Further Evidences of the Non-Sympathomimetic Action of Ephedrine.

Abstract

In a previous report 1 it was shown that the most favorable functional state of the sympathetic nerves in blood vessels, i. e., during sensitization by cocaine, failed to give responses to ephedrine, indicating that the cause of the pressor action of ephedrine was not sympathetic stimulation. Further evidence obtained recently along other lines confirms this result.

Three cats (4.5 to 7 cc. per kilo of Fledxt. Ergot, U. S. P.) and 1 dog (1 mgm. par Kg. ergotamine) were ergotized to the point of reversal of the original rises of blood pressure caused by epinephrine, to falls of pressure owing to paralysis of the constrictor sympathetic endings. In these same animals, the rises of blood pressure (before ergot) caused by different doses of ephedrine were invariably obtained when the vasomotor reversals to epinephrine were demonstrated. In other words, the pressor action of ephedrine still occurred after paralysis of the sympathetic constrictor endings, and therefore, was due to muscular stimulation. Figures 1 and 2 illustrate typical results with different doses of ephedrine and epinephrine before and after ergot in a cat and a dog.

Uteri responding by motor inhibition to treatment with epinephrine should respond similarly to ephedrine if the latter is sympathomimetic. However, this was not the case, for the same strips of excised uterus (in oxygenated Tyrode solution at 38°), which relaxed under epinephrine, were consistently contracted by the ephedrine. This biological test indicates that ephedrine stimulated the uterus through an action on the muscle. Figure 3 illustrates the contrast between epinephrine and ephedrine in their effects on excised guinea pig uterus. In a recent paper by Kreitniair, 2 appearing after this work was completed, the reported ephedrine stimulation of excised rabbit uterus, previously reversed with epinephrine with an ergot product, is consistent with our results. (See Fig, 3.)