliations

Botulinum toxin in gastric submucosa reduces stimulated HCl production in rats

Matteo Runfola et al. BMC Gastroenterol. .

Abstract

Background: Botulinum toxin blocks acetylcholine release from nerve endings and acts as a long term, reversible inhibitor of muscle contraction as well as of salivary, sweat gland, adrenal and prostatic secretions. The aim of the present study is to investigate whether gastric submucosal injection of botulinum toxin type A reduces stimulated gastric production of HCl.

Methods: Sixty-four rats were randomized in two groups and laparotomized. One group was treated with botulinum toxin-A 10 U by multiple submucosal gastric injections, while the second group was injected with saline. Two weeks later, acid secretion was stimulated by pyloric ligation and acid output was measured. Body weight, food and water intake were also recorded daily.

Results: HCl production after pyloric ligation was found to be significantly lower in botulinum toxin-treated rats (657 +/- 90.25 micromol HCl vs. 1247 +/- 152. P = 0.0017). Botulinum toxin-treated rats also showed significantly lower food intake and weight gain.

Conclusions: Botulinum toxin type A reduces stimulated gastric acidity. This is likely due either to inhibition of the cholinergic stimulation of gastric parietal cells, or to an action on the myenteric nervous plexuses. Reduction of growth and food intake may reflect both impaired digestion and decreased gastric motility.

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Figures

Figure 1
Figure 1
Time course of mean daily percentage variation of body weight in BTX and SALINE groups. Only survivors at day 14 were considered. 100% means basal body weight of each rat.
Figure 2
Figure 2
Time course of mean daily food intake in BTX and SALINE groups. Only survivors at day 14 were considered.
Figure 3
Figure 3
Time course of mean daily water intake in BTX and SALINE groups. Only survivors at day 14 were considered.
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References

    1. Das Gupta BR. Structure and biological activity of botulinum neurotoxin. J Physiol (Paris) 1990;84:220–228. - PubMed
    1. Jankovic J, Brin MF. Therapeutic uses of botulinum toxin. N Engl J Med. 1991;324:1186–1194. - PubMed
    1. Gui D, Rossi S, Runfola M, Magalini SC. Botulinum toxin in the therapy of gastrointestinal motility disorders. Aliment Pharmacol Ther. 2003;18:1–16. doi: 10.1046/j.1365-2036.2003.01598.x. - DOI - PubMed
    1. Maria G, Cassetta E, Gui D, Brisinda G, Bentivoglio AR, Albanese A. Botulinum toxin for chronic anal fissure. N Engl J Med. 1998;338:217–220. doi: 10.1056/NEJM199801223380402. - DOI - PubMed
    1. Brisinda G, Maria G, Bentivoglio AR, Cassetta E, Gui D, Albanese A. A comparison of injection of botulinum toxin and topical nitroglycerin ointment for the tratment of chronic anal fissure. N Engl J Med. 1999;341:65–69. doi: 10.1056/NEJM199907083410201. - DOI - PubMed

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