Acute cardiopulmonary effects of nitroglycerin in canine oleic acid pulmonary edema.

In a canine model of acute respiratory failure, the authors investigated acute cardiopulmonary effects of nitroglycerin (TNG) and compared the results with those obtained after phlebotomy. Oleic acid increased intrapulmonary shunt (Qs/Qt) from 7.4 to 31% (P less than 0.001) and decreased (P less than 0.01) cardiac output (CO). In the presence of assumed low-pressure pulmonary edema, TNG was infused to decrease mean blood pressure (BP) by 40%; this was associated with a 26% decrease (P less than 0.05) in CO. Qs/Qt increased from 31 to 42% (P less than 0.01). There was a slight increase (P less than 0.01) in pulmonary vascular resistance (PVR) with TNG, and mean pulmonary artery pressure (PAP) decreased (P less than 0.05). In contrast, when CO was decreased by a similar amount with phlebotomy, mean Qs/Qt did not significantly change. There were similar changes in PVR and PAP and mixed venous O2 tension with TNG and phlebotomy. Accordingly, current results rule out increased flow, increased PVO2, and mechanical alterations in pulmonary vascular pressures as contributory to the increase in Qs/Qt with TNG. Alternatively, 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.