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Adenosine on myocardial oxygen consumption
Insights
Adenosine infusion significantly reduced myocardial oxygen consumption and coronary artery pressure in dogs. This effect, independent of heart rate, suggests blood flow redistribution within the heart muscle.
Area of Science:
- Cardiovascular Physiology
- Cardiac Metabolism
Background:
- Adenosine is known to affect coronary circulation and myocardial function.
- Understanding adenosine's precise impact on myocardial oxygen consumption is crucial for cardiovascular research.
Purpose of the Study:
- To investigate the effects of intracoronary adenosine infusion on myocardial oxygen consumption and related hemodynamic parameters in a canine model.
- To determine if adenosine's impact on oxygen use is linked to coronary vasodilation or changes in heart rate and contractility.
Main Methods:
- Isolated supported dog heart preparation with constant coronary blood flow.
- Adenosine (50 mug/min) infused for 3 minutes.
- Measurements included coronary artery perfusion pressure, left ventricular systolic pressure, myocardial oxygen consumption, heart rate, myocardial contractile force, and maximal left ventricular dp/dt.
Main Results:
- Adenosine significantly decreased coronary artery perfusion pressure, left ventricular systolic pressure, and myocardial oxygen consumption.
- Myocardial contractile force and maximal left ventricular dp/dt remained unchanged.
- The reduction in myocardial oxygen consumption was more pronounced at higher heart rates, while pressure changes were similar across tested rates.
Conclusions:
- Adenosine-induced reduction in myocardial oxygen consumption is not primarily due to coronary vasodilation or direct negative chronotropic/inotropic effects.
- The findings suggest a potential mechanism involving functional shunting of blood flow within the myocardium or altered substrate utilization.
Abstract:
1 A 3 min intracoronary infusion of adenosine (50 mug/min) produced a significant decrease in coronary artery perfusion pressure, left ventricular systolic pressure and myocardial O2 consumption in the isolated supported heart preparation of the dog perfused at a constant coronary blood flow. Heart rate was controlled at 150, 190 or 230 beats/minute. 2 Myocardial contractile force and maximal left ventricular dp/dt were not changed by adenosine infusion. 3 The absolute decrease in myocardial O2 consumption was greater at increasing heart rates whereas the decrease in coronary artery perfusion pressure and peak left ventricular systolic pressure were similar. 4 The results suggest that the reduction in myocardial O2 consumption produced by adenosine is not related to coronary vasodilatation or to a negative chronotropic or inotropic action, but may be due to a functional shunting of blood flow from high O2 extracting regions of the myocardium to low O2 extracting ones and/or important effects on myocardial substrate utilization.