Mw. Frank et al., ENDOTHELIUM-DERIVED RELAXING FACTOR (NITRIC-OXIDE) HAS A TONIC VASODILATING ACTION ON CORONARY COLLATERAL VESSELS, Journal of the American College of Cardiology, 27(3), 1996, pp. 658-663
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.