title: Heparin inhibits reactive oxygen species generation by polymorphonuclear and mononuclear leucocytes.
abstract: To examine the hypothesis that heparin may affect leukocyte function and that it may have anti-inflammatory properties, we investigated the effect of heparin on reactive oxygen species (ROS) generation by leucocytes. Heparin was injected intravenously at a dose of 10000 units into eight normal subjects. Blood samples were collected from the antecubital vein sequentially, prior to and following heparin at 0, 0.5, 1, 2, and 4 hours. ROS generation was inhibited significantly by polymorphonuclear cells (PMNL) at 0.5, 1, and 2 hours and returned to baseline level at 4 hours. Similarly, ROS generation was inhibited markedly by mononuclear cells (MNC) at 0.5 hours, with a peak inhibition at 1 hour; it returned to baseline level by 4 hours. The maximum inhibition of ROS generation by PMNL was 57.3+/-19% of the basal, while that by MNC was 56.4+/-11% of the basal. Since ROS are proinflammatory and cause tissue damage, it is possible that heparin may have an anti-inflammatory effect in vivo, apart from its antithrombotic effect. Since ROS also bind to nitric oxide (NO) and reduce the bioavailability of NO, heparin may indirectly increase the bioavailability of NO and thus act as a vasodilator. This effect of heparin may be of particular relevance to its use in unstable angina and following thrombolysis in acute myocardial infarction in preventing reperfusion injury.
authors.affiliation: Department of Medicine, State University of New York at Buffalo and Kaleida Health, 14209, USA. pdandona@mfhs.edu
authors.forename: P
authors.initials: P
authors.lastname: Dandona
authors.forename: T
authors.initials: T
authors.lastname: Qutob
authors.forename: W
authors.initials: W
authors.lastname: Hamouda
authors.forename: F
authors.initials: F
authors.lastname: Bakri
authors.forename: A
authors.initials: A
authors.lastname: Aljada
authors.forename: Y
authors.initials: Y
authors.lastname: Kumbkarni
mesh_terms: D000328:Adult; D000578:Amidines / Q000378:metabolism; D019040:E-Selectin / Q000097:blood; D005260:Female; D006493:Heparin / Q000008:administration & dosage*; D006801:Humans; D007275:Injections, Intravenous; D007963:Leukocytes, Mononuclear / Q000187:drug effects* / Q000378:metabolism; D008163:Luminescent Measurements; D008297:Male; D009504:Neutrophils / Q000187:drug effects* / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism*; D012016:Reference Values; D013997:Time Factors; D019010:Vascular Cell Adhesion Molecule-1 / Q000097:blood; D014841:von Willebrand Factor / Q000378:metabolism
chemical_list: D000578:Amidines; D019040:E-Selectin; D017382:Reactive Oxygen Species; D019010:Vascular Cell Adhesion Molecule-1; D014841:von Willebrand Factor; C046728:2,2'-azobis(2-amidinopropane); D006493:Heparin