Responses to constant work rate bicycle ergometry exercise in primary pulmonary hypertension: the effect of inhaled nitric oxide.
OBJECTIVE
The purpose of this study was to investigate the responses of patients with primary pulmonary hypertension (PPH) to constant work rate exercise and to examine the effect of nitric oxide (NO) inhalation.


BACKGROUND
Maximal exercise tolerance is reduced in PPH, but gas exchange responses to constant work rate exercise have not been defined. We hypothesized that increased pulmonary vascular resistance in PPH would reduce the rate of rise of minute oxygen consumption in response to a given work rate. Because NO may lower pulmonary vascular pressures in PPH, we also postulated that inhaled NO might ameliorate gas exchange abnormalities.


METHODS
Nine PPH patients and nine matched normal subjects performed 6-min duration constant work rate cycle ergometry exercise (33.9+/-13.4 W). Patients performed two experiments: breathing air and breathing air with NO (20 ppm). Preexercise right ventricular systolic pressure was assessed by Doppler echocardiography. Normal subjects performed the air experiment only. Gas exchange and heart rate responses were characterized by fitting monoexponential curves.


RESULTS
In PPH patients, resting right ventricular systolic pressure fell after NO inhalation (from 83.8+/-16.9 to 73.9+/-21.6 mm Hg, p<0.01, analysis of variance with Tukey correction), but not after breathing air alone (from 88.0+/-20.8 to 86.7+/-20.6 mm Hg, p = NS). Nitric oxide did not affect any of the gas exchange responses. Minute oxygen consumption was similar by the end of exercise in patients and normals, but increased more slowly in patients (mean response time [MRT]: air, 63.17+/-14.99 s; NO, 61.60+/-15.45 s) than normals (MRT, 32.73+/-14.79, p<0.01, analysis of variance, Tukey test). Minute oxygen consumption kinetics during recovery were slower in patients (MRT air: 82.50+/-29.94 s; NO, 73.36+/-15.87 s) than in normals (MRT, 34.59+/-7.11 s, p<0.01). Heart rate kinetics during exercise and recovery were significantly slower in patients than in normals.


CONCLUSIONS
The cardiac output response is impaired in PPH. Nitric oxide lowered pulmonary artery pressure at rest, but failed to improve exercise gas exchange responses.
Riley
M S
MS
Division of Respiratory and Critical Care Physiology and Medicine, St. John's Cardiovascular Research Center, Harbor-UCLA Medical Center, Torrance, California, USA. mriley@compuserve.com
Pórszász
J
J
Engelen
M P
MP
Shapiro
S M
SM
Brundage
B H
BH
Wasserman
K
K
D000328:Adult; D002302:Cardiac Output / Q000187:drug effects; D015444:Exercise / Q000502:physiology*; D005080:Exercise Test; D005260:Female; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D006976:Hypertension, Pulmonary / Q000188:drug therapy* / Q000503:physiopathology*; D008875:Middle Aged; D009569:Nitric Oxide / Q000494:pharmacology* / Q000627:therapeutic use; D010101:Oxygen Consumption; D011659:Pulmonary Gas Exchange / Q000187:drug effects*; D014665:Vasodilator Agents / Q000494:pharmacology* / Q000627:therapeutic use
D014665:Vasodilator Agents; D009569:Nitric Oxide