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PROCEEDINGS OF THE PHYSIOLOGICAL SOCIETY

Provided adequate measures are taken to avoid the effects of sensory stimulation and of extensive operative procedures, asphyxia of the cerebral centres in a chloralosed cat, whether produced by general asphyxia, occlusion of the cerebral-arteries, cerebral compression, or by supplying asphyxial blood from another animal, causes a marked acceleration of the heart. This occurs after the vagi have been divided and the suprarenal glands have been removed. The acceleration takes place prior to the better known slowing of the heart which occurs in asphyxia or cerebral aneemia from central stimulation of the vagus. The acceleration is not related to any changes in pressure in the various blood vessels and must be looked upon as being due to the chemical effect of the asphyxia on the sympathetic. This is supported by the fact that the cardiac acceleration may be much delayed by over-ventilation of the animal prior to the production of cerebral anaemia. The central control of the heart rate may thus be somewhat similar to the control of respiration.