Gastric acid secretion after chemical sympathectomy

Adrenergic nerve terminals in several organs are selectively destroyed by 6-hydroxydopamine (6-OHDA) resulting in a chemical sympathectomy that is reversible. In this study the acute and chronic effects of 6-OHDA on gastric mucosa and acid secretion were evaluated. Four dogs were given 6-OHDA (40 mg/kg, intravenously). Gastric biopsies were taken before treatment and biweekly thereafter and were analyzed by fluorescence microscopy (Hillarp-Falck). Degeneration of adrenergic nerve terminals in the mucosa was complete at 1 week. Early regeneration was noted at 3 weeks and appeared to be complete at 9 weeks. In another group of seven dogs with a gastric fistula, dose-response curves to pnetagastrin (PPG, 0 to 5 microgram/kg/hr) were determined. Then 6-OHDA (40 mg/kg) was given to these dogs and secretory studies were repeated weekly thereafter for 8 weeks. After 6-OHDA administration, acid secretion increased in response to submaximal doses of PPG, whereas maximal secretion was unchanged. The peak increase occurred the second week; thereafter secretion gradually returned to control values. We conclude that chemical sympathectomy (6-OHDA) increases gastric acid secretion in response to submaximal PPG stimulation. This increase correlates well with the 6-OHDA--induced degeneration of adrenergic terminals in the mucosa. These data suggest that the adrenergic innervation of the stomach has an inhibitory effect on the control of acid secretion in the dog.