Perinatal pulmonary responses to arachidonic acid during normoxia and hypoxia

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Abstract
Dilator prostaglandins are released from the perinatal lung in response to ventilation and also may be involved in the pressor response to hypoxia. Arachidonic acid, precursor of bisenoic prostaglandins, causes pulmonary vasoconstriction when infused into the pulmonary circulation of perinatal goats. The effects of hypoxia on the arachidonic acid-induced increase in pulmonary vascular resistance (PVR) were evaluated in ventilated fetal and neonatal lambs using an in situ pump-perfused lower left lobe preparation. Pulmonary vascular effects in newborns due to arachidonic acid apparently are not altered by hypoxia. Ventilated fetuses show a greater response to arachidonic acid infused during hypoxia than during normoxia. This increase in PVR is merely additive to the hypoxic pressor response; thus, hypoxia does not appear to affect the actions of exogenous arachidonic acid in the perinatal pulmonary circulation. The decrease in systemic arterial pressure seen with arachidonic acid infusion is greater at the termination of the combined infusion and hypoxia than after infusion alone. This systemic hypotension is also of longer duration and may indicate a greater release of dilator prostaglandins from the lung following hypoxia and arachidonic acid.

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