Somatic depressor reflexes: results of specific 'depressor' afferents' excitation or an epiphenomenon of general anesthesia and certain decerebrations?

Abstract

In chloralose-urethane anesthetized cats and unanesthetized decerebrate cats graded electrical stimulation of the tibial nerve A-afferents was performed and the resulting changes in the tibial nerve compound action potentials, heart rate and systemic arterial pressure were recorded. Three subgroups of the tibial nerve A delta-afferents were distinguished and their excitability, conduction velocity and relation to the circulatory reflexes were characterized. Stimulation of the same A-afferents evoked only tachycardic reflexes in high-mesencephalic unanesthetized cats while both tachy- and bradycardic reflexes developed in anesthetized brain-intact cats. The volleys of A beta-afferents elicited depressor reflexes in 50% of anesthetized cats but were ineffective in the other anesthetized brain-intact cats and in all the unanesthetized decerebrate cats. In anesthetized cats, the volleys of two low-threshold subgroups of A delta-afferents evoked only depressor reflexes and volleys of high-threshold A delta-afferents evoked both depressor and pressor reflexes in dependence on the deepness of anesthesia. In unanesthetized cats, effects of A delta-stimulation depended on the level of decerebration, being exclusively pressor when the most high-threshold A delta-fibers were stimulated in high-mesencephalic cats, both pressor and depressor when only low-threshold subgroups of A delta-fibers were stimulated in these cats, and exclusively depressor in prebulbar cats. The dependence of the direction of reflex blood pressure changes on the level of decerebration and anesthesia is incompatible with the classical concept of the so-called somatic depressor afferents. Moreover, general anesthesia is shown to suppress and invert not only excitatory effects of spinal A-afferents' volleys on sympathetic vasoconstrictor and cardioaccelerator neurones but the inhibitory effects of these afferents' signals on the vagal cardioinhibitory neurones, too. Contrary to this concept, we regard the 'somatic depressor reflexes' and accompanying bradycardia not as a result of 'specific' afferents excitation, but as an epiphenomenon of general anesthesia and certain decerebrations. This hypothesis is founded: (1) on the results of electrophysiological investigations of somato-sympathetic and somato-vagal reflexes indicating the existence of parallel excitatory and inhibitory interneuronal pathways between the spinal afferents and sympathetic and vagal neurones; and (2) on the assumption of unequal sensitivity of these pathways to certain anesthetics.(ABSTRACT TRUNCATED AT 400 WORDS)