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Circulation. 1999;99:2090-2097

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(Circulation. 1999;99:2090-2097.)
© 1999 American Heart Association, Inc.


Clinical Investigation and Reports

Augmented {alpha}-Adrenergic Constriction of Atherosclerotic Human Coronary Arteries

Dietrich Baumgart, MD; Michael Haude, MD; Günter Görge, MD; Fengqi Liu, MD; Junbo Ge, MD; Claudia Große-Eggebrecht; Raimund Erbel, MD, FESC; Gerd Heusch, MD, FESC

From the Departments of Cardiology and Pathophysiology (G.H.), Center of Internal Medicine, University of Essen, Germany.

Correspondence to Dietrich Baumgart, MD, Universitätsklinikum Essen, Abteilung für Kardiologie, Hufelandstraße 55, 45122 Essen, Germany. E-mail dbaum3{at}t-online.de

Background—Although adrenergic activation plays a major role in the initiation of experimental myocardial ischemia, the significance of {alpha}-adrenergic coronary constriction in humans has been questioned. The present study assessed the impact of selective {alpha}-adrenergic receptor activation in patients with normal or atherosclerotic coronary arteries.

Methods and Results—In 39 patients, coronary blood flow (CBF, mL/min) was determined from combined angiography and Doppler measurements. In 8 patients with normal coronary arteries (group 1) and 9 with single coronary artery stenosis (group 2), doses of 1, 2.5, 5, and 10 mg IC of the {alpha}1-agonist methoxamine (M) were injected. Identical doses of the {alpha}2-agonist BHT933 (B) were injected in 8 patients with normal coronary arteries (group 3) and 8 with single stenosis (group 4). In 6 additional patients with single stenosis (group 5), aortocoronary sinus lactate differences were measured in response to M and B. CBF remained unchanged in group 1. In contrast, CBF was decreased dose-dependently in group 2, with a maximum at 10 mg M (39.0±9.4 versus 15.2±7.0). In groups 3 and 4, CBF was also decreased dose-dependently, with a maximum at 10 mg B (63.3±24.8 versus 49.1±27.9 and 41.5±19.0 versus 12.7±8.0, respectively). In group 5, there was more net lactate production with B than with M (-0.34±0.11 versus -0.04±0.09 mmol/L).

Conclusions—In normal coronary arteries, {alpha}1-adrenergic activation does not reduce CBF, whereas {alpha}2-adrenergic activation reduces CBF by microvascular constriction. Both {alpha}1- and {alpha}2-adrenergic epicardial and microvascular constriction are augmented by atherosclerosis and can induce myocardial ischemia.


Key Words: coronary disease • angiography • ultrasonics




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