Failure of methylprednisolone, ibuprofen, or prostacyclin to reduce HCl-induced pulmonary albumin leak in dogs.

The purpose of this study was to examine the effects of methylprednisolone (MP), ibuprofen (I), and prostacyclin (PGI2) pretreatment on cardiopulmonary hemodynamics, arterial oxygenation, and pulmonary alveolar-capillary membrane permeability, measured with a gamma-scintigraphic technique, after acid instillation in the dog. All animals were placed on their right side and 2 ml/kg 0.1 N HCl was instilled into the endotracheal tube. Five untreated control dogs showed a significant (p less than 0.05) rise in slope index (SI), a scintigraphic measurement of pulmonary albumin flux, 30 minutes after acid injury. After 120 minutes there was a significant rise in mean pulmonary arterial pressure (PAP) and pulmonary vascular resistance (PVR) and a decrease (p less than 0.05) in cardiac output (CO) and PaO2. Two groups of five dogs each were pretreated with MP (30 mg/kg) and I (12.5 mg/kg), respectively. Thirty minutes after acid instillation both groups showed a significant rise in the SI, which was significantly greater than the values in the control animals in the case of MP. By 120 minutes after acid injury all changes in PAP, PVR, PaO2, and CO were not significantly different from those of control animals with the exception of the I group, which resisted any change in CO throughout the study. Another group of five dogs were pretreated with a constant infusion of PGI2 (3 micrograms/kg/min) starting 75 minutes before acid instillation. PGI2 produced a significant increase in CO that was also greater (p less than 0.05) than the CO in control animals before instillation of HCl. Pre-HCl SI in the dogs treated with PGI2 was slightly, but significantly, increased over control dogs. The SI and CO remained significantly higher than values in control animals 30 minutes after acid injury. The SI remained significantly higher than that of control animals at 120 minutes. After 2 hours changes in PAP, PVR, PaO2, and CO were without significant difference from those of control animals. These data support the conclusion that PGI2, I, or MP are not effective therapy for acid aspiration and that PGI2 and I may worsen the protein leak by increasing flow across the damaged capillary membrane.