The effects of infusion of arachidonic acid, the precursor of the bisenoic prostaglandins, were investigated in the feline pulmonary vascular bed under conditions in which pulmonary blood flow varied naturally or was controlled, and when vascular tone was at basal levels or elevated. In approximately half of the animals studied, arachidonic acid infusions caused small decreases in pulmonary arterial pressure, and the depressor response was enhanced when pulmonary vascular resistance was actively increased. In the others, arachidonic acid infusions increased pulmonary arterial pressure. In all experiments, infusions of large amounts of the precursor acid, as well as bolus injections, increased pulmonary arterial pressure and pulmonary vascular resistance. Responses to arachidonic acid were attenuated by meclofenamic acid, a cyclooxygenase inhibitor. In half the animals studied, the pressor response to hypoxia was decreased by arachidonic acid, whereas in the others, hypoxic vasoconstriction was enhanced. In two-thirds of the experiments in which pulmonary blood flow was held constant and pulmonary vascular tone was elevated, arachidonic acid infusions decreased pulmonary vascular resistance. These experiments indicate that both vasodilator and vasoconstrictor products in the cyclooxygenase pathway can be formed from arachidonic acid in the lung of the intact-chest cat, and that resulting responses to the prostaglandin precursor may be dependent on substrate concentration, rate and mode of administration, activity of biosynthetic enzymes, and basal level of tone in the pulmonary vascular bed.
|Original language||English (US)|
|Number of pages||7|
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|State||Published - 1980|
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Physiology (medical)