The effect of analgesic and neuroplegic agents on the coronary chemoreflex

Abstract

It is known that certain substances, intravenously administered, can cause a reflex fall of blood pressure and bradycardia. These reflexes are evoked by stimulation of the receptors of the lungs and heart, and their afferent routes terminate in the body of the vagus nerves. Dawes and Comroe were the first to use the name "coronary chemoreflex = for the reflex from the cardiac receptors [14]. This reflex is caused by Veratrum alkaloids, serotonim, ATP, isourea derivatives, as well as by serum, plasma, and blood.* All these substances induce bradycardia and hypotension only when they enter the cardiac receptors, through the coronary vessels (the name of the reflex is related to this fact) [9,14].The question of which cardiac receptors are responsible for the development of the coronary chemoreflex is still largely unsolved.Veratrum alkaloids are known to induce the coronary chemoreflex by stimulating the cardiac mechanoreceptors [20]; according to the data of Mort and Peintal [18,21], serotonin stimulates a different type of cardiac receptor, and it is not yet clear which receptors react to sermn, ATP, and isourea derivatives.Our knowledge of the "coronary chemoreflex," therefore, cannot be considered complete from the physiological standpoint. Moreover, the existing data do not give sufficient basis for a more rational classification of the reflexes incorporated under this name.The coronary chemoreflex is known to be one of the causes of hypotension in myocardial infraction, stenocardia, operations on the heart, and post-transfusion complications: it plays a substantial role in the "action mechanism of certain medicinal preparations used to treat hypertonic conditions [12,[14][15][16]. It has therefore become necessary to seek pharmacological agents which will influence the coronary chemoreflex.We began our research in this direction with a study of the effect of analgesics, aminazine (chloropromazinc), and reserpine on the coronary chemoreflex. The ability of these substances to alter the course of many viscero'-visceral reflexes is generally known [2,8,17]. It therefore seemed wholly possible that they could affect the subject reflexes from the heart. Other important reasons for our choice of these substances were the extensive use of aminazine and analgesics in myocardial infarction, stenocardia, and operations on the heart and the attempts which have been made to use reserpine combined with veratrine to treat hypertonic conditions [1,15.16].* Serum, plasma, and blood acquire the ability to induce coronary chemoreflex only after long storage (2-3 weeks). 51