Heparins increase endothelial nitric oxide bioavailability by liberating vessel-immobilized myeloperoxidase.
Standard
Heparins increase endothelial nitric oxide bioavailability by liberating vessel-immobilized myeloperoxidase. / Baldus, Stephan; Rudolph, Volker; Roiss, Mika; Ito, Wulf D; Rudolph, Tanja Katharina; Eiserich, Jason P; Sydow, Karsten; Lau, Denise; Szöcs, Katalin; Klinke, Anna; Kubala, Lukas; Berglund, Lars; Schrepfer, Sonja; Deuse, Tobias; Haddad, Munif; Risius, Tim; Klemm, Hanno; Reichenspurner, Hermann; Meinertz, Thomas; Heitzer, Thomas.
In: CIRCULATION, Vol. 113, No. 15, 15, 2006, p. 1871-1878.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
Harvard
APA
Vancouver
Bibtex
}
RIS
TY - JOUR
T1 - Heparins increase endothelial nitric oxide bioavailability by liberating vessel-immobilized myeloperoxidase.
AU - Baldus, Stephan
AU - Rudolph, Volker
AU - Roiss, Mika
AU - Ito, Wulf D
AU - Rudolph, Tanja Katharina
AU - Eiserich, Jason P
AU - Sydow, Karsten
AU - Lau, Denise
AU - Szöcs, Katalin
AU - Klinke, Anna
AU - Kubala, Lukas
AU - Berglund, Lars
AU - Schrepfer, Sonja
AU - Deuse, Tobias
AU - Haddad, Munif
AU - Risius, Tim
AU - Klemm, Hanno
AU - Reichenspurner, Hermann
AU - Meinertz, Thomas
AU - Heitzer, Thomas
PY - 2006
Y1 - 2006
N2 - BACKGROUND: Neutrophils and monocytes are centrally linked to vascular inflammatory disease, and leukocyte-derived myeloperoxidase (MPO) has emerged as an important mechanistic participant in impaired vasomotor function. MPO binds to and transcytoses endothelial cells in a glycosaminoglycan-dependent manner, and MPO binding to the vessel wall is a prerequisite for MPO-dependent oxidation of endothelium-derived nitric oxide (NO) and impairment of endothelial function in animal models. In the present study, we investigated whether heparin mobilizes MPO from vascular compartments in humans and defined whether this translates into increased vascular NO bioavailability and function. METHODS AND RESULTS: Plasma MPO levels before and after heparin administration were assessed by ELISA in 109 patients undergoing coronary angiography. Whereas baseline plasma MPO levels did not differ between patients with or without angiographically detectable coronary artery disease (CAD), the increase in MPO plasma content on bolus heparin administration was higher in patients with CAD (P=0.01). Heparin treatment also improved endothelial NO bioavailability, as evidenced by flow-mediated dilation (P
AB - BACKGROUND: Neutrophils and monocytes are centrally linked to vascular inflammatory disease, and leukocyte-derived myeloperoxidase (MPO) has emerged as an important mechanistic participant in impaired vasomotor function. MPO binds to and transcytoses endothelial cells in a glycosaminoglycan-dependent manner, and MPO binding to the vessel wall is a prerequisite for MPO-dependent oxidation of endothelium-derived nitric oxide (NO) and impairment of endothelial function in animal models. In the present study, we investigated whether heparin mobilizes MPO from vascular compartments in humans and defined whether this translates into increased vascular NO bioavailability and function. METHODS AND RESULTS: Plasma MPO levels before and after heparin administration were assessed by ELISA in 109 patients undergoing coronary angiography. Whereas baseline plasma MPO levels did not differ between patients with or without angiographically detectable coronary artery disease (CAD), the increase in MPO plasma content on bolus heparin administration was higher in patients with CAD (P=0.01). Heparin treatment also improved endothelial NO bioavailability, as evidenced by flow-mediated dilation (P
U2 - 10.1161/CIRCULATIONAHA.105.590083
DO - 10.1161/CIRCULATIONAHA.105.590083
M3 - SCORING: Zeitschriftenaufsatz
VL - 113
SP - 1871
EP - 1878
JO - CIRCULATION
JF - CIRCULATION
SN - 0009-7322
IS - 15
M1 - 15
ER -
