Decreased BasalProduction ofNitric OxideinPatients WithHeartDisease

Study objectives: Thepathophysiologic role ofnitric oxide(NO) released inthelung isnotwell understood. Todetermine whether theproduction ofendogenous NO iscorrelated withany hemodynamic parameters, we measured theamountofNO released fromthelung tissue of patients withheart disease. Methods: Twenty patients (14 withischemic heartdisease, 4withdilated cardiomyopathy, and2 withmitral stenosis) and16normal control subjects were enrolled inthestudy. We measured exhaled airsamples byusing amethoddeveloped inourlaboratory. TheNO release ratefromthe lungs was calculated fromtheamountofexhaled NO andtheduration oftheexhalation. Results: TherateofNO release was significantly lower inthepatients withmoderate-to-severe heart failure (New YorkHeartAssociation [NYHA] IIorIII) thaninthose withmildheart failure (NYHA I) or innormal control subjects. TherateofNO release was positively correlated withthe cardiac index (r=0.50, p<0.05), andwas negatively correlated witheither thesystemic (r= .0.58, p<0.01) orpulmonary vascular resistance (r=.0.45, p<0.05). Inthepatients withmoderate-tosevereheart failure, theamountofNO released andtheoxygen tension inthepulmonary artery were significantly lowercompared withthoseparameters inpatients withmildheart failure. Conclusions: Results suggest that thebasalproduction ofendogenous NO inthelung tissue of patients withheart failure isimpaired, perhaps leading totheelevated pulmonary vascular tone seen inpatients withmoderate-to-severe heart failure. (CHEST 1998; 113:317-22)