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The effect of histamine-H2-receptor-antagonists on gastric acid secretion, gastric mucosal blood flow and acid base balance in cats

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Summary

  1. 1.

    In anaesthetized acute gastric fistula cats the effect was studied of the histamine-H2-receptor-antagonists burimamide and metiamide on histamine-stimulated gastric acid secretion, gastric mucosal blood flow, and acid base balance of the arterial blood and the gastric venous drainage.

  2. 2.

    Both burimamide and metiamide inhibit gastric secretion and gastric mucosal blood flow. The effects of metiamide are more pronounced than those of burimamide. On acid base balance both histamine-H2-receptor-antagonists have essentially the same effects which reflect the reduced loss of H+ from the stomach.

  3. 3.

    The inhibitory effects of burimamide on the stomach are at least in part antagonized by the histamine-H1-receptor-antagonist mepyramine (which presumably prevents burimamide from releasing catecholamines) and by the α-adrenergic blocking agent phenoxybenzamine, providing indirect evidence for the view that these effects of burimamide are mediated by catecholamines.

  4. 4.

    Phenoxybenzamine and mepyramine do not antagonize the gastric inhibitory effects of metiamide indicating that metiamide is void of catecholamine releasing properties.

  5. 5.

    Phenoxybenzamine and mepyramine influence acid base balance only when the inhibition of gastric acid secretion by burimamide was diminished. They prevented the histamine-mediated drop in arterial pO2, indicating that this histamine effect can be attributed to catecholamines, too.

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  1. Pharmakologisches Institut, Wilhelmstraße 56, D-7400, Tübingen, Federal Republic of Germany

    Margitta Albinus & K. -Fr. Sewing

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  1. Margitta Albinus
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  2. K. -Fr. Sewing
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Supported by a grant from the Deutsche Forschungsgemeinschaft.

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Albinus, M., Sewing, K.F. The effect of histamine-H2-receptor-antagonists on gastric acid secretion, gastric mucosal blood flow and acid base balance in cats. Naunyn-Schmiedeberg's Arch. Pharmacol. 285, 337–353 (1974). https://doi.org/10.1007/BF00501463

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  • DOI: https://doi.org/10.1007/BF00501463

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