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The peripheral vascular effects and supraspinal control of a spinal cardiovascular reflex Szeto, Peter Ming


It has been reported that a mechanical stretch of the walls of the thoracic aorta without obstruction of aortic blood flow induced significant increases in arterial blood pressure, heart rate and cardiac contractility (indicated by LV dP/dt max), and that these reflex hemodynamic changes were present in both intact and spinal cats (Lioy et al, 1974). We decided therefore to study (1) the relative contribution of the external iliac, the superior mesenteric and the renal vascular beds to the pressor response of this spinal thoracic: aorta reflex (TAR), and (2) the effects of the carotid baroreceptor and chemoreceptor reflexes on the TAR pressor response. Experiments were carried out in adult cats with intact brain-stem and anesthetized with chloralose-urethan. The cervical vagi were cut and the common carotids were occluded or the carotid sinuses denervated. The animals were artifically ventilated and the blood gases and pH were kept within physiological limits. (1) By measuring blood flows in the external iliac, superior mesenteric and renal arteries using ultrasonic Doppler flowmeters, we found that aortic stretch (AS) induced, in all the vascular beds a vasoconstriction which could be prevented by the administration of an alpha-adrenergic blocker (phenoxybenzamine). The increase in vascular resistance was most marked in the superior mesenteric bed, and least in the renal bed. The latter maintained a constant flow in the presence of a higher perfusion pressure, probably because of autoregulation. After alpha-adrenergic blockade, the external iliac vasoconstriction was reversed to vasodilatation that could be blocked by atropine. The possibility that AS reflexly activates the sympathetic cholinergic vasodilator system is suggested. (2) The baroreceptor and chemoreceptor reflexes were activated by stimulating the carotid sinus nerve or by perfusing the sinus. We found that both these supraspinal reflexes inhibit but do not abolish the pressor effects of the TAR. The possible mechanisms of these inhibitions and the implications of these results on the nervous control of circulation are discussed.

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