Effects of synthetic prostaglandin analogues on platelet aggregation and secretion [proceedings].

plasma; 2 cat lungs cat plasma; 2 cat lungs cat whole blood; 1 guinea-pig lung Krebs Ringer solution and 2 guinea-pig lungs horse plasma. The lungs were perfused (370C) in a recirculating system with constant volume inflow (approximately 150 mi/mn for cat and rabbit lungs, 20-30 mmin for guinea-pig lungs). They were ventilated with 5% CO2 in air at a constant tidal volume. Ten ml/min of the venous effluent was pumped to superfuse a rat stomach strip, a rat calon and a chick rectum for the continuous bioassay of PGs (Vane, 1969). The superfusate was then returned to the lung perfusion circuit. The tissues were sensitive to calibrating doses of 1 ng/ml PGE2 and PGFM. Pulmonary oedema was induced by elevating the outflow pressure of the lungs to 10-30 mmHg for 10-70 minutes. In all lungs this manoeuvre caused gross alveolar oedema as evidenced by cessation of ventilatory movement, translucent appearance of lungs and foam in the trachea. In none of the 14 experiments did raised outflow pressure or oedema development cause any release of PGs which could be detected on the tissues. Theoretically, PG-release of less than 0.5-1 ng/ml might have escaped detection. However, in four experiments, serial radioimmunological determinations of PGF2 were performed on extracts of the perfusate. These experiments verified the findings with bioassay that no PGs were released during raised outflow pressure or subsequent oedema. In conclusion, the present experiments suggest that neither vascular distension nor oedema is a stimulus for increased synthesis of prostaglandins in isolated, perfused lungs.