Abstract 13040: Alpha-Adrenergic Coronary Vasoconstriction and Myocardial Function in Humans
Sympathetically mediated coronary vasoconstriction is regulated by stimulation of alpha-adrenergic receptors. This process may be protective in animals since it evokes blood flow redistribution to the subendocardium. The role of sympathetic coronary vasoconstriction in humans is unclear. We previously found that lower body negative pressure (LBNP) can increase sympathetic activation and evoke coronary vasoconstriction. In order to determine whether sympathetic coronary vasoconstriction plays a beneficial role in human coronary regulation, we tested the effects of LBNP on coronary vasoconstriction and myocardial function in 8 healthy subjects before and after treatment with Phentolamine, an alpha-adrenergic receptor antagonist. Transthoracic Doppler echocardiography and Tissue Doppler imaging were used to record peak coronary blood flow velocity (CBV) and myocardial longitudinal systolic and diastolic velocities (Sm and Em), indices of systolic and diastolic function, respectively. LBNP at −5 mmHg induced a significant decrease in CBV (22±2 cm/s vs. 18±1 cm/s, P < 0.05) while myocardial systolic and diastolic functions were preserved. Intravenous administration of Phentolamine did not change CBV at rest but attenuated the coronary vasoconstriction seen during LBNP; this diminution was associated with a significant decline in Em (Figure). These data demonstrate: 1) in the coronary circulation, there is little alpha-adrenergic constrictor tone at rest and 2) adrenergic coronary vasoconstriction is beneficial in maintaining subendocardial myocardial function in humans. This study provides indirect evidence to support the concept that sympathetic coronary vasoconstriction preserves subendocardial blood flow in humans during cardiac stress.
- Coronary circulation
- Alpha-adrenergic receptor blockers
- Tissue doppler
- © 2010 by American Heart Association, Inc.