Effect of Two Types of β-Adrenergic Blockade on Gastric Acid Secretion During Pentagastrin Stimulation in Non-vagotomized and in Vagotomized Gastric Fistula Dogs

Abstract

The effect of β-adrenoceptor blockade by propranolol and practolol on submaximally pentagastrin-stimulated gastric acid secretion was studied in conscious non-vagotomized and in vagotomized gastric fistula dogs. Propranolol (0.5 mg/kg) intravenously augmented gastric acid output in vagotomized dogs, more after truncal and selective vagotomy than after parietal cell vagotomy. Vagally innervated dogs also showed an increase, but to a lesser degree and not statistically significant. The increase restored the acid output to preoperative levels in the vagotomized dogs. Practolol (1.0 mg/kg) intravenously resulted in a slight and insignificant increase in acid output in dogs with truncal vagotomy and had only a negligible effect in vagally innervated dogs and after selective and parietal cell vagotomy. It is concluded that propranolol augments pentagastrin-stimulated acid output in vagotomized dogs, and this augmentation was most pronounced in the totally vagotomized stomach. Practolol had minor influence on gastric acid secretion. This effect of the two β-blocking agents indicates that β₂-blockade is most important for the secretory augmentation. The restoration of postvagotomy acid secretion to preoperative levels suggests that adrenergic influence is important for the decrease in pentagastrin-stimulated acid secretion after vagotomy.

Key-words:

• β-adrenergic blockade
• dog
• gastric fistula
• gastric secretion
• pentagastrin
• vagotomy