Bp. Guery et al., PULMONARY STRESS INJURY WITHIN PHYSIOLOGICAL RANGES OF AIRWAY AND VASCULAR PRESSURES, Journal of critical care, 13(2), 1998, pp. 58-66
Purpose: The aim of this study was to assess the respective role of a
small elevation in pulmonary capillary pressure, airway pressure, or b
oth on alveolar capillary barrier permeability in an isolated perfused
rat lung model. Materials and Methods: Four groups were studied with
low or high airway pressure (LA: 10 mL/kg (tidal volume); HA: 20 mL/kg
), low or high pulmonary artery pressure (LP: 9 mm Hg; HP: 12 mm Hg):
LALP, HALF, LAMP, and HAHP. The lungs were ventilated and perfused ex
vivo for 30 minutes. Quantification of fluorescein isothiocyanate-labe
led (FITC) dextran in bronchoalveolar lavage (BAL) fluid and radiolabe
led tracers assessed alveolar capillary barrier permeability. Results:
BALF FITC-dextran was similar in the three groups with either one or
two low-pressure parameters (LALP, LAHP, HALP), but high amounts were
found in the HAHP group (375.2 x 10(-6) mg/mL v, respectively, 21.4, 2
6.2, and 30 x 10(-6) mg/mL, P = .0001). These results were consistent
with the albumin space and extravascular lung water: higher values onl
y in the HAHP group statistically different from the other groups (P <
.002). Interalveolar pore examined with scanning electron microscopy s
howed an increase in diameters between LALP and HAHP (P < .0001). Conc
lusions: We can conclude that elevation of either the pulmonary artery
pressure from 8 to 11 mm Hg or the alveolar pressure from 10 to 15 mm
Hg alone does not change the permeability of the alveolar capillary m
embrane; however, there is an additive effect of these pressures, Copy
right (C) 1998 by W.B. Saunders Company.