Platelet antiaggregatory substances inhibit arachidonic acid induced coronary constriction.

Isolated perfused hearts of rats and guinea pigs reacted to arachidonic acid (AA) with coronary vasoconstriction followed by vasodilatation. The infusion of prostacyclin (PGI2), Iloprost, hydralazine (HYD), and nifedipine (NFP) elicited a vasodilatation that nullified the coronary flow reserve, therefore the AA-induced vasodilatation was abolished. Dipyridamole (DPY) and 1-methyl-3-isobutylxanthine (MIX) produced a slight coronary dilatation without restricting the dilatation induced by AA.

Arachidonic acid induced coronary reactions and their inhibition by docosahexaenoic acid.

The objective of the present study was to further investigate the influence exerted by docosahexaenoic acid (DHA) on the coronary reactions induced in isolated perfused hearts of rats and guinea pigs by bolus doses of arachidonic acid (AA). As in previous studies, we found that AA produced a coronary constriction followed by a longer lasting dilatation. The present data demonstrate that a 5-min infusion of DHA at 0.

Modulation of positive inotropy and metabolic coronary dilatation by myocardial alpha-adrenoceptors.

Cardiac hyperactivity and its consequent metabolically induced coronary vasodilation (MCD) were studied in isolated, perfused, electrically paced rat hearts. The alpha-adrenoceptor agonists, phenylephrine and methoxamine, produced a concentration-dependent inhibition of the inotropic responses to noradrenaline, dobutamine, isoprenaline, tyramine, and glucagon, while relatively potentiating their MCD reactions. This inhibition was unrelated to the alpha-agonists' known inotropic action and was not affected by catecholamine depletion of the heart.

Blockade of coronary reactions to arachidonic acid by glyceryl trinitrate and tranylcypromine.

Isolated perfused hearts of rats or guinea pigs reacted to bolus doses of arachidonic acid (AA) with a coronary constriction followed by a protracted vasodilatation phase. Glyceryl trinitrate (GTN; 55-95 microM) produced coronary dilatation during which the AA-induced constriction remained unaltered, or even enhanced. After 'acute tolerance' developed by sustained GTN infusion, the constrictor phase of AA was inhibited while the vasodilatation continued unaltered or slightly enhanced.

Reduced glutathione modulates the arachidonic acid induced coronary reactions.

Coronary flow was recorded from spontaneously beating isolated perfused hearts of rats and guinea pigs. Arachidonic acid (AA), in single bolus doses, produced a fast short lasting coronary constriction followed by a slow developing but persisting vasodilation. These reactions (biphasic type) were characteristic of the guinea pig heart.