Effect of bulbar perfusion with acid, hypertonic solutions, and acetylcholine on gastric acid secretion in dogs.
Dogs were provided with innervated pouches of the fundic stomach and the duodenal bulb. One dog also had an isolated pouch of the distal duodenum. Acid secretion was stimulated by intravenous infusion of a low dose of pentagastrin (ICI 50 123). Bulbar pouches were perfused with solutions of 0.9% Na C1, 0.1 N HC1, 40% glucose, 40% NaC1, and 40% peptone or with 0.1% solutions of acetylcholine chloride. Acidification of the bulbar pouches profoundly inhibited the acid output from the gastric ppoches. Perfusion with acetylcholine produced a transient inhibition of acid secretion. When hypertonic solutions were perfused through the bulbar pouches or the pouch of distal duodenum, no inhibition occurred. It is concluded that hypertonic solutions are not activators of the bulbar inhibitory mechanism that has been shown to respond to reduction of the intrabulbar pH. Inhibition following bulbar perfusion with acetylcholine may mean that liberation of the hypothetical humoral agent, bulbogastrone, to some extent is under cholinergic control.
D000109:Acetylcholine / Q000494:pharmacology*; D000818:Animals; D003864:Depression, Chemical; D004285:Dogs; D004386:Duodenum / Q000187:drug effects / Q000502:physiology; D005750:Gastric Juice / Q000378:metabolism*; D005947:Glucose / Q000494:pharmacology; D006851:Hydrochloric Acid / Q000494:pharmacology*; D006982:Hypertonic Solutions / Q000494:pharmacology; D010418:Pentagastrin / Q000494:pharmacology; D010461:Peptones / Q000494:pharmacology; D010477:Perfusion; D012636:Secretory Rate / Q000187:drug effects; D012965:Sodium Chloride / Q000494:pharmacology; D013268:Stimulation, Chemical; D013270:Stomach / Q000502:physiology
D006982:Hypertonic Solutions; D010461:Peptones; D012965:Sodium Chloride; D010418:Pentagastrin; D005947:Glucose; D000109:Acetylcholine; D006851:Hydrochloric Acid