Acute Cardiopulmonary Effects of Nitroglycerin in Canine Oleic Acid Pulmonary Edema

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Abstract
In a canine model of acute respiratory failure, the acute cardiopulmonary effects of nitroglycerin (TNG) were investigated and compared the results with those obtained after phlebotomy. Oleic acid increased intrapulmonary shunt (Qs/Qt) from 7.4-31% (P < 0.001) and decreased (P < 0.01) cardiac output (CO). In the presence of assumed low-pressure pulmonary edema, TNG was infused to decrease mean blood pressure .**GRAPHIC**. by 40%; this was associated with a 26% decrease (P < 0.05) in CO. Qs/Qt increased from 31-42% (P < 0.01). There was a slight increase (P < 0.01) in pulmonary vascular resistance (PVR) with TNG, and mean pulmonary artery pressure .**GRAPHIC**. decreased (P < 0.05). When CO was decreased by a similar amount with phlebotomy, mean Qs/Qt did not significantly change. There were similar changes in PVR and .**GRAPHIC**. and mixed venous O2 tension with TNG and phlebotomy. Current results rule out increased flow, increased P.hivin.vO2, and mechanical alterations in pulmonary vascular pressures as contributory to the increase in Qs/Qt with TNG. The increase in Qs/Qt with TNG may be explained by a direct pharmacologic decrease in pulmonary hypoxic vasoconstriction and/or by nonspecific pharmacologic effects.