Lung edema caused by high peak inspiratory pressures in dogs. Role of increased microvascular filtration pressure and permeability.
Mechanical ventilation with high peak airway pressures (Paw) has been shown to induce pulmonary edema in animal experiments, but the relative contributions of transvascular filtration pressure and microvascular permeability are unclear. Therefore, we examined the effects of positive-pressure ventilation on two groups of open-chest dogs ventilated for 30 min with a peak Paw of 21.8 +/- 2.3 cm H2O (Low Paw) or 64.3 +/- 3.5 cm H2O (High Paw). No hemodynamic changes were observed in the Low Paw group during ventilation, but mean pulmonary artery pressure (Ppa) increased by 9.9 cm H2O, peak inspiratory Ppa by 24.6 cm H2O, and estimated mean microvascular pressure by 12.5 cm H2O during High Paw ventilation. During the same period, lung lymph flow increased by 435% in the High Paw and 35% in the Low Paw groups, and the terminal extravascular lung water/blood-free dry weight ratios were 5.65 +/- 0.27 and 4.43 +/- 0.13 g/g, respectively, for the two groups. Lung lymph protein clearances and minimal lymph/plasma ratios of total protein were significantly higher (p less than 0.05) after 2 h of increased left atrial pressure (PLA) in the High Paw group versus the Low Paw group, which indicates a significant increase in microvascular permeability. Lymph prostacyclin concentration in pulmonary lymph, measured as the stable metabolite 6-0-PGF1 alpha, was increased significantly by 70 to 150% from baseline (p less than 0.05) in both groups during the periods of increased Paw and increased PLA, but it was not significantly different between the groups.(ABSTRACT TRUNCATED AT 250 WORDS)
Parker
J C
JC
Department of Physiology, University of South Alabama, College of Medicine, Mobile 36688.
Hernandez
L A
LA
Longenecker
G L
GL
Peevy
K
K
Johnson
W
W
D000818:Animals; D002199:Capillary Permeability / Q000502:physiology; D004285:Dogs; D011464:Epoprostenol / Q000378:metabolism; D015633:Extravascular Lung Water / Q000502:physiology; D008168:Lung / Q000378:metabolism; D008196:Lymph / Q000502:physiology; D011175:Positive-Pressure Respiration / Q000009:adverse effects*; D011652:Pulmonary Circulation / Q000502:physiology*; D011654:Pulmonary Edema / Q000209:etiology* / Q000503:physiopathology; D013928:Thromboxane A2 / Q000378:metabolism; D014882:Water-Electrolyte Balance
D013928:Thromboxane A2; D011464:Epoprostenol