Related Experiment Videos
Endogenous adenosine and coronary vasoconstriction in hypoperfused myocardium during exercise
D J Duncker1, D D Laxson, P Lindstrom
1Department of Internal Medicine, University of Minnesota Medical School, Minneapolis 55455.
Cardiovascular Research
|September 1, 1993
Summary
Endogenous adenosine dilates coronary vessels during ischemia, but does not block vasoconstriction from thromboxane A2 (U46619). This suggests adenosine and U46619 act on different coronary vessel sizes.
Area of Science:
- Cardiovascular Physiology
- Myocardial Ischemia Research
- Pharmacology
Background:
- Coronary circulation remains responsive to stimuli during myocardial ischemia.
- Endogenous adenosine's role in modulating vasoconstriction during ischemia is not fully understood.
Purpose of the Study:
- To investigate if endogenous adenosine attenuates coronary vasoconstriction induced by the thromboxane A2 analogue, U46619.
- To understand the interaction between adenosine and thromboxane A2 in ischemic coronary circulation.
Main Methods:
- Nine instrumented dogs underwent treadmill exercise with induced coronary stenosis and hypoperfusion.
- Myocardial blood flow was measured using radioactive microspheres during U46619 infusion.
- Adenosine receptor blockade was achieved using 8-phenyltheophylline and adenosine deaminase.
Main Results:
- U46619 decreased myocardial blood flow in the stenosed region.
- Adenosine blockade alone reduced blood flow, indicating endogenous adenosine's vasodilatory role in ischemia.
- Adenosine blockade did not enhance U46619-induced vasoconstriction.
Conclusions:
- Endogenous adenosine contributes to vasodilation in hypoperfused myocardium, even with U46619 present.
- Endogenous adenosine does not attenuate the vasoconstrictive effects of U46619.
- Findings suggest thromboxane A2 and adenosine act on different coronary vascular segments.