Basal nitric oxide expresses endogenous cardioprotection during reperfusion by inhibition of neutrophil-mediated damage after surgical revascularization

Ischemia-reperfusion damages endothelium and impairs basal production of nitric oxide. Basally released nitric oxide is cardioprotective by its inhibition of neutrophil activities. Loss of endogenous nitric oxide with endothelial injury may occur during two phases: cardioplegic ischemia and reperfus...

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Veröffentlicht in:	The Journal of thoracic and cardiovascular surgery 1997-02, Vol.113 (2), p.399-409
Hauptverfasser:	Sato, Hiroki, Zhao, Zhi-Qing, Jordan, James E., Todd, James C., Riley, Robert D., Taft, C.Spencer, Hammon Jr, John W., Li, Ping, Ma, Xin-liang, Vinten-Johansen, J.
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Cardioplegic Solutions Disease Models, Animal Dogs Endothelium, Vascular - physiology Female Heart Arrest, Induced Hemodynamics Male Myocardial Contraction Myocardium - enzymology Myocardium - pathology Neutrophils - enzymology Neutrophils - physiology Nitric Oxide - physiology Peroxidase - metabolism Reperfusion Injury - pathology Reperfusion Injury - physiopathology
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