The Splanchnic Efferent Outflow of Impulses in the Light of Ergotamine Action

It was found that the effect of faradic stimulation of the peripheral end of the splanchnic nerve, which normally causes a rapid rise in the blood pressure, became more and more delayed and depressed, until after large doses the effect was reversed.

Abstract

Summary. For an analysis of the action of ergotamine upon the arterial blood pressure of the cat we have recorded the action potentials from efferent fibres of the splanchnic nerve. When ergotamine is given in a moderate dose of 0.05 mg per kg body weight, asphyxiation or the inhalation of air rich in carbon dioxide produces a fall instead of the usual rise in blood pressure. The electric response, however, differs from that to ergotamine only in that the response now starts earlier and is more accentuated. After a pithing of the brain and the medulla oblongata the efferent outflow in the splanchnic nerve reacts to asphyxiation and carbon dioxide in a way very similar to the reaction in the intact cat, but the response is more rapid and more pronounced than in the intact animal. Ergotamine does notproduce any change whatever in the splanchnic efferent outflow in the spinal cat. This shows that inhibitory influences upon the spinal vaso‐motor centres are exerted from higher centres, which influence is abolished by ergotamine even in moderate doses, as has been shown by ROTHLIN, WRIGHT and EULER and SCHMITERLÖW. When giving increasing doses of ergotamine it was found that the effect of faradic stimulation of the peripheral end of the splanchnic nerve, which normally causes a rapid rise in the blood pressure, became more and more delayed and depressed, until after large doses the effect was reversed. At his stage the adrenaline effect was also reversed. These observations have been discussed in the light of the prevailing theories on the nature of peripheral sympathetic effect. It was found that the simplest explanation would be to assume that the sympathetic nerve activity leads to a peripheral liberation of adrenaline. The phenomena observed under ergotamine may, however, be equally well understood by assuming that the constrictor excitation is mediated by sympathin E. In such case we may assume that the vasodilation produced by direct stimulation of the splanchnic nerve is due either to the action of antidromic afferent impulses or to the liberation of sympathin I in fibres running to the intestinal walls, or to a combination of both these influences. Thus even in this scheme the supposition of specific sympathetic vaso‐dilator fibres in the splanchnic nerve of the cat does not seem to be necessary.