ON THE MECHANISM OF STIMULATION OF CAROTID GLAND CHEMORECEPTORS

Publisher Website
Google Scholar
Abstract
By a special perfusion arrangement the carotid sinuses and glands of anesthetized dogs were subjected to anoxia, hypercapnia and asphyxia before and after poisoning with mono-iodo-acetic acid. Ventilation of the animal progressively increases during the poisoning. Concns. of poison which abolish the reflex anoxic hyperpnea or convert it to a late depression may affect the pressure reflexes very little. Under certain conditions the anoxic response may be thus abolished or converted while the hypercapnic response persists strongly. Hypercapnia appears able to stimulate the poisoned chemoreceptors under a degree of anoxia which by itself is unable to stimulate. It is concluded that anoxic stimulation of carotid gland chemoreceptors requires the process of formation of intermediary or final acid products of glycolysis, and that hypercapnic stimulation is at least partly independent of such processes. The question is brought up concerning whether anoxemia and hypercapnia. each with its own acid mechanism, actually act upon a single set of receptors, or require 2 distinct sets.