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Endothelium-derived relaxing factor (nitric oxide) has a tonic vasodilating action on coronary collateral vessels
M W Frank1, K R Harris, K A Ahlin
1Feinberg Cardiovascular Research Institute, Northwestern University Medical School, Chicago, Illinois 60611-3008, USA.
Insights
Nitric oxide (NO) plays a key role in dilating coronary collateral vessels, improving blood flow after heart attacks. Impaired NO function can significantly reduce this vital collateral perfusion.
Area of Science:
- Cardiovascular Physiology
- Endothelial Function
- Myocardial Ischemia
Background:
- Coronary collateral circulation is crucial for supplying blood to ischemic heart muscle.
- While responsive to various vasoactive agents, the specific role of endogenous nitric oxide (NO) in collateral function remains incompletely understood.
Purpose of the Study:
- To investigate the tonic vasodilating effect of endothelium-derived relaxing factor (nitric oxide) on coronary collateral channels.
- To determine if NO influences blood flow regulation in collateral vessels developed post-myocardial ischemia.
Main Methods:
- Coronary collateral channels were established in dogs using ameroid implantation or repeated coronary artery occlusion.
- Systemic administration of NG-nitro-L-arginine methyl ester, a nitric oxide synthesis inhibitor, was used to assess its impact.
- Measurements included aortic and circumflex pressures and coronary blood flow before and after NO inhibition.
Main Results:
- Inhibition of nitric oxide synthesis significantly increased coronary collateral resistance by 173% (p < 0.01).
- This increase in resistance was associated with a reduced flow in the collateral-dependent region.
- Administration of L-arginine partially reversed the elevated collateral resistance, confirming the role of NO.
Conclusions:
- Nitric oxide exerts a substantial tonic vasodilating influence on coronary collateral vessels.
- Dysfunctional endothelial nitric oxide production in disease states may critically impair collateral blood flow to the heart.
Objectives:
We sought to determine whether endothelium-derived relaxing factor (nitric oxide) exerts a tonic vasodilating effect on coronary collateral channels developed in response to myocardial ischemia.
Background:
Although the coronary collateral circulation is known to react to several vasoactive agents, the role of endogenously produced nitric oxide is unclear.
Methods:
Coronary collateral channels were induced in the left circumflex artery bed of 12 chronically instrumented dogs by either ameroid implantation or repeated occlusion of the left circumflex coronary artery. With the native circumflex artery occluded, aortic and circumflex pressures and microsphere flows were measured before and after systemic administration of NG-nitro-L-arginine methyl ester, an arginine analogue known to block the synthesis of nitric oxide.
Results:
NG-nitro-L-arginine methyl ester increased mean aortic pressure from a mean +/- SEM of 92 +/- 4 to 114 +/- 4 mm Hg, whereas pressure 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 flow in the circumflex bed (from 1.31 to +/- 0.14 to 1.09 +/- 0.15 ml/min per g), resulting in an increase in coronary collateral resistance averaging 173 +/- 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 oxide normally exerts a substantial tonic dilating effect in coronary collateral vessels. Disease-induced alterations in endothelial function may limit collateral perfusion importantly.