Abstract
Chen 1 and Kreitmair 2 believe that the pharmacological action of ephedrin in small doses is identical with that of adrenalin, that is, a stimulation of the sympathetic myoneural junction (commonly spoken of as nerve endings), while that of larger doses is due to direct stimulation of smooth muscle comparable to that produced by barium. Among other effects described by these investigators, are those of inhibition of the intestinal movements and relaxation of spasm of bronchial muscle. The former of these effects has been questioned by Nagel, 3 who failed to obtain any inhibition of the gut but solely a pressor effect.
Like Nagel, we have not (in over 100 experiments) obtained any evidence of a depressant action of ephedrin on the isolated rabbit gut although we have meticulously followed the methods and employed the dosage of Chen and Kreitmair. Other publications4-5 have called in question the view that ephedrin produces certain of its effects by sympathicometic action. The question is not of merely theoretical interest for if ephedrin does not stimulate the sympathetic nerve endings in the gut, it is highly unlikely that it stimulates similar inhibitory nerve endings in the bronchi. As such assumed pharmacological action is the basis of the use of ephedrin as a substitute for adrenalin in the treatment of asthma, a repetition of Chen and Kreitmair's investigations appeared desirable. In a limited number of experiments conducted in this laboratory, a broncho-dilating effect of ephedrin has been observed only exceptionally. Perhaps the divergent reports of the efficacy of ephedrin in bronchial asthma may have their explanation in the fact that ephedrin relaxes bronchial spasm only under certain conditions.
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