Reflex pulmonary vasoconstriction due to stimulation of the aortic body by nicotine

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Abstract
To study the hemodynamic effects of stimulation of the aortic and carotid body chemoreceptors, we injected 2.5– 20 µg/kg nicotine into the ascending aorta of anesthetized, artificially ventilated open-chest dogs. Pressures in the pulmonary artery, left atrium, and systemic arteries, and the stroke output of the right ventricle were measured simultaneously. Pulmonary and systemic vascular resistances (PVR, SVR) were calculated. Changes began 1.5–3.0 sec after the injection; the following two 5-sec periods were compared to a 5-sec control period immediately preceding injection. The injection of nicotine was followed by a significant reflex rise in PVR; the sensory receptors for the reflex were aortic chemoreceptors and the efferent paths were sympathetic fibers. Similar effects were not elicited by stimulation of the carotid body. Bronchoconstriction, changes in bronchial flow, shifts of blood volume between the vascular beds, and liberation of catecholamine were excluded as factors in the PVR increase. Bradycardia, increased SVR, and decreased flow also occurred after combined stimulation of the aortic and carotid chemoreceptors; however, when bradycardia was prevented by atropinization, no significant change in flow occurred.