Vasomotor activity of moderately well-developed canine coronary collateral circulation

This study examined the ability of moderately well-developed coronary collateral vasculature to undergo vasoconstriction in response to α-adrenergic agonists, vasopressin and angiotensin, and vasodilation in response to nitroglycerine. Studies were performed in 20 dogs 4-16 wk after left anterior descending coronary artery occlusion had been produced by an Ameroid constrictor or hollow intravascular plug. Collateral flow was estimated from retrograde flow from the cannulated left anterior descending artery. Tissue flow was measured with microspheres. Agonists were introduced into the left main coronary artery to reach collaterals arising from the left circumflex and septal arteries. Vasopressin and angiotensin II decreased retrograde flow from 22.7 ± 5.5 to 15.5 ± 2.7 and from 19.2 ± 2.8 to 14.3 ± 1.9 ml/min, respectively (each P < 0.05). Both agents also significantly decreased tissue flow to normally perfused and collateral dependent myocardium. Neither the selective α₁-adrenergic agonist phenylephrine nor the α₂-agonist B-HT 933 decreased retrograde flow. Nitroglycerin increased retrograde flow by 63 ± 27% (P < 0.01). Thus, although the moderately well-developed coronary collateral circulation is capable of vasoconstriction in response to vasopressin and angiotensin II, these data fail to support a role for α-adrenergic mechanisms in modulating collateral flow.