Pulmonary stress injury within physiological ranges of airway and vascular pressures**
Review articleOpen access

Purpose:The aim of this study was to assess the respective role of a small elevation in pulmonary capillary pressure, airway pressure, or both on alveolar capillary barrier permeability in an isolated perfused rat lung model.Materials and Methods:Four groups were studiedwith 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, HALP, LAHP, and HAHP The lungs were ventilated and penfused ex vivo for 30 minutes. Quantification of fluorescein isothiocyanate-labeled (FITC) dextran in bronchoalveolar lavage (BAL) fluid and radiolabeled tracers assessed alveolar capillary barrier permeability.Results:BALF FITC-dextran was similar in the threegroups with either one or two low-pressure parameters (LALP, LAHP, HALP), but high amounts were found in the HARP group (375.2 × 10−6 mg/mL v, respectively, 21.4, 26.2, and 30 × 10−6 mg/mL, P = .0001). These results were consistent with the albumin space and extravascular lung water: higher values only in the HARP group statistically different from the other groups (P < .002). Interalveolar pore examined with scanning electron microscopy showed an increase in diameters between LALP and HAHP (P < .0001).Conclusions:We can conclude that elevation of eitherthe 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 membrane; however, there is an additive effect of these pressures.

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