FLOW-DEPENDENT, ENDOTHELIUM-MEDIATED DILATION OF EPICARDIAL CORONARY-ARTERIES IN CONSCIOUS DOGS - EFFECTS OF CYCLOOXYGENASE INHIBITION

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  • 1 January 1984
    • journal article
    • research article
    • Vol. 6  (6) , 1161-1169
Abstract
Endothelial damage or removal abolishes the dilation of epicardial coronary arteries induced by increments in flow through these arteries in vitro. Whether or not the release of a cyclooxygenase product from endothelial cells in vivo is the mechanism of this flow-dependent dilation was tested. In 8 conscious dogs, instrumented to register the external diameter of 2 epicardial branches, anterior descending and circumfles, or the left coronary artery, increments in coronary flow increased and reductions in coronary flow decreased the diameter of the left circumflex epicardial artery by 182 .+-. 11 .mu.m/100% change in flow. When mean coronary flow in 1 epicardial branch was kept constant by a distal, flow-limiting stenosis during the application of flow-augmenting stimuli (temporal coronary occlusion or 80-400 .mu.g/kg adenosine i.v.), no dilation of this artery was observed. Cyclooxygenase inhibition (suppressing the bradykinin-induced elevation of plasma 6-keto-PG(prostaglandin)F1.alpha.) by indomethacin (5 mg/kg) or by diclofenac (10 mg/kg) increased smooth muscle tone in both epicardial arteries, but did not modify the flow-diameter relation (181 .+-. 10 and 179 .+-. 9 .mu.m/100% change in flow, respectively). Evidently, a tonic, instantaneous influence of coronary flow on the smooth muscle tone of the epicardial coronary arteries exists in vivo. Apparently, prostacyclin or another prostanoid is not a mediator of this endothelium-mediated influence of flow on smooth muscle tone.

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