Hypoxia–Reoxygenation Potentiates Zymosan Activated Plasma-Induced Endothelial Injury

The pathophysiology of ischemia–reperfusion injury and the role played by the interaction of plasma proteins, including complement, with reperfused endothelium remains incompletely understood. Venular endothelial changes due to hypoxia followed by reoxygenation (H-R) are vital because venules are th...

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Veröffentlicht in:	The Journal of surgical research 1998-07, Vol.77 (2), p.91-98
Hauptverfasser:	Gupta, N., Jacobs, D.L., Miller, T.A., Smith, G.S., Dahms, T.E.
Format:	Artikel
Sprache:	eng
Schlagworte:	Actins - metabolism Antibodies, Monoclonal - pharmacology Anticoagulants - pharmacology Biological and medical sciences Blood Proteins - pharmacology Blood Proteins - physiology Bucladesine - pharmacology Cardiovascular system Cells, Cultured Colforsin - pharmacology Complement System Proteins - physiology Cyclic AMP - metabolism Cytoskeleton - drug effects Cytoskeleton - metabolism Endothelium, Vascular - drug effects Endothelium, Vascular - metabolism Hemostatics - pharmacology Heparin - pharmacology Humans Hypoxia - metabolism Medical sciences Oxygen - pharmacology Pharmacology. Drug treatments Receptors, Complement Solubility Thrombin - pharmacology Umbilical Veins - cytology Vascular wall Zymosan - pharmacology
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