Abstract
Since eserine permits a greater accumulation of acetylcholine at junctional points of activated ganglion cells, muscle fibers and other end organs, and granting the same for increased acidity, it is to be anticipated that eserine and carbon dioxide would complement each other in their effects upon the body. 1-6 This preconceived idea was put to a simple test in anesthetized dogs connected with rebreathing tanks for alternate administration of room air and carbon dioxide mixtures.
The cardio-inhibitory reflex initiated by faradic stimulation of the superior laryngeal nerve served as the physiological indicator. The superior laryngeal nerve was stimulated for a period of 5 seconds at intervals of 2 minutes with faradic shocks of uniform intensity.
It was demonstrated, by the administration of a 10% mixture of carbon dioxide in 40% oxygen, that hypercapnia increased the reflexogenic inhibition of the heart. Intravenous injection of eserine superimposed upon a continuing hypercapnia increased and prolonged the reflexogenic cardio-inhibition still more. Return to room air while the effects of eserine were still evident produced an abrupt diminution in the degree of cardio-inhibition. These results permit 4 conclusions. 1. Hypercapnia potentiates the cardio-inhibitory reflex initiated by stimulation of the superior laryngeal nerve. 2. Eserine produces a comparable potentiation. 3. The potentiation produced by eserine is addible to that of hypercapnia. 4. The potentiating action of hypercapnia is subtractible from that of eserine.
Because the frequency of the heart beat is probably the end effect of the influences of many junctional stations, parasympathetic, sympathetic and central, a quantitative allocation of the acid-neurohumoral effects at the several stations is at present impossible.
Get full access to this article
View all access options for this article.