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Cardiac Stress Test Induced by Dobutamine and Monitored by Cardiac Catheterization in Mice
Published on: February 10, 2013
Dobutamine enhances cardiodepressant effects of receptor-mediated coronary endothelial stimulation
J Bartunek1, A M Shah, M Vanderheyden
1Cardiovascular Center, Aalst, Belgium.
Insights
Beta-adrenergic stimulation with dobutamine enhances the heart-relaxing effects of substance P in patients with heart transplants and cardiomyopathy. This interaction may involve nitric oxide, improving myocardial contractile performance.
Area of Science:
- Cardiology
- Pharmacology
- Physiology
Background:
- Intracoronary substance P infusion reduces left ventricular pressures by promoting earlier relaxation via paracrine action of endothelial mediators.
- Beta-adrenergic stimulation also induces earlier left ventricular relaxation.
Purpose of the Study:
- To investigate the effects of beta-adrenergic stimulation on the myocardial contractile response to intracoronary substance P infusion in humans.
Main Methods:
- Data collected from 13 heart transplant recipients and 3 patients with dilated cardiomyopathy.
- Left ventricular pressure recordings obtained during intracoronary substance P infusion.
- Measurements repeated during concurrent intravenous dobutamine administration.
Main Results:
- Dobutamine significantly increased the fall in left ventricular end-systolic pressure and peak systolic pressure induced by substance P in both patient groups.
- The cardiodepressant effect of substance P was enhanced by dobutamine.
Conclusions:
- Dobutamine potentiates the cardiodepressant effects of substance P on myocardial contractile performance in transplant recipients and cardiomyopathy patients.
- This enhancement may stem from an interaction between beta-adrenergic stimulation and endothelial mediators like nitric oxide.
Background:
In humans, intracoronary infusion of substance P reduces left ventricular end-systolic pressure and left ventricular peak systolic pressure because of earlier onset of left ventricular relaxation induced by paracrine myocardial action of mediators released from the coronary endothelium. The present study investigated in humans the effects of beta-adrenergic stimulation, which also induces earlier left ventricular relaxation, on the left ventricular myocardial contractile response to intracoronary infusion of substance P.
Methods And Results:
Data were obtained in 13 patients after cardiac transplantation and in 3 patients with dilated nonischemic cardiomyopathy. Microtip left ventricular pressure recordings were obtained during a 5-minute intracoronary infusion of substance P (20 pmol/min) under control conditions and then repeated during concurrent intravenous administration of dobutamine. In the presence of dobutamine, intracoronary substance P caused a greater fall in left ventricular end-systolic pressure (transplantation control, -9 +/- 11 versus transplantation dobutamine, -20 +/- 18 mm Hg [P < .05]; cardiomyopathy control, -4 +/- 1 versus cardiomyopathy dobutamine, -10 +/- 3 mm Hg [P < .05]) and in left ventricular peak systolic pressure (transplantation control, -14 +/- 10 versus transplantation dobutamine, -30 +/- 22 mm Hg [P < .01]; cardiomyopathy control, -9 +/- 7 versus cardiomyopathy dobutamine, -15 +/- 6 mm Hg [P = .1]).
Conclusions:
Dobutamine enhances the cardiodepressant effect on myocardial contractile performance of receptor-mediated coronary endothelial stimulation in transplant recipients and in patients with dilated nonischemic cardiomyopathy. This enhancement could result from a potentiating interaction of the relaxation-hastening effect exerted by beta-adrenergic stimulation and by mediators released from the coronary endothelium, such as nitric oxide.
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