ORIGIN OF THE HIND LIMB VASODILATATION EVOKED BY STIMULATION OF THE MOTOR CORTEX IN THE CAT

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 vasodilation 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 sympathic 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. © 1979 The Physiological Society