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2008 - Society for Cardiothoracic Surgery

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<strong>Society</strong> <strong>for</strong> <strong>Cardiothoracic</strong> <strong>Surgery</strong> • Edinburgh<br />

Monday 10th March Session 1<br />

08:10 – 08:20 Ochil Abstract No. 2<br />

NAPDH Oxidase-derived Superoxide Generation Contributes to Venous<br />

Endothelial Dysfunction in Human Heart Failure.<br />

Authors: A Momin 1 ; R Dworakowski 1 ; S Walker 1 ; M Kearney 1 ; A Shah 1<br />

Author’s Institution: 1 GKT School of Medicine King’s College, London, United Kingdom<br />

Objectives: Venous endothelial dysfunction contributes to the pathophysiology of human<br />

heart-failure, by altering venous capacitance, vascular volume and ventricular preload.<br />

The aim of this study was to compare venous endothelial function in human subjects<br />

with and without heart-failure and to investigate potential underlying mechanisms.<br />

Methods: Segments of saphenous vein harvested from consecutive CABG patients, 18<br />

had heart failure diagnosed by conventional criteria and 34 had preserved LV (Control).<br />

Vascular function assessed in organ-baths from vasomotor dose-response curves to<br />

acetylcholine and sodium nitroprusside (endothelium-dependent and independent<br />

agonists). The mRNA-expression of NADPH-oxidase components (Nox1, Nox2, Nox4, p47,<br />

p67) and eNOS in venous segments was quantified by real-time PCR using the SYBR-<br />

Green and standard-curve method. Superoxide production in venous homogenates<br />

measured by lucigenin-enhanced chemiluminescence. All patients had measurement of<br />

lipids, glucose, CRP, interleukin-1 and TNF-alpha levels.<br />

Results: Patients with heart failure had greater endothelial dysfunction than controls<br />

(16±3 vs 40±8%; p

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