Coronary vasodilator responses to hypoxia before and after aminophylline

Afonso, Skoda; Ansfield, Thomas J.; Berndt, Theodore B.; Rowe, George G.

doi:10.1113/jphysiol.1972.sp009769

Cited by 35 publications

(19 citation statements)

References 7 publications

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“…This would then induce dilatation of the coronary resistance vessels. Nevertheless, doubts concerning this hypothesis have been raised by several authors (Bittar & Pauly, 1971;Afonso, Ansfield, Berndt & Rowe, 1972) who showed that the administration of aminophylline left reactive hyperaemia responses unchanged but blocked the responses to adenosine. Moreover, it has been shown that adenosine 5'-triphosphate (ATP), adenosine 5'-pyrophosphate (ADP) and adenosine 5'-phosphate (AMP) are more potent coronary vasodilators than adenosine (Moir & Downs, 1972; ATP has been found in the perfusate of hypoxic guinea-pig heart (Paddle & Burnstock, 1974).…”

Section: Resultsmentioning

confidence: 99%

Coronary Reactions to Cardiac Hyperactivity and to Hypoxia in Isolated Perfused Heart of Rat

Sen

Sunahara

Talesnik

et al. 1977

British J Pharmacology

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I 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 The heart rate was controlled by electrical pacing. Coronary vasodilatation resulted from cardiostimulation or hypoxia. This coronary response was greater at higher heart rates. 3 In parallel experiments administration of noradrenaline to hearts paced at different frequencies resulted in a rate-dependent elevation of adenosine-3',5'-cyclic monophosphate (cyclic AMP). 4 Duration of hypoxia leading to different degrees of reactive hyperaemia did not change the cardiac cyclic AMP levels. SCoronary vasodilatation due to increased cardiac metabolism produced by noradrenaline, Ca2+ or tachycardia was enhanced by the phosphodiesterase inhibitors diazoxide and papaverine while it was inhibited during the administration of prostaglandin E2. 6 Reactive hyperaemia was unaffected by diazoxide, papaverine or prostaglandin E2. 7 Catecholamine depletion by reserpine did not influence metabolic coronary dilatation nor the reactive hyperaemic responses. 8 We postulate that there are at least two types of coronary reactions: one in response to hypoxia, 'reactive hyperaemia', and another resulting from cardiac hyperactivity, 'metabolic coronary dilatation'. The latter, blocked by prostaglandin E2 and enhanced by diazoxide or papaverine, would be triggered by cyclic AMP while reactive hyperaemia would result from other mechanisms.

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Section: Resultsmentioning

confidence: 99%

Coronary Reactions to Cardiac Hyperactivity and to Hypoxia in Isolated Perfused Heart of Rat

Sen

Sunahara

Talesnik

et al. 1977

British J Pharmacology

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“…Berne (1963) hypothesized that adenosine was the physiologic regulator of blood flow during reactive hyperemia, and this hypothesis dominated the field for the next decade, although clear supporting evidence was lacking (see Nees et al, 1985;Zucchi et al, 1989). For example, an adenosine receptor antagonist, theophylline, failed to block reactive hyperemia, although it blocked the vasodilator actions of exogenously applied adenosine (Afonso et al, 1972;Bünger et al, 1975). Intracoronary adenosine and ATP increased coronary blood flow, but reactive hyperemia in the dog heart after occlusion was not blocked by the adenosine receptor antagonist aminophylline (Eikens and Wilcken, 1973a,b;Giles and Wilcken, 1977;Clemens et al, 1985a).…”

Section: E Coronary Vesselsmentioning

confidence: 99%

Purinergic Signaling and Blood Vessels in Health and Disease

2013

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“…The influence of oxygen tension on vascular resistance is a well-known phenomenon (Markwalder & Starling, 1913;Green & Wegria, 1941;Berne et al 1957;Carrier, Walker & Guyton, 1964;Daugherty, Scott, Dabney & Haddy, 1967;Detar & Bohr, 1968;Afonso, Ansfield, Berndt & Rowe, 1972;Duvelleroy et al 1973;Gellai, Norton & Detar, 1973). The possible roles of oxygen tension as the underlying mechanisms ofautoregulation and metabolic vasodilation have also been discussed (Belloni, 1979).…”

Section: Theoretical Backgroundmentioning

confidence: 99%

Oxygen and coronary vascular resistance during autoregulation and metabolic vasodilation in the dog.

Drake-Holland¹,

Laird²,

Noble³

et al. 1984

The Journal of Physiology

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SUMMARY1. The hypothesis that tissue oxygen tension controls coronary vascular resistance during changes in perfusion pressure and oxygen consumption was expressed in a simplified mathematical form capable of making quantitative predictions.2. The predictive value of this formulation of the hypothesis was tested in experiments on anaesthetized mongrel dogs subjected to constant-pressure perfusion of the left main coronary artery, with measurements of coronary blood flow and arterio-venous oxygen content differences. Coronary venous oxygen content was used as an index of tissue oxygenation. t 3. The responses of coronary blood flow and arterio-venous oxygen content difference, made over a range of perfusion pressures (which caused autoregulation) and heart rates (which caused metabolic regulation) were predicted qualitatively by the model. 4. Coronary vascular conductance was positively related to metabolic rate only during metabolic regulation (heart rate changes); during autoregulation the relationship between these two variables was inverse.5. Coronary vascular conductance and resistance values taken from both interventions (both perfusion pressure and heart rate variations) were closely related to coronary venous oxygen content and calculated Po2.6. These findings suggest that further examination of oxygen tension, as the controller of the coronary vascular bed under physiological conditions should be considered.

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Coronary vasodilator responses to hypoxia before and after aminophylline

Cited by 35 publications

References 7 publications

Coronary Reactions to Cardiac Hyperactivity and to Hypoxia in Isolated Perfused Heart of Rat

Coronary Reactions to Cardiac Hyperactivity and to Hypoxia in Isolated Perfused Heart of Rat

Purinergic Signaling and Blood Vessels in Health and Disease

Oxygen and coronary vascular resistance during autoregulation and metabolic vasodilation in the dog.

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