• John T Reeves, John H Linehan, and Kurt R Stenmark.
• University of Colorado Health Sciences Center, 4200 E. 9th Ave., Denver, CO 80262, USA.
• Am. J. Physiol. Lung Cell Mol. Physiol. 2005 Mar 1;288(3):L419-25.

AbstractIncreasing pulmonary arterial (Ppa) and wedge (Pw) pressures at high flow (Q) during exercise could distend the thin-walled vessels. A mechanical descriptor of vascular distension, the distensibility (alpha, fractional diameter change/mmHg pressure), has been reported to be approximately 0.02 for isolated large and small arteries, i.e., a 2% change in diameter per millimeter mercury pressure. In this review we used a pulmonary hemodynamic model to estimate alpha for data from exercising humans to determine whether interpretable results might be obtained. In 59 normal sea level subjects having published measurements of Ppa and Pw over a range of Q, we found values of alpha (0.02 +/- 0.002) giving calculated Ppa, which matched measured Ppa to within 1.3 +/- 0.1 (SE) mmHg. When subjects were exposed to chronic hypoxia (n = 6, in Operation Everest II), alpha decreased (0.022 +/- 0.002 vs. 0.008 +/- 0.001, P < 0.05), but when subjects were exposed to acute hypoxia (Duke chamber study, n = 8), alpha did not decrease (0.014 +/- 0.002 vs. 0.012 +/- 0.002, P = not significant). Values of alpha tended to decrease with age in men >60 yr. Thus at rest and during exercise, normal values of alpha in young persons were similar to those measured in vitro, and the values decreased in chronic hypoxia and with aging where vascular remodeling or vascular wall stiffening was expected. We propose that the estimation of pulmonary vascular distensibility in humans may be a useful descriptor of pulmonary hemodynamics.

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