Ischemia-induced coronary collateral growth is dependent on vascular endothelial growth factor and nitric oxide

We hypothesized that ischemia-induced expression of vascular endothelial growth factor (VEGF) and the production of NO stimulate coronary collateral growth. To test this hypothesis, we measured coronary collateral blood flow and VEGF expression in myocardial interstitial fluid in a canine model of r...

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Bibliographic Details
Published in:Circulation (New York, N.Y.) N.Y.), 2000-12, Vol.102 (25), p.3098-3103
Main Authors: MATSUNAGA, Toshiro, WARLTIER, David C, WEIHRAUCH, Dorothee W, MONIZ, Melinda, TESSMER, John, CHILIAN, William M
Format: Article
Language:English
Subjects:
Animals
Arterial Occlusive Diseases - complications
Biological and medical sciences
Blotting, Western
Cardiology. Vascular system
Collateral Circulation
Coronary heart disease
Coronary Vessels
Dogs
Endothelial Growth Factors - metabolism
Enzyme Inhibitors - pharmacology
Female
Heart
Hemodynamics
Hyperemia - etiology
Lymphokines - metabolism
Male
Medical sciences
Myocardial Ischemia - etiology
Myocardial Ischemia - metabolism
Myocardial Ischemia - physiopathology
NG-Nitroarginine Methyl Ester - pharmacology
Nitric Oxide - biosynthesis
Nitric Oxide Synthase - antagonists & inhibitors
Reverse Transcriptase Polymerase Chain Reaction
RNA, Messenger - metabolism
Vascular Endothelial Growth Factor A
Vascular Endothelial Growth Factors
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Summary:We hypothesized that ischemia-induced expression of vascular endothelial growth factor (VEGF) and the production of NO stimulate coronary collateral growth. To test this hypothesis, we measured coronary collateral blood flow and VEGF expression in myocardial interstitial fluid in a canine model of repetitive myocardial ischemia under control conditions and during antagonism of NO synthase. Collateralization was induced by multiple (1/h; 8/d), brief (2 minutes) occlusions of the left anterior descending coronary artery for 21 days. In controls, collateral blood flow (microspheres) progressively increased to 89+/-9 mL. min(-1). 100 g(-1) on day 21, which was equivalent to perfusion in the normal zone. Reactive hyperemic responses (a measure of the severity of ischemia) decreased as collateral blood flow increased. In N(G)-nitro-L-arginine methyl ester (L-NAME)- and L-NAME+nifedipine-treated dogs, to block the production of NO and control hypertension, respectively, collateral blood flow did not increase and reactive hyperemia was robust throughout the occlusion protocol (P
ISSN:0009-7322
1524-4539
DOI:10.1161/01.cir.102.25.3098