ENDOTHELIUM-DERIVED RELAXING FACTOR (NITRIC-OXIDE) HAS A TONIC VASODILATING ACTION ON CORONARY COLLATERAL VESSELS

Objectives. We sought to determine whether endothelium-derived relaxin g factor (nitric oxide) exerts a tonic vasodilating effect on coronary collateral channels developed in response to myocardial ischemia, Bac kground. Although the coronary collateral circulation is known to reac t to several vasoactive agents, the role of endogenously produced nitr ic oxide is unclear, Methods. Coronary collateral channels were induce d in the left circumflex artery bed of 12 chronically instrumented dog s by either ameroid implantation or repeated occlusion of the left cir cumflex coronary artery, With the native circumflex artery occluded, a ortic and circumflex pressures and microsphere flows were measured bef ore and after systemic administration of N-G-nitro-L-arginine methyl e ster, an arginine analogue known to block the synthesis of nitric oxid e, Results. N-G-nitro-L-arginine methyl ester increased mean aortic pr essure from a mean +/- SEM of 92 +/-4 to 114 +/- 4 mm Hg, whereas pres sure in the occluded circumflex artery decreased from 61 +/- 4 to 55 /- 4 mm Hg. The increase in aortic-circumflex pressure gradient (from 31 +/- 4 to 59 +/- 5 mm Hg) was accompanied by a decrease in how in th e circumflex bed (from 1.31 +/- 0.14 to 1.09 +/- 0.15 ml/min per g), r esulting in an increase in coronary collateral resistance averaging 17 3 +/- 37% (from 26 +/- 4 to 64 +/- 9 mm Hg/ml per min per g, p < 0.01) , The increase in collateral resistance could be partially reversed by administration of L-arginine, Conclusions. We conclude that nitric ox ide normally exerts a substantial tonic dilating effect in coronary co llateral vessels, Disease-induced alterations in endothelial function may limit collateral perfusion importantly.