Source: Annual Congress 2011 - Physiology of human pulmonary hypertension
Disease area: Pulmonary vascular diseases

Abstract

Introduction
Exercise-induced pulmonary arterial hypertension (PAH) is a clinically important stage in the spectrum of PAH. The pathophysiology of abnormal pulmonary vascular responses to exercise is poorly characterized. Endogenous nitric oxide (NO) is an important mediator of vasodilation and accumulating data suggests impaired NO signaling PAH.
Aims
The objective was to test the hypothesis that changes in stable NO metabolites (NOx) in blood during exercise in patients with resting or exercise-induced PAH would differ from NOx in individuals with normal exercise pulmonary arterial pressures. Patients were selected from a population referred to the MGH Cardiopulmonary Exercise Lab for invasive incremental cardiopulmonary exercise testing with pulmonary and radial artery catheters. Simultaneous samples of arterial (a) and mixed venous (mv) blood at rest, peak exercise, and one hour post-exercise were obtained from 10 patients with PAH (VO2max <85% predicted, Qtmax <80% predicted, PAP >30 mmHg, and PVR >80 dyne·s·cm-5) and 10 controls (VO2max and Qtmax both >80% predicted). These were analyzed for [NOx] using chemiluminescence. Data are median [interquartile ranges]. Comparisons used the Mann-Whitney test.
Results
NOx_mv increased from rest to exercise in controls (45%, [4, 77], p=0.02), but not in PAH (0%, [-27, 15], p=0.97).

NOx_a increased in both groups (11% [-2, 26] v 7% [-7, 40], p=0.80). NOx flux [Qtmax · (mv-a [NOx])] in controls was greater than PAH (370% [-100, 4869] v -96% [-460, 6], p=0.04).

There were no differences in [NOx] during recovery.
Conclusions
Normal pulmonary vasodilation and recruitment during exercise may be dependent on NOx bioavailability in mixed venous blood.

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Citations should be made in the following way:
W. Oldham, A. Janocha, P. Pappagianopoulos, S. Erzurum, A. Waxman, G. Lewis, D. Systrom (Boston, Cleveland, United States Of America). Nitric oxide metabolite flux during exercise in pulmonary arterial hypertension. Eur Respir J 2011; 38: Suppl. 55, 2308

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