To determine how hypoxia may alter determinants of pulmonary transvascular fluid flux, adult male ferrets were exposed to either room air (C) or hypoxia (H; Fl(O2) = 0.12) for 24 h. After anesthesia and ventilation with C or H, the mean pulmonary artery pressures were 18.4 ± 2.2 (SEM) and 27.3 ± 2.9 mm Hg, respectively (p < 0.025). The right lung was then removed for gravimetric analysis of lung water and the left lung was blood-perfused (~142 ml/kg/min) and continuously weighed for 15 min at left atrial pressures of 20, 25, and 30 mm Hg. Filtration coefficient (K(f)) was estimated from the slopes of the relationships of rate of weight gain versus change in vascular pressure over the last 5 min of each interval. Extravascular lung water/blood-free dry lung weight for C and H were 2.95 ± 0.06 (SEM) and 3.53 ± 0.09 ml/g, respectively (p < 0.01). K(f) for C and H were 0.0645 ± 0.0190 (SEM) and 0.0662 ± 0.0085 ml/min/mm Hg/100 g, respectively (NS). In a second group of experiments, in which lungs were removed from ferrets after 24 h exposures to C or H, protein reflection coefficients (σ) were estimated by comparing the increases in perfusate hematocrit and protein concentrations during edema formation. Reflection coefficients for albumin were 0.64 ± 0.03 (SEM) and 0.39 ± 0.07 with C and H, respectively (p < 0.01). The σ values for IgG and IgM were not affected. In a third group of experiments, isolated perfused ferret lungs were ventilated with Fl(O2) = 3.3% O2 for 76 ± 33 min (SD), followed by 18% O2 for 92 ± 34 min or vice versa. With these brief exposures to hypoxia, there was no effect on σ for albumin, IgG, or IgM. We conclude that 24 h hypoxia may promote pulmonary edema formation in ferret lungs by increasing the permeability of the vasculature to albumin, thereby decreasing the effectiveness of the plasma-interstitial oncotic pressure gradient. Hypoxic vasoconstriction-induced increases in vascular pressure may contribute further to edema formation.
|Original language||English (US)|
|Number of pages||6|
|Journal||American journal of respiratory and critical care medicine|
|State||Published - May 1994|
ASJC Scopus subject areas
- Pulmonary and Respiratory Medicine
- Critical Care and Intensive Care Medicine