Hemodynamic cause of the pressor response to carotid occlusion

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Abstract
Dogs were prepared for hemodynamic study of baroreceptor reflexes by section of the aortic depressor nerves and removal of one carotid sinus; the other sinus was supplied by a common carotid artery exteriorized in a van Leersum loop. An electromagnetic flow transducer was implanted on the ascending aorta, and a catheter in the aortic arch. In 2 dogs the depressor nerves were intact. Occlusion of the exteriorized common carotid artery caused cardiac output, peripheral resistance, and heart rate to increase. Stroke volume was moderately decreased. Increases in heart rate and arterial pressure were regular and reproducible but there was pronounced variation in the relative contributions of cardiac output and peripheral resistance to the rise in pressure. In about half the responses cardiac output was dominant; in the other half, peripheral resistance. The variability appeared in the individual dogs, either from day to day, or in successive responses. In the dogs with intact aortic depressor nerves the pressor response was due entirely to increased peripheral resistance. It is proposed that the pre-existing hemodynamic state conditions the mechanism of response to carotid occlusion.