α-Adrenergic Vasoconstrictor Tone Limits Right Coronary Blood Flow in Exercising Dogs

Abstract

In exercising dogs, increased myocardial O₂ consumption (MVO₂) of the left ventricle is met primarily by hyperemia, whereas increased O₂ extraction makes a greater contribution to right ventricular (RV) O₂ supply. We hypothesized that α-adrenergic vasoconstrictor tone limits right coronary (RC) blood flow during exercise, forcing increased O₂ extraction. This tone might also contribute to lesser RC vascular conductance at rest. Accordingly, RV O₂ balance was examined at rest and during graded treadmill exercise before and during α-adrenergic blockade with phentolamine (1 mg/kg, iv, n = 6). The transmural distribution of RC flow was measured with radiolabeled microspheres in 4 additional dogs. At rest, α-adrenergic receptor blockade did not significantly increase RC flow or conductance. During exercise, α-adrenergic blockade increased RC flow and conductance responses to increased RV MVO₂ by 25% and 60%, respectively. The transmural distribution of RC flow was not altered by exercise or by α-adrenergic blockade. Before α-adrenergic blockade, hyperemia provided 39%–66% of the additional O₂ consumed by the right ventricle during graded exercise; after α-adrenergic blockade, hyperemia contributed 74%–85%. After α-adrenergic blockade, the slope of the relationship between RC venous PO₂ and RV MVO₂ became less steep, reflecting less O₂ extraction due to enhanced hyperemia. Additional experiments were conducted on 5 anesthetized, open-chest dogs with constant RC perfusion pressure and β-adrenergic blockade. The RC flow response to intracoronary norepinephrine was shifted to the left compared with that measured in the left coronary circulation, consistent with observations in the conscious exercising dogs. In conclusion, α-adrenergic vasoconstrictor tone does not restrict resting RC blood flow, but during exercise, this tone transmurally blunts RC hyperemia and forces the right ventricle to mobilize its O₂ extraction reserve. This effect is more pronounced than has been reported for the left ventricle.