Postvagotomy Acid Secretion and Mucosal Blood Flow during β-Adrenoceptor Stimulation and Universal Chemical Sympathectomy in Dogs

Abstract

The aim of the present study was to examine the effect of β-adrenoceptor stimulation, α 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 β₁ receptors non-competitively. The effect of isoprenaline was more pronounced after vagotomy than before vagotomy and significantly more pronounced than the effect on para-sympathomimetically 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.

Key-words:

• α-Blocking drugs
• β-blocking drugs
• dogs
• chemical sympathectomy
• dose response
• gastric mucosal blood flow
• gastric secretion
• isoprenaline
• parietal cell vagotomy
• pentagastrin