Failure of Ischemia to Break the Dog’s Gastric Mucosal Barrier

Abstract

Vagally denervated (Heidenhain) pouches of the dog’s oxyntic gland area of the stomach were irrigated with 100 mN HC1, and net fluxes of H+ and Na+ together with aminopyrine clearances were measured. An increase in output of Na+ and an increase in disappearance of H+, in absence of secretion, were sought as indices of damage to the gastric mucosal barrier. Ischemia was produced by repeated subcutaneous injection of vasopressin (20 U every 30 min), by a single hemorrhage (estimated 30% of blood volume), by repeated hemorrhages holding the dog’s mean arterial blood pressure at 80 mm Hg, and by intravenous infusion of vasopressin (4 U per hr) or norepinephrine (2-μg base per kg-min). Infusion of vasoconstrictor drugs was combined with infusion of histamine (50-μg base per kg-hr), bethanechol chloride (50 μg per kg-hr), or pentagastrin (8 μg per kg-hr). In no instance did ischemia lasting 4, 5, or 6 hr have any effect upon the integrity of the gastric mucosal barrier. Repeated subcutaneous injection of vasopressin or a single, rapid hemorrhage does not induce ischemia lasting longer than 5 to 6 hr. When histamine or bethanechol and pentagastrin are given, the vasoconstrictor drugs are incapable of causing lasting mucosal ischemia.