THE CENTRAL ACTION OF LIGNOCAINE AND ITS EFFECT ON CARDIAC OUTPUT

Fifty-nine tests were performed on twenty-four anaesthetized dogs in a study of the effects of lignocaine on circulatory and respiratory functions. In single-dog experiments, it was shown that lignocaine (1 to 2 mg./kg. body weight) increased ventilation somewhat, but had no effect on O(2) consumption. Cardiac output was increased due to a rise in both heart rate and stroke volume. There was an elevation of arterial blood pressure. The central blood volume was increased, but central venous pressure, total peripheral resistance and the ventilationperfusion ratio were decreased. The increase in cardiac output after lignocaine was abolished both in decerebrate and in vagotomized dogs. In cross-circulation experiments with dogs, it was demonstrated that the primary site of action of lignocaine on cardiac output was central. The effect of lignocaine on cardiac output could be blocked by intravenous procaine.