Pneumonia was induced in rats by instillation of carrageenin (0.5 ml of 0.7 % solution) into the trachea. Three or four days after instillation, the lungs were isolated, perfused with blood of healthy rat blood donors, and ventilated with air + 5 % C02 or with various hypoxic gas mixtures. Pulmonary vascular reactivity to acute hypoxic challenges was significantly lower in lungs of rats with pneumonia than in lungs of controls. The relationship between 02 concentration in the inspired gas and Po2 in the blood effluent from the preparation was shifted significantly to lower Po2 in lungs with pneumonia compared to control ones. These changes were not present in rats allowed to recover for 2- 3 weeks after carrageenin instillation. We suppose that blunted hypoxic pulmonary vasoconstriction may contribute to hypoxaemia during acute pulmonary inflammation. Decreased Po2 in the blood effluent from the isolated lungs with pneumonia implies significant increase of oxygen consumption by the cells involved in the inflammatory process.
Acute lung injury was induced by intravenous injection of 20 //I of a mixture of equivalent volumes of capronic acid, caprilic acid and olive oil in intact anaesthetized rats and in isolated perfused rat lung preparations. Lung injury in intact rats resulted in an increase in lung weight related to body weight and in a decrease in the lung dry/wet weight ratio. Lung compliance, measured in a body plethysmograph, was decreased. Pao2 decreased and Pac02 increased in 10 and 20 min, respectively, after the beginning of the experiment. Mean blood pressure in pulmonary artery increased immediately after the injection. Isolated rat lungs were perfused at constant flow with physiological saline solution containing bovine albumin and meclofenamate. The injection of a mixture of capronic acid, caprilic acid and olive oil increased the baseline perfusion pressure and led to a release of endothelial cells into the perfusate. The perfusion flow-pressure relationship was shifted upwards. Both the extrapolated pressure axis, intercept and slope of the plot were significantly elevated. The described experimental lung injury is a suitable model for studies on the effects of vascular wall damage and transvascular fluid leak in pulmonary vasculature.