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.

Effects of thyroid state on respiration of perfused rat and guinea pig hearts

1987 ◽  
Vol 253 (3) ◽  
pp. H519-H523 ◽  
Author(s):  
L. C. Read ◽  
P. G. Wallace ◽  
M. N. Berry
Keyword(s):  
Oxygen Consumption ◽  
Guinea Pig ◽  
Thyroid Hormones ◽  
Isolated Heart ◽  
Basal Respiration ◽  
Perfused Heart ◽  
Guinea Pig Heart ◽  
Thyroid State ◽  
Contraction Frequency ◽  
Rat Hearts

The effects of thyroid state on the respiration of the isolated heart were investigated using retrograde perfused rat and guinea pig hearts. In both species, hypothyroidism caused a marked depression in circulating thyroid hormone concentrations and in the respiration of the isolated, retrograde perfused heart. The effects on myocardial respiration could be attributed to changes in the contraction frequency and in the oxygen consumption per beat, with little contribution from basal respiration. Treatment of animals with thyroxine elevated plasma thyroid hormones to a similar extent in rats and guinea pigs. In the latter, thyroxine treatment was associated with substantial increases in the contraction frequency and the oxygen consumption per beat of the isolated heart. In contrast, only small changes were apparent in the retrograde perfused rat heart, observations that were confirmed in rat hearts perfused at near physiological work loads. It was concluded that rat hearts isolated from normal animals function at near maximal thyroid state, in contrast to the guinea pig heart, which requires higher circulating concentrations of thyroid hormones to attain maximal responses.

Dissociation between adenosine release, MVO2, and energy status in working guinea pig hearts

1997 ◽  
Vol 272 (1) ◽  
pp. H371-H381 ◽  
Author(s):  
U. K. Decking ◽  
S. Arens ◽  
G. Schlieper ◽  
K. Schulze ◽  
J. Schrader
Keyword(s):  
Guinea Pig ◽  
Isolated Heart ◽  
Adenosine Kinase ◽  
Energy Status ◽  
Perfusion Medium ◽  
Guinea Pig Heart ◽  
Atp Formation ◽  
Fluorocarbon Emulsion ◽  
Cardiac Energy ◽  
Arterial Po2

Rapid adaptation of ATP formation and coronary flow is required when cardiac work is altered. Cardiac energy status was proposed to control both oxygen consumption (MVO2) and release of vasoactive adenosine (AR). To investigate the hypothesis of a linear relation between free AMP and AR, we employed 31P nuclear magnetic resonance (NMR) in a newly elaborated guinea pig heart performing pressure-volume work. Under basal conditions, MVO2 was 7.8 +/- 1.0 mumol.min-1.g-1, free AMP 297 +/- 189 nM and AR 226 +/- 179 pmol.min-1.g-1 (n = 29). Decreasing arterial PO2 by 50% reduced MVO2 and increased free AMP by 29%; however, AR rose threefold (n = 5). Doubling oxygen content of the perfusion medium (fluorocarbon emulsion) did not alter MVO2, free AMP, or AR (n = 6). When afterload was doubled, MVO2 increased (+45%) and AR decreased (-60%) despite no change in ADP or AMP (n = 6). Dobutamine increased MVO2 (+50%) and AMP (-98%); however, AR rose more than five times (n = 8). Switching substrates from glucose + pyruvate to glucose diminished MVO2 and increased ADP twofold and AMP fourfold, whereas AR remained constant (n = 6). Our findings demonstrate that cardiac energy status is also not the prime regulator of oxidative phosphorylation in the isolated heart. Changes in the oxygen supply-to-demand ratio induced a rise in AR that exceeded by far the increase in free AMP. Thus, additional factors, possibly inhibition of adenosine kinase, influence the release of vasoactive adenosine.

