The origin of the hind limb vasodilatation evoked by stimulation of the motor cortex in the cat.

Abstract

SUMMARY1. In cats under Althesin anaesthesia, the hind limb area of the motor cortex has been stimulated by means of monopolar, semi-micro-electrodes with careful experimental control so as to avoid reflex effects evoked through stimulation of meningeal afferent fibres or stimulus spread to non-cortical structures.2. Localized cortical stimulation which elicited muscle contractions in the contralateral hind limb also elicited vasodilatation in the same limb: the stimulus threshold was the same for both effects, and the magnitude of the dilatation was related to the strength of contraction.3. Reduction of the somatic motor response, caused by lesions in the medullary pyramidal tract, was accompanied by a parallel reduction of the vascular response.4. Prevention of the motor response by gallamine or by spinal cord section at L4-L5 (which leaves the sympathetic outflow to the hind limbs intact) led to abolition of the vascular response. During recovery from gallamine, contraction and vasodilatation returned in parallel.5. The muscle vasodilatation was insensitive to atropine or guanethidine. 6. It is concluded that the hind limb vasodilatation observed on stimulation of the motor cortex is simply a post-contraction hyperaemia, and that it is independent of the sympathetic nervous system. Previous conclusions of a sympathetically mediated vasodilatation probably resulted from inadequate control of the stimulus or a failure to recognize weak muscle contractions.

An analysis of the purinergic component of active muscle vasodilatation obtained by electrical stimulation of the hypothalamus in rabbits

“…Our evidence indicates that it is not. There are marked differences in the characteristics of blood flow responses evoked in the experiments of Hilton et al (1979) and those which we observed. Even during powerful muscle contractions, the magnitude of their hyperaemic blood flow responses was minor when compared with the magnitudes of both active muscle vasodilatation in cats and the vasodilatation which we observed.…”

“…Contrary to the earlier findings of Eliasson et al (1952), Hilton et al (1979 have recently claimed that muscle vasodilatation produced by motor cortical stimulation in cats is not due to an active vasodilatation but, instead, is secondary to muscular contractions: a functional hyperaemia. Hilton's work poses the question of whether or not our vasodilatation might also be a functional hyperaemia.…”

Large vasodilatations in skeletal muscle of resting conscious dogs and their contribution to blood pressure variability

“…A mediation through the motor nerves is a particularly attractive explanation, since a similar atropine resistant vasodilatation had been observed in response to electrical stimulation in the motor cortex of the cat (Hilton et al 1979). The authors of that study had attributed the dilator response to the release of metabolic vasodilators secondary to even minor contractions of the skeletal muscle.…”

Central Nervous Regulation of Vascular Resistance

“…A study in the cat in which the stimulation of the motor cortex was carefully controlled to avoid refl ex effects through stimulation of meningeal afferents or current spread to noncortical structures (45) found no vasodila .. tQ! effects in skeletal muscles evoked via their sympathetic outfl ow.…”