The dopamine-induced coronary vasoconstrictor response is potentiated by adenosine administration in the dog heart

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Abstract

The ineffectiveness of β-adrenergic blockade in abolishing adenosine-induced coronary vasodilation was utilized to demonstrate that dopamine (DA) is capable of eliciting very strong coronary vasoconstrictor actions in vivo. In 2 separate groups of dogs anesthetized with pentobarbital, responses to DA were assessed either by flowmeter recordings or by computer-aided infrared thermography, which senses coronary blood flow-dependent heat emission from the epicardium. In untreated controls, submaximal DA infusions (16 μg·kg-1·min-1 iv) elicited a coronary vasodilator response. The thermographic equivalent of this hemodynamic action was an increased epicardial temperature. Pretreatment with oxprenolol (0.5 mg·kg-1 iv) preserved both basic heart activity and cardiac heat emission at levels which were comparable to the control state, but prevented DA mediated excitation of cardiac and coronary β-adrenoceptors. In this state, DA infusion constricted the coronary arteries and tended to decrease heat emission. However, both types of effects were moderate, and the only hemodynamic effect was statistically significant. If DA was given after the coronary bed had been dilated submaximally by adenosine (30 μg·kg-1·min-1 infused into the left heart), the flow-reducing effect of DA became a dramatic phenomenon, and the DA-induced epicardial cooling was significantly potentiated. The results show that after eliminating conventioinal β-effects, DA affects the coronary arteries through vasoconstrictor mechanisms. This finding suggests that the DA-induced constriction is limited in undilated coronary arteries by the metabolic autoregulatory capacity of the vessels.

Original languageEnglish
Pages (from-to)709-721
Number of pages13
JournalJapanese Heart Journal
Volume30
Issue number5
Publication statusPublished - 1989

Fingerprint

Vasoconstrictor Agents
Adenosine
Dopamine
Dogs
Coronary Vessels
Hot Temperature
Hemodynamics
Oxprenolol
Flowmeters
Pericardium
Pentobarbital
Vasodilator Agents
Constriction
Vasodilation
Adrenergic Agents
Adrenergic Receptors
Temperature

Keywords

  • β-Adrenergic blockade
  • Coronary vascular conductance
  • Epicardial heat emission
  • Oxprenolol
  • Thermography

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

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title = "The dopamine-induced coronary vasoconstrictor response is potentiated by adenosine administration in the dog heart",
abstract = "The ineffectiveness of β-adrenergic blockade in abolishing adenosine-induced coronary vasodilation was utilized to demonstrate that dopamine (DA) is capable of eliciting very strong coronary vasoconstrictor actions in vivo. In 2 separate groups of dogs anesthetized with pentobarbital, responses to DA were assessed either by flowmeter recordings or by computer-aided infrared thermography, which senses coronary blood flow-dependent heat emission from the epicardium. In untreated controls, submaximal DA infusions (16 μg·kg-1·min-1 iv) elicited a coronary vasodilator response. The thermographic equivalent of this hemodynamic action was an increased epicardial temperature. Pretreatment with oxprenolol (0.5 mg·kg-1 iv) preserved both basic heart activity and cardiac heat emission at levels which were comparable to the control state, but prevented DA mediated excitation of cardiac and coronary β-adrenoceptors. In this state, DA infusion constricted the coronary arteries and tended to decrease heat emission. However, both types of effects were moderate, and the only hemodynamic effect was statistically significant. If DA was given after the coronary bed had been dilated submaximally by adenosine (30 μg·kg-1·min-1 infused into the left heart), the flow-reducing effect of DA became a dramatic phenomenon, and the DA-induced epicardial cooling was significantly potentiated. The results show that after eliminating conventioinal β-effects, DA affects the coronary arteries through vasoconstrictor mechanisms. This finding suggests that the DA-induced constriction is limited in undilated coronary arteries by the metabolic autoregulatory capacity of the vessels.",
keywords = "β-Adrenergic blockade, Coronary vascular conductance, Epicardial heat emission, Oxprenolol, Thermography",
author = "A. Kollar and V. K{\'e}kesi and A. Juh{\'a}sz-Nagy",
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T1 - The dopamine-induced coronary vasoconstrictor response is potentiated by adenosine administration in the dog heart

AU - Kollar, A.

AU - Kékesi, V.

AU - Juhász-Nagy, A.

PY - 1989

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N2 - The ineffectiveness of β-adrenergic blockade in abolishing adenosine-induced coronary vasodilation was utilized to demonstrate that dopamine (DA) is capable of eliciting very strong coronary vasoconstrictor actions in vivo. In 2 separate groups of dogs anesthetized with pentobarbital, responses to DA were assessed either by flowmeter recordings or by computer-aided infrared thermography, which senses coronary blood flow-dependent heat emission from the epicardium. In untreated controls, submaximal DA infusions (16 μg·kg-1·min-1 iv) elicited a coronary vasodilator response. The thermographic equivalent of this hemodynamic action was an increased epicardial temperature. Pretreatment with oxprenolol (0.5 mg·kg-1 iv) preserved both basic heart activity and cardiac heat emission at levels which were comparable to the control state, but prevented DA mediated excitation of cardiac and coronary β-adrenoceptors. In this state, DA infusion constricted the coronary arteries and tended to decrease heat emission. However, both types of effects were moderate, and the only hemodynamic effect was statistically significant. If DA was given after the coronary bed had been dilated submaximally by adenosine (30 μg·kg-1·min-1 infused into the left heart), the flow-reducing effect of DA became a dramatic phenomenon, and the DA-induced epicardial cooling was significantly potentiated. The results show that after eliminating conventioinal β-effects, DA affects the coronary arteries through vasoconstrictor mechanisms. This finding suggests that the DA-induced constriction is limited in undilated coronary arteries by the metabolic autoregulatory capacity of the vessels.

AB - The ineffectiveness of β-adrenergic blockade in abolishing adenosine-induced coronary vasodilation was utilized to demonstrate that dopamine (DA) is capable of eliciting very strong coronary vasoconstrictor actions in vivo. In 2 separate groups of dogs anesthetized with pentobarbital, responses to DA were assessed either by flowmeter recordings or by computer-aided infrared thermography, which senses coronary blood flow-dependent heat emission from the epicardium. In untreated controls, submaximal DA infusions (16 μg·kg-1·min-1 iv) elicited a coronary vasodilator response. The thermographic equivalent of this hemodynamic action was an increased epicardial temperature. Pretreatment with oxprenolol (0.5 mg·kg-1 iv) preserved both basic heart activity and cardiac heat emission at levels which were comparable to the control state, but prevented DA mediated excitation of cardiac and coronary β-adrenoceptors. In this state, DA infusion constricted the coronary arteries and tended to decrease heat emission. However, both types of effects were moderate, and the only hemodynamic effect was statistically significant. If DA was given after the coronary bed had been dilated submaximally by adenosine (30 μg·kg-1·min-1 infused into the left heart), the flow-reducing effect of DA became a dramatic phenomenon, and the DA-induced epicardial cooling was significantly potentiated. The results show that after eliminating conventioinal β-effects, DA affects the coronary arteries through vasoconstrictor mechanisms. This finding suggests that the DA-induced constriction is limited in undilated coronary arteries by the metabolic autoregulatory capacity of the vessels.

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