EFFECTS OF INTRA-ARTERIAL PERFUSIONS ON ELECTRICAL ACTIVITY AND ELECTROLYTE CONTENTS OF DOG SMALL INTESTINE

Abstract

The mechanisms underlying the periodic depolarizations (slow waves) in longitudinal muscle of the small intestine were studied in vivo in dogs by means of intra-arterial perfusions of solutions with altered electrolyte concentrations or with added metabolic inhibitors. Perfusion of solutions containing reduced sodium, potassium, or chloride concentrations markedly altered electrolyte concentrations in intestinal muscle but did not necessarily alter intestinal slow waves seriously. However, when lithium ion was substituted for sodium ion serious depression of slow waves occurred. This was also found with ouabain, NaF, and Na₂EDTA, substances which, like lithium, are believed to inhibit the active transport process directly. Iodoacetate and dinitrophenol had little depressant effect on intestinal slow waves in amounts sufficient to cause downhill ion movements. NaCN or 1,10-phenanthroline depressed slow waves, but the effect of NaCN was largely prevented by prior reserpinization of the dog. The depressant effects of lithium ion, ouabain, NaF, and Na₂EDTA were diminished but not abolished by reserpinization. It was concluded that lower amounts of inhibitors of the active transport process abolished intestinal slow waves by causing the release of catecholamines from intrinsic nerve endings in the intestine. The released catecholamines then depressed slow waves. In higher amounts, inhibitors of the active transport process depressed intestinal slow waves by a direct action, unaffected by reserpinization. Intestinal slow waves were therefore postulated to originate from the oscillatory activity of an electrogenic sodium pump.Perfusates with elevated sodium or potassium concentration initiated action potentials in intestinal longitudinal muscle. These action potentials were blocked by atropine and hexamethonium. In reserpinized animals, Na₂EDTA or large amounts of ouabain also initiated action potentials which were stopped or prevented by atropine. It was postulated that all these procedures caused acetylcholine release from intrinsic parasympathetic nerves and that the common mechanism was displacement of mediator by net entrance of sodium ion. This same mechanism may also have accounted for the release of catecholamines from intrinsic sympathetic nerves mentioned above.