D4776
De-N-sulfated heparin sodium salt
Completely de-N-sulfated and approx. 20% N-acetylated
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About This Item
Produtos recomendados
fonte biológica
heparin from Porcine (mucosa)
Formulário
solid
temperatura de armazenamento
2-8°C
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Aplicação
N-Acetylheparin, derivitized porcine mucosal heparin without anticoagulant properties, may be used to protect cardiac, vascular and neural tissues by inhibiting complement activation and neutrophil infiltration of the damage site.
Nota de preparo
Prepared from porcine mucosal heparin by a modification of the method of Nagasawa, K. and Inoue, Y., Methods Carb. Chem., 8, 291 (1980).
Código de classe de armazenamento
11 - Combustible Solids
Classe de risco de água (WGK)
WGK 3
Ponto de fulgor (°F)
Not applicable
Ponto de fulgor (°C)
Not applicable
Equipamento de proteção individual
Eyeshields, Gloves, type N95 (US)
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J L Park et al.
Pharmacology, 58(3), 120-131 (1999-02-02)
The ability of the heparin derivative, N-acetylheparin (NHEP) to protect the heart from regional ischemia/reperfusion injury was examined in vivo. NHEP (2 mg/kg i.v.) or vehicle was administered 2 h before occlusion of the left circumflex coronary (LCX) artery. Open-chest
P C Kouretas et al.
Circulation, 99(8), 1062-1068 (1999-03-02)
Coronary endothelial dysfunction after brief ischemia-reperfusion (IR) remains a clinical problem. We investigated the role of heparin and N-acetylheparin, a nonanticoagulant heparin derivative, in modulating coronary endothelial function after IR injury, with an emphasis on defining the role of the
P C Kouretas et al.
Journal of molecular and cellular cardiology, 30(12), 2669-2682 (1999-02-17)
Heparin, which is widely used clinically, has recently been shown to have specific properties affecting the vascular endothelium. We hypothesized that heparin stimulates endothelial nitric oxide synthase (eNOS) activity by a mechanism independent of its anticoagulant properties and dependent on
Y Hua et al.
Journal of neurosurgery, 92(6), 1016-1022 (2000-06-06)
Brain edema formation following intracerebral hemorrhage (ICH) appears to be partly related to erythrocyte lysis and hemoglobin release. Erythrocyte lysis may be mediated by the complement cascade, which then triggers parenchymal injury. In this study the authors examine whether the
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