Respiratory responses to intravenous sodium cyanide, a function of the oxygen-cyanide relationship.

Abstract

The fast intravenous injection of sodium cyanide in an adequate dosage in man almost invariably produces a deep inspiratory gasp. This fact was first investigated in detail by Loevenhart and associates (1) and was subsequently used for the determination of the circulation time by Robb and Weiss (2, 3). Heymans (4) discovered by cross-circulation experiments in animals that this respiratory stimulation of cyanide was mediated exclusively through the carotid and aortic chemoreceptors. At the intracellular level, the exact mechanism for this reaction is still a controversial one. It is known, however, that cyanide inhibits cytochrome oxidase in very low concentrations and, therefore, must depress aerobic intracellular respiration. Unmetabolized acid products consequently accumulate rapidly, stimulate the chemoreceptor nerve endings which send up volleys of impulses to the respiratory center, which is, in turn, reflexly stimulated to produce a gasp and hyperpnea. Von Euler and associates (5) demonstrated in a very elegant manner the effect of sodium cyanide in anesthetized cats. He dissected afferent strands of nerve fibers from the carotid body and recorded directly their action potentials. A cyanide infusion was found to increase markedly the rate and amplitude of these impulses. With concomitant oxygen inhalation, however, it was noted that the traffic of impulses was greatly diminished or even abolished. It seemed, therefore, that pure oxygen is able to overcome in