Effects of alveolar hypoxia and reoxygenation on pulmonary capillary pressure and lung fluid balance in dogs

Abstract

Pulmonary oedema formation during alveolar hypoxia and reoxygenation is considered to be the result of increased capillary pressure and/or increased capilllary permeability because of endothelial cell damage. To test this hypothesis pulmonal arterial pressure (PAP), pulmonary capillary pressure (Pc), extravascular lung water (EVLW) and pulmonary capillary permeability-surface area (PS) were measured for urea in in vivo dog lungs during constant blood flow during prolonged alveolar hypoxia and reoxygenation. Twenty dogs (nine time controls and 11 test animals) were investigated in vivo during constant blood flow. Pc and segmental vascular resistance was determined by analysis of pulmonal arterial occlusion pressure-profiles. The multiple indicator-dilution technique was used to study EVLW and PS-urea. During hypoxic pulmonary vasoconstriction, PAP increased with time in a biphasic fashion. Pc remained unchanged because of a predominant precapillary constriction. During reoxygenation, PAP, Pc and segmental vascular resistance were similar to base-line values. EVLW increased significantly during hypoxia and reoxygenation, whereas PS-urea remained unchanged.Table 2Table 2: abstract 3). Table of median values (95% confidence interval) Pulmonary oedema formation during hypoxia and reoxygenation is not because of increased capillary filtration nor to increased capillary permeability, but rather is a consequence of increased water flow through hydraulic pathways in capillary endothelial cells.