Comparison of buffer and red blood cell perfusion of guinea pig heart oxygenation

2003 ◽  
Vol 285 (5) ◽  
pp. H1819-H1825 ◽  
Author(s):  
Kenneth A. Schenkman ◽  
Daniel A. Beard ◽  
Wayne A. Ciesielski ◽  
Eric O. Feigl
Keyword(s):  
Oxygen Consumption ◽  
Guinea Pig ◽  
Oxygen Saturation ◽  
Red Blood Cells ◽  
Ventricular Function ◽  
Oxygen Tension ◽  
Blood Cells ◽  
Low Oxygen ◽  
Guinea Pig Heart ◽  
Perfused Hearts

Myocardial mean myoglobin oxygen saturation was determined spectroscopically from isolated guinea pig hearts perfused with red blood cells during increasing hypoxia. These experiments were undertaken to compare intracellular myoglobin oxygen saturation in isolated hearts perfused with a modest concentration of red blood cells (5% hematocrit) with intracellular myoglobin saturation previously reported from traditional buffer-perfused hearts. Studies were performed at 37°C with hearts paced at 240 beats/min and a constant perfusion pressure of 80 cmH2O. It was found that during perfusion with a hematocrit of 5%, baseline mean myoglobin saturation was 93% compared with 72% during buffer perfusion. Mean myoglobin saturation, ventricular function, and oxygen consumption remained fairly constant for arterial perfusate oxygen tensions above 100 mmHg and then decreased precipitously below 100 mmHg. In contrast, mean myoglobin saturation, ventricular function, and oxygen consumption began to decrease even at high oxygen tension with buffer perfusion. The present results demonstrate that perfusion with 5% red blood cells in the perfusate increases the baseline mean myoglobin saturation and better preserves cardiac function at low oxygen tension relative to buffer perfusion. These results suggest that caution should be used in extrapolating intracellular oxygen dynamics from buffer-perfused to blood-perfused hearts.

scholarly journals ANAPHYLAXIS IN THE ISOLATED HEART

1938 ◽  
Vol 67 (2) ◽  
pp. 169-180 ◽  
Author(s):  
Herbert B. Wilcox ◽  
E. Cowles Andrus
Keyword(s):  
Guinea Pig ◽  
Intact Animal ◽  
Isolated Heart ◽  
Horse Serum ◽  
Coronary Vessels ◽  
Cardiac Rate ◽  
Isolated Hearts ◽  
Flow Through ◽  
Perfused Hearts ◽  
Electrocardiographic Abnormalities

The isolated hearts of guinea pigs sensitized to horse serum have been shown to react characteristically upon exposure to small amounts of antigen. The cardiac rate is temporarily accelerated and transient alterations in amplitude of contraction are to be observed. Electrocardiographic abnormalities, previously recorded by remote leads during anaphylactic shock in the intact animal, have been recorded by direct leads from the isolated perfused hearts of sensitized animals during this reaction. An additional effect of anaphylaxis in the isolated heart of the guinea pig is reported: a striking reduction in the rate of flow through the coronary vessels. The anaphylactic reaction of the isolated heart of the guinea pig has been compared with the action of histamine upon the same preparation and the effect of atropine upon each has been observed. The implications of certain quantitative differences in the influence of atropine upon these reactions are discussed.

Prostacyclin-thromboxane interactions in the platelet-perfused in vitro heart

1981 ◽  
Vol 241 (1) ◽  
pp. H18-H25
Author(s):  
K. Schror ◽  
P. Kohler ◽  
M. Muller ◽  
B. A. Peskar ◽  
P. Rosen
Keyword(s):  
Arachidonic Acid ◽  
Guinea Pig ◽  
Human Platelets ◽  
Coronary Vascular Resistance ◽  
Guinea Pig Heart ◽  
Vascular Bed ◽  
Bioassay Data ◽  
Induced Changes ◽  
Thromboxane Formation

A preparation of an isolated platelet-perfused guinea pig heart is described, which was utilized to study prostacyclin-thromboxane interrelationships. Infusion of washed human platelets (4 X 10(8)/min) through the coronary vascular bed stimulated the vascular PGI2 production from 114 +/- 27 to 350 +/- 30 pg/ml (P less than 0.01) and was associated with a significant increase in platelet cAMP from 1.2 +/- 0.4 to 2.6 +/- 0.9 pmol/10(8) platelets (P less than 0.05). Administration of arachidonic acid (AA) (45 micrograms) to the system led to a further increase (eight- to ninefold) of PGI2 and yielded marked thromboxane formation (20-25 ng/ml). Treatment of the hearts with aspirin (1 mM) prevented the PGI2 formation and AA-induced increase in platelet cAMP. Treatment of platelets with aspirin prevented thromboxane formation but did not influence AA-induced changes in platelet cAMP and vascular PGI2 production. Bioassay data of PGI2 and rabbit aortic contracting substance gave results comparable to radioimmunoassay of 6-keto-PGF1 alpha and thromboxane B2. AA always decreased the coronary vascular resistance whether thromboxanes were formed or not.

