The aim of the present work was to investigate whether
prostaglandins (PGs) are synthetized and released from isolated blood-perfused rat and cat lungs secondary to vasoconstriction induced by alveolar
hypoxia. The lungs were perfused with autologous blood with constant volume inflow via the pulmonary artery in a recirculating system. They were ventilated with constant volume positive pressure, and acute alveolar
hypoxia was induced by ventilation with a gas containing 2% O2. A superfusion bioassay technique was used to measure PG-like activity in the perfusate from the lungs, the blood being re-oxygenated before reaching the assay tissues. The
oxygenator prevented the perfusate
hypoxia induced by ventilation
hypoxia to affect the bioassay tissues. The assay tissues were rat stomach strip, rat colon and chick rectum. They were sensitive to calibrating doses of 0.5--1 ng/ml
PGE2 and 1--2 ng/ml
PGF2alpha. In another series of experiments PGs of the F-series were measured in lung tissue from normoxic and hypoxic lungs with radioimmunoassay technique. No increase in PG-like activity could be detected in the venous effluent by means of bioassay during
hypoxia, nor was the lung tissue content of immunoactive
PGF increased by
hypoxia. The present findings indicate that alveolar
hypoxia does not stimulate PG-synthesis in lungs, refuting that PGs are important mediators of the pulmonary
vasoconstrictor response to alveolar
hypoxia. It is concluded that PGs play no significant role in producing the pressor response to alveolar
hypoxia.