Effects of Arachidonic Acid in the Rabbit Pulmonary and Systemic Vascular Beds in vivo

Abstract

We studied the effects of arachidonic acid (AA) in the pulmonary and systemic circulations of rabbit under constant blood flow conditions in vivo, using a total heart bypass model. AA (100–150 µg/kg) injected into the pulmonary artery produced a dose-dependent increase in pulmonary arterial pressure (P_pa), without altering systemic arterial pressure (P_sa). Conversely, injection of AA into the aorta reduced P_sa in a dose-dependent fashion, but did not significantly alter P_pa. FPL55712, a leukotriene receptor antagonist, did not affect any of these responses to AA. Indometacin, a cyclo-oxygenase inhibitor, totally prevented the pulmonary pressor response to intravenously administered AA and reduced the systemic depressor response to intra-arterially administered AA. The thromboxane A₂ synthetase inhibitor, 7-(l-imidazolyl)heptanoic acid, totally abolished the increase in P_pa in response to intravenously adminstered AA, but did not alter the dose-dependent decrease in P_sa in response to intra-arterially administered AA. These results suggest that in rabbits (1) AA produces pulmonary vasoconstriction and systemic vasodilation, (2) blood metabolites of AA mediate these effects and are then rapidly deactivated, and (3) AA-induced pulmonary vasoconstriction appears to be largely dependent on thromboxane A₂.

Milrinone Relaxes Pulmonary Veins in Guinea Pigs and Humans

“…However, results from the systemic circulation can’t be transferred to the pulmonary circulation in general, as both vascular beds express a remarkable distinct behaviour concerning the regulation of vascular permeability [43], the response to hypoxia [44], to cardiovascular agents [45], [46], to arachidonic acid [47], as well as differences in the NO-pathway [48], [49]. Therefore, questions concerning the pulmonary circulation can only be solved by examining pulmonary vessels themselves.…”