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Abstract

Ross A., Gao Z., Heffernan M., Leuenberger U., Sinoway L., Muller M. Penn State Hershey Heart and Vascular Institute, Pennsylvania State University College of Medicine, Hershey, PA

The rise in heart rate (HR) and cardiac contractility during exercise is due to activation of myocardial b-adrenergic receptors. b-receptors are also located on coronary blood vessels and are thought to participate in exercise hyperemia, thereby helping to preserve the balance between myocardial oxygen supply and demand. However, experimental data in human subjects are lacking. Purpose: We hypothesized that intravenous b-adrenergic blockade would attenuate the reflex tachycardia and coronary hyperemia in response to isometric handgrip (i.e., a stimulus known to increase both cardiac metabolism and coronary blood flow). Methods: Six men (66 ± 2 yrs) performed isometric handgrip exercise at 40% of maximal voluntary contraction for 2 minutes after receiving intravenous propranolol; control trials occurred on separate days. HR and blood pressure were monitored continuously and rate-pressure product (RPP) was calculated as an index of myocardial oxygen demand. Coronary blood flow velocity (CBFV) was measured by transthoracic Doppler echocardiography (left anterior descending coronary artery) and coronary vascular resistance (CVR) was calculated. The ratio of RPP/CVR was used as an index of myocardial oxygen supply. Physiological parameters were statistically compared at baseline and in response to exercise between conditions. Results: Refer to Table. Conclusion: The novel finding of this study is that under resting conditions propranolol raises coronary resistance (impaired oxygen supply) despite also lowering cardiac metabolism (reduced oxygen demand). These data support the concept that coronary b-adrenergic receptors contribute to myocardial blood flow regulation both at rest and during exercise in humans.

Supported by NIH P01 HL096570 and UL1 TR000127

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