EXHALED NITRIC BRIDE DURING EXERCISE IN PRIMARY PULMONARY-HYPERTENSION AND PULMONARY FIBROSIS

Study objectives: Nitric oxide (NO), a potent vasodilator, is present in the exhaled air of humans. We wished to quantify NO production in p atients with abnormalities of the pulmonary circulation, Participants: Nine patients with primary pulmonary hypertension (PPH), six with pul monary fibrosis (PF), and 20 normal volunteers were studied, Intervent ions: All subjects were studied at rest and during continuous incremen tal (ramp) cycle ergometry exercise, All patients with PPH and nine ma tched normal volunteers also performed constant exercise at equal abso lute work rates, Measurements and results: The concentration of NO was measured continuously in mixed expired air, and the rate of NO produc tion (VNO) calculated, Peak exercise capacity was markedly impaired in both patient groups, VNO was similar at rest in the PPH patients (142 +/-84 nL/min) and the normal subjects (117+/-45 nL/min), but lower in the PF patients (66+/-13 nL/min; p<0.05; analysis of variance with Bon feronni correction), While VNO in normal subjects more than doubled by peak exercise to 268+/-85 nL/min, there was no significant rise with exercise in either patient group (PPI-I, 155+/-81 nL/min; PF, 91+/-67 nL/min), Constant work rate exercise induced a significant rise in VNO in the normal subjects (rest, 101+/-68 nL/min; exercise, 147+/-87 nL/ min; p<0.001) but no significant change in the PPH patients (rest, 127 +/-111 nL/min; exercise, 68+/-65 nL/min), Conclusions: We conclude tha t the low resting VNO in PF may be due to loss of normal functional pu lmonary capillary bed, The increase in VNO seen in normal subjects may be associated with dilatation and recruitment of the pulmonary capill ary bed during exercise, and failure to increase VNO during exercise i n disease states may reflect an inability to recruit the capillary bed .