The ability of moderately well-developed coronary collateral vessels to undergo vasoconstriction in response to α-adrenergic stimulation and to ergonovine was studied. Studies were performed in 15 dogs 4-16 wk after embolic occlusion of the left anterior descending coronary artery had been performed to stimulate collateral vessel gowth. Interarterial collateral flow was measured as retrograde flow from the cannulated left anterior descending coronary artery, while microvascular collateral flow was measured as continuing tissue flow determined with radioactive microspheres administered during the retrograde flow collection. Studies were performed after β-adrenergic blockade with propranolol. Neither cardiac sympathetic nerve stimulation nor α1-adrenergic stimulation with phenylephrine caused significant change in retrograde blood flow or myocardial tissue flow. The selective α2-adrenergic agonist, B-HT 933, decreased tissue flow in the collateral-dependent region but did not significantly alter retrograde flow. Although these data indicate that intramural microvascular collateral communications are capable of vasoconstriction in response to α2-adenergic stimulation, the larger interarterial collaterals are unresponsive to α-adrenergic influences. However, under the conditions of the experiment, adrenergic activity did not appear to influence collateral function, since neither α1-adrenergic blockade with prazosin nor α2-adrenergic blockade with rauwolscine altered collateral flow. Ergonovine, 0.2-0.8 lmg · kg-1 · min-1, caused a 22 ± 4% decrease in retrograde flow (P < 0.01) but did not alter microvascular collateral flow. Thus, of the agents tested, only ergonovine caused vasoconstriction of the large interarterial coronary collateral vessels.
|Original language||English (US)|
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|Issue number||4 30-4|
|State||Published - 1991|
- B-HT 933
- coronary occlusion