Reflex Vascular Responses to Left Ventricular Outflow Obstruction and Activation of Ventricular Baroreceptors in Dogs

Allyn L. Mark; Francois M. Abboud; Phillip G. Schmid; Donald D. Heistad

doi:10.1172/JCI107281

Reflex Vascular Responses to Left Ventricular Outflow Obstruction and Activation of Ventricular Baroreceptors in Dogs

Allyn L. Mark, Francois M. Abboud, Phillip G. Schmid, and Donald D. Heistad

Published May 1, 1973 - More info

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Abstract

Reflex vascular responses to acute left ventricular outflow obstruction were studied in anesthetized dogs. The studies were done to compare the effects of activation of ventricular baroreceptors on vascular resistance in skeletal muscle (gracilis muscle) and skin (hindpaw); to identify afferent and efferent pathways which mediate the reflex vasodilatation; and to assess the relative contribution of ventricular baroreceptors and baroreceptors in left atrium and pulmonary vessels in responses to left ventricular outflow obstruction. The gracilis artery and the cranial tibial artery to the paw were perfused separately at constant flow. Changes in perfusion pressure to each bed reflected changes in vascular resistance. Outflow obstruction was produced by inflating a balloon in the left ventricular outflow tract for 15 s while pressures in the left ventricle and aortic arch were measured.

Inflation of the balloon increased left ventricular pressure and decreased pressure in the aortic arch. Low and high levels of obstruction produced dilator responses averaging -5±3 (SE) and -42±11 mm Hg in muscle and -1±1 and -3±2 mm Hg in paw. Denervation, phentolamine, and glyceryltrinitrate caused greater dilatation in paw than did left ventricular outflow obstruction. This indicates that dilator responses in the paw were not limited by a low level of resting neurogenic constrictor tone or by a negligible dilator capacity of these vessels.

Obstruction to left ventricular inflow increased left atrial pressure, but did not cause reflex vasodilatation. This suggests that low pressure baroreceptors in atria or pulmonary vessels did not contribute to vasodilator responses to left ventricular outflow obstruction.

Vasodilator responses to outflow obstruction were blocked by bilateral vagotomy, sectioning the sciatic and obturator nerves, and administration of phentolamine, but were not decreased by atropine or tripelennamine.

The results indicate that activation of left ventricular baroreceptors produces striking vasodilatation in skeletal muscle, but only slight vasodilatation in skin. The data suggest that the difference in dilator responses in the two beds results from greater withdrawal of adrenergic constrictor tone to skeletal muscle than to skin. Activation of sympathetic cholinergic or histaminergic dilator pathways does not contribute to the dilatation.

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