A COMPARISON OF THE RESPONSES OF SYMPATHETIC GANGLIA AND CHEMORECEPTORS TO CHOLINOMIMETIC AGENTS AND SODIUM CYANIDE

¹ Department of Pharmacology, Schools of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania

An electrophysiological study was made of the responses to drugs of the terminal portions of the sympathetic supply to the region of the carotid bifurcation. Administered intraarterially, acetylcholine (ACh), tetramethylammonium, and nicotine evoked firing in external carotid nerves that had been surgically separated from the superior cervical ganglion. Since firing was evoked by sodium cyanide in the external carotid nerve, it was suggested that the drug-induced responses were recorded from sensory fibers which arose in the chemoreceptors of the carotid body and passed with the external carotid nerve. The mean threshold dose of ACh needed for the activation of the firing was comparable to that required for the activation of orthodromic postganglionic firing. The response to ACh of the external carotid nerve was enhanced following the inhibition of the cholinesterases by 217 AO and was blocked by hexamethonium (C₆) , tetraethylammonium, and d-tubocurarine. Unlike ACh , methacholine (MCh) did not produce firing in the external carotid postganglionic nerve. Small doses of atropine, which prevented the orthodromic postganglionic responses to MCh, had no effect on the firing induced by ACh. These findings were discussed in relation to the distribution of C₆-and atropine-sensitive sites in sympathetic ganglia and unmyelinated nerves.

Sodium cyanide evoked a long-lasting negative potential in the superior cervical ganglion. The cyanide-induce potential (1) was not accompanied by postganglionic firing, (2) had no effect on ganglionic transmission or responses to injected ACh, and (3) was not altered by C₆ or atropine. Accordingly, it is unlikely that the potential originated in the ganglion cells. The possibility was considered that the source of the cyanide-evoked potential was either the glial cells or the vascular smooth muscle cells of the ganglion.