Postvagotomy acid secretion and mucosal blood flow during beta-adrenoceptor stimulation and universal chemical sympathectomy in dogs.
The aim of the present study was to examine the effect of beta-adrenoceptor stimulation, alpha blockade, and elimination of the adrenergic nerve function on mucosal blood flow and acid secretion in parietal-cell-vagotomized (PCV) gastric fistula dogs. Isoprenaline inhibited pentagastrin-stimulated gastric acid secretion via the beta 1 receptors non-competitively. The effect of isoprenaline was more pronounced after vagotomy than before vagotomy and significantly more pronounced than the effect on parasympathomimetically stimulated (bethanechol) gastric acid secretion. The animals were subjected to chemical sympathectomy with 6-hydroxy-dopamine, a false neurotransmitter that selectively destroys the adrenergic nerve terminals. Chemical sympathectomy increased the pentagastrin-stimulated gastric acid secretion and stabilized the mucosal blood flow at the level before vagotomy, but with an increased ratio between blood flow and acid secretion. One may conclude that the sympathetic nerve system influences gastric function after vagotomy.
D000318:Adrenergic beta-Agonists / Q000494:pharmacology*; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology*; D000818:Animals; D004285:Dogs; D005260:Female; D005744:Gastric Acid / Q000378:metabolism*; D005753:Gastric Mucosa / Q000098:blood supply*; D006801:Humans; D007545:Isoproterenol / Q000494:pharmacology; D008297:Male; D010418:Pentagastrin / Q000494:pharmacology; D012039:Regional Blood Flow / Q000187:drug effects; D013563:Sympathectomy, Chemical; D014628:Vagotomy; D014629:Vagotomy, Proximal Gastric
D000318:Adrenergic beta-Agonists; D000319:Adrenergic beta-Antagonists; D010418:Pentagastrin; D007545:Isoproterenol