Prostaglandin content in blood and lung tissue during alveolar hypoxia

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Abstract
The aim of the present work was to investigate whether prostaglandins (PG) are synthesized 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 from affecting 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 PGE2.alpha.. In another series of experiments PG 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. Alveolar hypoxia does not stimulate PG-synthesis in lungs, refuting the idea that PG are important mediators of the pulmonary vasoconstrictor response to alveolar hypoxia. PG play no significant role in producing the pressor response to alveolar hypoxia.