Mechanical ventilation increases microvascular permeability in oleic acid-injured lungs

The pulmonary pathology for which a patient receives ventilatory support may increase the risk of developing barotrauma, because an underlying disease process may weaken the vasculature and render the lung more susceptible to damage by mechanical ventilation. We determined the response of isolated young rabbit lungs to mechanical ventilation after oleic acid (OA) injury. New Zealand White rabbits (0.7-1.3 kg) were anesthetized with pentobarbital sodium (30 mg/kg), tracheotomized, and exsanguinated. The heart and lungs were isolated and perfused with autologous blood at a constant flow. The capillary filtration coefficient (Kf,c, in ml.min-1.cmH2O-1.100 g wet wt-1) and pulmonary arterial (Ppa) and venous pressures were determined before and 30 and 60 min after oleic acid administration (OA group; 0.2 ml into the venous reservoir), ventilation alone (Vent group; peak inspiratory pressure = 25 cmH2O), or oleic acid combined with ventilation (OA + Vent group). Ppa transiently increased by 4.21 +/- 0.822 cmH2O after OA administration but then returned to approximately control values. Baseline Kf,c values for OA (0.288 +/- 0.042), Vent (0.296 +/- 0.035), or OA + Vent (0.276 +/- 0.028) groups were not significantly different from each other. Kf,c after either OA administration (0.45 +/- 0.066) or Vent (0.35 +/- 0.75) were not significantly different from each other or from baseline measurements. In the group ventilated after OA administration (OA + Vent), Kf,c (0.883 +/- 0.148) increased significantly from baseline (P less than 0.001) and was significantly different from all other treatment groups. We conclude that the combination of minimal OA injury and ventilation was more deleterious to the lung than either one alone.