Effect of Adrenal-Demedullation on Acceleration of Denervated Heart by Acetylcholine Hypotension. ∗

Abstract

Evidence has been presented that adrenaline and sympathin are liberated reflexly in unanesthetized dogs as a result of the brief hypotension produced by intravenous injection of acetylcholine. 1 The diphasic action of acetylcholine on intestinal motility was interpreted as resulting from a direct stimulatory effect of the compound on the intestinal smooth muscle followed by inhibition of the intestine by sympathomimetic substances. Adrenal demedullation prolonged the direct excitatory phase and reduced the inhibitory phase. It was considered that the inhibition that still resulted after adrenal demedullation was caused by sympathin liberated at the endings of adrenergic nerves activated reflexly by the fall in blood pressure.

Wiggers and Green have suggested that the evidence that a part of the acceleration of the denervated heart after acetylcholine injection is caused by adrenalin would have been more convincing had it been shown that the acceleration is reduced after excision of the adrenal medullae. 2 Such an experiment should also determine the cardiac effects of the sympathin produced during acetylcholine hypotension. The effect of a given dose of acetylcholine on the rate of the denervated heart can not be readily determined for the same dog before and after adrenal-demedullation, because the nutritional state of the animals with denervated hearts does not permit carrying them through additional operations. However, records have been obtained from 2 series of dogs with denervated hearts, one series having intact adrenal glands and the other series having the adrenals demedullated prior to the cardiac denervation.

Data obtained by the methods previously described 1 show that adrenal demedullation greatly reduces, but does not entirely eliminate, the acceleration of the denervated heart following acetylcholine injections. These facts provide additional evidence that acetylcholine causes the liberation of sympathomimetic substances from both adrenal and extra-adrenal sources.