Journal of Applied Physiology AJP: Gastrointestinal and Liver Physiology
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J Appl Physiol 49: 66-72, 1980;
8750-7587/80 $5.00
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Journal of Applied Physiology, Vol 49, Issue 1 66-72, Copyright © 1980 by American Physiological Society


ARTICLES

Adrenal component to pulmonary hypertension caused by nicotine administration in the dog

M. B. Maron, D. A. Rickaby and C. A. Dawson

In this study, we investigated the possibility that the adrenal gland contributes to nicotine-induced pulmonary hypertension using a canine left lower lung lobe (LLL) preparation that was pump-perfused with mixed venous blood at constant flow and outflow pressure. Main pulmonary artery, left atrial, and LLL arterial pressures were monitored to assess the responses of the animal's intact right lung and isolated LLL. With the adrenal venous return intact, injection of 10-26 micrograms/kg nicotine into the left ventricle or ascending aorta resulted in a 42% increase in LLL arterial pressure and a 70% increase in the pulmonary arterial-left atrial pressure gradient (Ppa-Pla). When the adrenal venous return was interrupted, the increases in LLL arterial pressure and Ppa-Pla were reduced to 6 and 10%, respectively. The LLL response could be eliminated by alpha-adrenergic receptor blockade, suggesting that adrenal catecholamines may contribute to the pulmonary hypertension induced by nicotine infusion.





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