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The Journal of Thoracic and Cardiovascular Surgery, Vol 81, 537-545, Copyright © 1981 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association

ARTICLES

Reversal of experimental pulmonary hypertension with sodium nitroprusside

TJ Bixler, VL Gott and TJ Gardner

Pulmonary vascular resistance may be elevated by the use of vasoconstrictive agents or by alveolar hypoxia. The present study was designed to determine the precise vasoconstrictive effects of the two inotropic agents, dopamine and epinephrine, as well as the effects of alveolar hypoxia on the pulmonary vascular system. In addition, the vasoactive effects of a known vasodilator, nitroprusside, were studied. A canine pulmonary lobar preparation was isolated in situ with its pulmonary artery and bronchus selectively cannulated in order to maintain a constant lobar pulmonary blood flow and in order to vary the inspired oxygen concentration from 95% to 0%. Pulmonary vascular pressures were determined by direct measurements and pulmonary vascular resistance units (PVRU) were calculated. Dopamine, epinephrine, and nitroprusside were infused into the isolated pulmonary artery singly and in combination, and the inspired oxygen concentration was varied during each drug infusion. The results of the study demonstrate that dopamine, epinephrine, and alveolar hypoxia all significantly elevate pulmonary vascular resistance. When these two drugs are used together in the presence of hypoxia, the effect on pulmonary resistance is additive. Furthermore, nitroprusside prevents the elevation of pulmonary vascular resistance caused by alveolar hypoxia, and when used with dopamine or epinephrine in the presence of hypoxia, nitroprusside reduces pulmonary vascular resistance toward normal.

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