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975871 
Journal Article 
Abstract 
Liberation of vessel adherent myeloperoxidase by enoxaparin improves endothelial nitric oxide bioavailability 
Rudolph, T; Rudolph, V; Klinke, A; Lau, D; Heitzer, T; Meinertz, T; Baldus, S 
2008 
Yes 
Free Radical Biology and Medicine
ISSN: 0891-5849
EISSN: 1873-4596 
45 
Suppl. 
S135-S135 
English 
WOS:000260867900380 
is part of a larger document 3452652 SFRBM's 15th Annual Meeting: Program and Abstracts
Aim: Myeloperoxidase (MPO), a leukocyte-derived heme enzyme binds to the endothelium and depletes vascular nitric oxide (NO) bioavailability in animal models. Unfractionated heparins release vessel-bound MPO and increase endothelial NO bioavailability. Whether low molecular weight heparins also affect circulating MPO levels and NO dependent vasoreactivity however remains elusive.

Methods and Results: in a randomized, double-blind, placebo controlled trial patients with stable coronary artery disease received either 1 mg/kg enoxaparin or an equivalent volume of sodium chloride (NaCl) subcutaneously. Enoxaparin led to a significant improvement of FMD (5.51±2.92% vs. 6.55±3.16%, p=0.01) accompanied by a significant increase in plasma MPO levels (2.51 [IR: 2.04-3.62] ng/ml vs. 3.70 [IR: 2.80-5.50] ng/ml; p<0.001) whereas NaCl revealed neither a change in FMD (5.56±3.62% vs. 5.34±3.32%, p=ns) nor in plasma MPO levels (3.04 [IR: 2.22-4.67] ng/ml vs. 2.90 [IR:1.95-4.32] ng/ml; p=ns). The extent of enoxaparin-induced MPO release and the improvement in endothelial function correlated (r=0.67, P<0.001).

Conclusion: This study confirms the concept that heparins enhance vascular NO bioavailability by mobilizing vessel bound MPO. These data not only support the notion of extracoagulant, anti-inflammatory properties of heparins but reinforce the concept of MPO-dependent NO oxidation as a central mechanism for regulation of vascular tone in inflammatory vascular disease. 
Society for Free Radical Biology and Medicine 15th Annual Meeting 
Indianapolis, IN 
November 19-23, 2008