H2O2-induced Vasodilatation Compensates Diabetes-induced Microvascular Endothelial Dysfunction during Acute Coronary Occlusion in Canine Coronary Native Collateral Microvessels in Vivo
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概要
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Background: It has been previously demonstrated that endothelial Cu, Zn-SOD and caveolin-1 play crucial roles of hydrogen peroxide (H2O2) production as an endothelium-derived hyperpolarizing factor (EDHF) in mouse mesenteric arteries. We thus examined whether this mechanism is involved in the EDHF-mediated responses in diabetes mellitus (DM) during acute coronary occlusion.Methods: Canine subepicardial coronary collateral small arteries (CSA>100µm) and arterioles (CA <100µm) were visually traced by an intravital microscope between left anterior descending artery (LAD) and left circumflex coronary artery (LCX) with an injection of indocyanine green. We examined bradykinin-induced vasodilatation of native coronary collaterals before and after myocardial ischemia by proximal LAD occlusion (90min) under the following conditions (n=6 each); (i) control and (ii) DM (alloxan, 1 week prior to study, IV) with cyclooxygenase blockade (ibuprofen, 12.5 mg/kg, IV) before the onset of the ischemia. Myocardial levels of Cu,Zn-SOD, caveolin-1 and H2O2 (Amplex Red) and plasma levels of 8-OHdG, as a marker of oxidative stress and tetrahydrobiopterin in the coronary sinus were measured by ELISA and high-performance liquid chromatography. Results: Although the levels of Cu, Zn-SOD, tetrahydrobiopterin and caveolin-1 in the LAD area were comparable between the control and DM groups, caveolin-1 levels were greater in coronary microvessels than in coronary conduit arteries in the control group. Nitric oxide (NO)-mediated coronary vasodilatation of CSA by bradykinin significantly decreased in DM compared with control, and was restored by compensation of EDHF/H2O2 in CA with H2O2 production for the loss of NO. Oxidative stress (8-OHdG) was significantly increased in DM compared with control. Conclusions: NO-mediated, endothelium-dependent vasodilatations of CSA during acute coronary occlusion are impaired in DM and are compensated by EDHF/H2O2 in dogs in vivo.
- 日本微小循環学会の論文
著者
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Yada Toyotaka
Department of Medical Engineering & Systems Cardiology, Kawasaki Medical School
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Hiramatsu Osamu
Department of Medical Engineering & Systems Cardiology, Kawasaki Medical School
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Kajiya Fumihiko
Department Of Medical Engineering And Systems Cardiology
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Kajiya Fumihiko
Department Of Cardiovascular Physiology Okayama University
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Goto Masami
Department Of Anesthesiology Kanagawa Cardiovascular And Respiratory Center
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Shimokawa Hiroaki
Department Of Cardiology Tohoku University School Of Medicine
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Nakamoto Hiroshi
Department Of Medical Engineering And Systems Cardiology
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Ogasawara Yasuo
Department Of Food Science And Nutrition School Of Human Environmental Sciences Mukogawa Women'
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Shimokawa Hiroaki
Department of Cardiovascular Medicine, Tohoku University Graduate School of Medicine, Japan
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