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Exhaled Nitric Oxide During Exercise in Primary Pulmonary Hypertension and Pulmonary Fibrosis

Marshall S. Riley; János Pórszász; Joe Miranda; Mariëlle P.K.J. Engelen; Bruce Brundage; Karlman Wasserman
Author and Funding Information

Affiliations: From the Division of Respiratory and Critical Care Physiology and Medicine, St. John's Cardiovascular Research Center, Harbor-UCLA Medical Center, Torrance, Calif.,  From the Division of Cardiology, St. John's Cardiovascular Research Center, Harbor-UCLA Medical Center, Torrance, Calif.

Affiliations: From the Division of Respiratory and Critical Care Physiology and Medicine, St. John's Cardiovascular Research Center, Harbor-UCLA Medical Center, Torrance, Calif.,  From the Division of Cardiology, St. John's Cardiovascular Research Center, Harbor-UCLA Medical Center, Torrance, Calif.


1997 by the American College of Chest Physicians


Chest. 1997;111(1):44-50. doi:10.1378/chest.111.1.44
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Abstract

Study objectives: Nitric oxide (NO), a potent vasodilator, is present in the exhaled air of humans. We wished to quantify NO production in patients with abnormalities of the pulmonary circulation.

Participants: Nine patients with primary pulmonary hypertension (PPH), six with pulmonary fibrosis (PF), and 20 normal volunteers were studied.

Interventions: All subjects were studied at rest and during continuous incremental (ramp) cycle ergometry exercise. All patients with PPH and nine matched normal volunteers also performed constant exercise at equal absolute work rates.

Measurements and results: The concentration of NO was measured continuously in mixed expired air, and the rate of NO production (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 Bonferonni 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 (PPH, 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 that the low resting VNO in PF may be due to loss of normal functional pulmonary capillary bed. The increase in VNO seen in normal subjects may be associated with dilatation and recruitment of the pulmonary capillary bed during exercise, and failure to increase VNO during exercise in disease states may reflect an inability to recruit the capillary bed.


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