scholarly journals EFFECTS OF ARACHIDONIC ACID AND BRADYKININ ON THE CORONARY FLOW, RELEASE OF PGI2 AND CARDIAC FUNCTIONS IN THE PERFUSED GUINEA-PIG HEART

1982 ◽  
Vol 32 (2) ◽  
pp. 351-358
Author(s):  
Zen-ichi TERASHITA ◽  
Hiroshi FUKUI ◽  
Kohei NISHIKAWA ◽  
Minoru HIRATA ◽  
Shintaro KIKUCH
Keyword(s):  
Arachidonic Acid ◽  
Guinea Pig ◽  
Coronary Flow ◽  
Guinea Pig Heart ◽  
Cardiac Functions

Species differences in the positive inotropic response to DPI 201-106, a novel cardiotonic agent

1989 ◽  
Vol 67 (11) ◽  
pp. 1460-1463 ◽  
Author(s):  
Stephen J. Haleen ◽  
Robert P. Steffen ◽  
Ronald E. Weishaar
Keyword(s):  
Guinea Pig ◽  
Sodium Channel ◽  
Species Differences ◽  
Isolated Heart ◽  
Inotropic Response ◽  
Inotropic Effects ◽  
Isolated Hearts ◽  
Cardiotonic Agent ◽  
Rat Hearts ◽  
First Time

The positive inotropic activity of the novel cardiotonic DPI 201-106 was investigated in rat and guinea pig isolated hearts. For comparative purposes, the adenylate cyclase stimulant forskolin and the sodium channel agonist veratridine were also evaluated in both species. DPI 201-106 and veratridine produced greater inotropic effects in rat hearts than in guinea pig hearts, whereas forskolin produced comparable effects. In both species the inotropic response to DPI 201-106 and veratridine, but not forskolin, was reversed by the sodium channel antagonist tetrodotoxin. These results confirm that the positive inotropic effect of DPI 201-106 is due to stimulation of the sodium channel and demonstrate for the first time that species differences exist in the inotropic response to this novel cardiotonic drug.Key words: cardiac muscle, contractility, cardiotonic drug, sodium channel, isolated heart.

Arachidonic acid induced coronary reactions and their inhibition by docosahexaenoic acid

1986 ◽  
Vol 64 (1) ◽  
pp. 77-84 ◽  
Author(s):  
Jaime Talesnik
Keyword(s):  
Fatty Acids ◽  
Arachidonic Acid ◽  
Docosahexaenoic Acid ◽  
Isolated Heart ◽  
Isolated Perfused Heart ◽  
Perfused Heart ◽  
Dependent Inhibition ◽  
Perfused Hearts ◽  
Vascular Compartment

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 0.17–0.68 μM caused a concentration-dependent inhibition of the AA-induced constriction. The vasodilatation determined by AA was also depressed, but only after about 30 min of a sustained DHA infusion. The precursor of AA, linoleic acid (LA), was also infused for about 30 min, and like DHA it inhibited the coronary reactions induced by AA. LA is not converted into AA by the isolated heart, but like DHA, was probably incorporated into the cells of the coronary vascular compartment. It is known that LA, administered "in vivo" to mammals, is converted into AA and increases the production of eicosanoids, whereas DHA does not follow this metabolic pathway. The incorporation of these essential polyunsaturated fatty acids by the isolated perfused heart would inhibit the cyclooxygenase in the coronary vessel walls, interfering with the generation of vasomotor metabolites from AA. We postulate that the systemic administration of DHA, by inhibiting the synthesis of a constrictor metabolite, could be beneficial in reducing the damage due to microvascular constriction in myocardial ischaemia.

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.

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