Platelet antiaggregatory substances inhibit arachidonic acid induced coronary constriction

1986 ◽  
Vol 64 (4) ◽  
pp. 398-405 ◽  
Author(s):  
Petros Ioannou ◽  
Jaime Talesnik
Keyword(s):  
Arachidonic Acid ◽  
Guinea Pigs ◽  
Coronary Flow ◽  
Inhibitory Action ◽  
Coronary Vasoconstriction ◽  
Coronary Constriction ◽  
Vascular Walls ◽  
Flow Reserve ◽  
Vasodilator Action ◽  
Perfused Hearts

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. Regardless of their vasodilator action, all these drugs acted by inhibiting the AA-induced coronary constriction, while their infusion lasted. We postulated that a thromboxane-like substance, formed from AA in the vascular walls, would be responsible for the coronary vasoconstriction caused by AA. The inhibition of the AA-induced coronary constriction by PGI2, Iloprost, HYD, NFP, DPY, and MIX may be explained by an inhibitory action of these drugs on the synthetic processes of the thromboxane-like substance.

Reduced glutathione modulates the arachidonic acid induced coronary reactions

1984 ◽  
Vol 62 (10) ◽  
pp. 1261-1267 ◽  
Author(s):  
Jaime Talesnik ◽  
James N. Tsoporis
Keyword(s):  
Arachidonic Acid ◽  
Guinea Pig ◽  
Reduced Glutathione ◽  
Isolated Heart ◽  
Prostaglandin E ◽  
Guinea Pig Heart ◽  
Rat Hearts ◽  
Resistance Vessels ◽  
Vasodilator Action ◽  
Perfused Hearts

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. In about 50% of the rat hearts the vasoconstrictor action predominated while the biphasic response was obtained in the rest of the experiments. Pretreatment of rats with aspirin prevented the responses to AA in the isolated heart. The administration of reduced glutathione (GSH) (about 1 mM to the rat or 0.5–0.75 mM to the guinea pig hearts) produced a marked development and (or) enhancement of the vasodilator action of AA. Repeated or single large doses of AA produced a change of pattern of responses from biphasic to constrictor type; the addition of GSH restored the vasodilator phase. Since GSH directs the endoperoxide metabolism towards the synthesis of prostaglandin E2 (PGE2), we postulate that the coronary dilatation of resistance vessels produced by AA would be due to a great extent to PGE2.

scholarly journals THE EFFECTS OF ANAPHYLAXIS, AND OF HISTAMINE, UPON THE CORONARY ARTERIES IN THE ISOLATED HEART

1939 ◽  
Vol 69 (4) ◽  
pp. 545-553 ◽  
Author(s):  
E. Cowles Andrus ◽  
Herbert B. Wilcox
Keyword(s):  
Coronary Arteries ◽  
Guinea Pigs ◽  
Coronary Flow ◽  
Isolated Heart ◽  
Horse Serum ◽  
Isolated Hearts ◽  
Specific Polysaccharide ◽  
Egg Albumen ◽  
Perfused Hearts ◽  
Anaphylactic Response

Anaphylaxis in the isolated, perfused hearts of cats has been shown to be accompanied by a considerable, though transient, increase in coronary flow. This result is contrasted with that observed in the hearts of guinea pigs and rabbits in which the coronary arteries are constricted during anaphylaxis. Attention is directed to the fact that, in the hearts of these three species, the effects of anaphylaxis and of histamine are qualitatively parallel. The characteristic anaphylactic response in the isolated hearts of guinea pigs has been evoked: (a) in the organs removed from immune animals, (b) by each of two antigens (horse serum and egg albumen) under conditions of double sensitization, and (c) upon exposure of the hearts of passively sensitized animals to the type-specific polysaccharide of the pneumococcus. It is evident that, among the effects of anaphylaxis upon smooth muscle in various organs, there must be considered that upon the coronary arteries.

scholarly journals Limited coronary flow reserve after dipyridamole in patients with ergonovine-induced coronary vasoconstriction.

Circulation ◽  
1987 ◽  
Vol 75 (1) ◽  
pp. 163-174 ◽  
Author(s):  
R O Cannon ◽  
W H Schenke ◽  
M B Leon ◽  
D R Rosing ◽  
J Urqhart ◽  
...  
Keyword(s):  
Coronary Flow Reserve ◽  
Coronary Flow ◽  
Coronary Vasoconstriction ◽  
Flow Reserve

Role of parabrachial nucleus in baroreflex-mediated coronary vasoconstriction

1996 ◽  
Vol 271 (3) ◽  
pp. H1079-H1086 ◽  
Author(s):  
D. D. Gutterman ◽  
A. Goodson
Keyword(s):  
Arterial Pressure ◽  
Kainic Acid ◽  
Coronary Flow ◽  
Carotid Occlusion ◽  
Parabrachial Nucleus ◽  
Coronary Vasoconstriction ◽  
Coronary Constriction ◽  
Bilateral Carotid Occlusion ◽  
Bilateral Carotid

Coronary vasoconstriction is a component of the baroreflex response to bilateral carotid occlusion. The central pathways responsible for this reflex constriction are incompletely understood, but previous studies show that activation of parabrachial nucleus (PBN) elicits coronary vasoconstriction and that PBN shares prominent anatomic connections with other central baroreflex centers, including the nucleus of the tractus solitarius. Therefore, we examined whether PBN plays a role in baroreflex mediated coronary constriction and whether cell bodies rather than fibers passing through this region are involved. Anesthetized cats were instrumented for continuous measurements of heart rate, arterial pressure, and coronary flow velocity. Bilateral carotid occlusion following propranolol and vagotomy increased arterial pressure (63 +/- 10%) and an index of coronary vascular resistance (34 +/- 6%). Bilateral microinjections of lidocaine (1%, 400 nl) into PBN reversibly attenuated the coronary constriction (19 +/- 5%) with little effect on the change in arterial pressure. It was further demonstrated that autoregulatory responses to the increase in pressure could not fully account for the observed changes in coronary constriction. In a separate group of animals, kainic acid (50 mM, 300 nl) abolished the baroreflex increase in coronary resistance (43 +/- 1 vs. -9 +/- 9% after) without affecting the increase in arterial pressure (54 +/- 12% increase before vs. 55 +/- 20% increase after kainic acid). We conclude that PBN is a necessary component of the baroreflex pathway mediating coronary vasoconstriction. Furthermore, cell bodies in PBN, rather than simply fibers passing through that region, participate in the reflex coronary vasoconstriction.

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