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.

Enhancement by glutathione of the inotropic actions of catecholamines and glucagon.

We have previously shown that cardiostimulation produced by catecholamines, glucagon, tachycardia or CaCl2, resulted in a metabolically induced increase in coronary flow [9, 11, 12]. Slow infusion of prostaglandin E2 (PGE2) or its precursor, arachidonic acid, inhibited the development of metabolic coronary dilatation without major alterations of the effects of the cardiostimulating agents on the cardiac activity [9, 11, 12]. Since PGE2 synthesis is known to be enhanced by glutathione we thought that its addition to the perfused heart would intensify the inhibition of the metabolic coronary dilatation produced by arachidonic acid.

Enhancement of metabolic coronary vasodilatation by nicotinic acid or amide.

Cardiostimulation produced by noradrenaline, glucagon, or tachycardia on the isolated perfused rat heart produced a metabolic coronary dilatation that was potentiated by nicotinic acid or its amide [NIC; 0.05-1.0 mM] without affecting the cardiostimulation.

Coronary flow reactions to arachidonic acid are inhibited by docosahexaenoic acid.

Arachidonic acid (AA) administered to isolated perfused rat hearts produced coronary vasoconstriction followed by vasodilatation due to biotransformation of AA into vasoactive metabolites. The formation of these metabolites may be blocked with ibuprofen or fenclorac. Slow infusions of docosahexaenoic acid (DHx) resulted in an inhibition of the coronary responses to AA.

Coronary vasoconstrictor and vasodilator actions of arachidonic acid in the isolated perfused heart of the rat.

The administration of arachidonic acid (AA) to the isolated perfused heart of the rat usually produced biphasic coronary responses characterized by initial vasoconstriction followed by prolonged vasodilatation. However, some responses were predominantly vasoconstrictor or vasodilator. The non-steroidal anti-inflammatory agents (NSAA) indomethacin (1-5 mg/l) and naproxen (12.

Enhancement of noradrenaline-induced metabolic coronary dilatation by ethanol.

Isolated perfused rat hearts receiving noradrenaline as a cardiostimulatory agent show the characteristic metabolic coronary dilatations which correlate with the inotropic effect elicited by noradrenaline. Addition of ethanol (20-400 mg/dl) to the perfusion fluid produced a concentration-dependent enhancement of the metabolic coronary dilatation. The latter was increased by 50% at about 125 mg ethanol/dl.

Myocardial synthesis of prostaglandin-like substances and coronary reactions to cardiostimulation and to hypoxia.

1 Continuous recording of cardiac contractions and coronary flow from isolated perfused hearts of rats permitted the study of coronary reactions to: (a) cardiostimulation induced by single doses or slow infusions of noradrenaline, CaCl2, glucagon or electrically induced tachycardia; (b) short interruptions of coronary inflow (hypoxia). 2 Except during tachycardia the heart rate was kept constant at 210 beats/min by electrical pacing. 3 Metabolic coronary vasodilatation (MCD) resulting from cardiac hyperactivity induced by noradrenaline, Ca2+, tachycardia or glucagon was inhibited by administration of prostaglandin E2.

Coronary reactions to cardiac hyperactivity and to hypoxia in isolated perfused heart of rat.

1. Continuous recording of cardiac force of contraction, heart rate and coronary flow from isolated perfused hearts of rats was used to study coronary reactions: (a) to cardiostimulation with noradrenaline, CaCl2, or electrically induced tachycardia; (b) to short duration stoppage of coronary inflow (hypoxia). 2.

Prostaglandin E2 and cyclic AMP in the coronary vasodilatation due to cardiac hyperactivity.

In the isolated perfused rat heart, the dose-related cardiostimulation produced by norepinephrine (NE) or calcium chloride (Ca2+) was followed by a corresponding increase in coronary flow (CF) and in the cardiac level of adenosine 3',5'-cyclic phosphate (cAMP). Prolonged prostaglandin E2 (pge2) infusion did not change the basic force of contraction, CF, or cAMP level but when NE or Ca2+ were administered, only the responses of the CF and the cAMP were diminished. A phosphodiesterase inhibitor, diazoxide (Dx), caused insignificant increase in the basal cAMP, without affecting the force of contraction or CF.