Absence of inducible nitric oxide synthase modulates early reperfusion-induced NF-kappaB and AP-1 activation and enhances myocardial damage.

@article{Zingarelli2002AbsenceOI,
  title={Absence of inducible nitric oxide synthase modulates early reperfusion-induced NF-kappaB and AP-1 activation and enhances myocardial damage.},
  author={Basilia Zingarelli and Paul W. Hake and Zequan Yang and Michael O'connor and Alvin G. Denenberg and Hector R Wong},
  journal={FASEB journal : official publication of the Federation of American Societies for Experimental Biology},
  year={2002},
  volume={16 3},
  pages={327-42}
}
The role of nitric oxide (NO) generated by the inducible NO synthase (iNOS) during myocardial ischemia and reperfusion is not understood. We investigated the role of iNOS during early reperfusion damage induced in genetically deficient iNOS (iNOS-/-) mice and wild-type littermates. In wild-type mice, ischemia (60 min) and reperfusion (60 min) induced an elevation in serum levels of creatine phosphokinase and myocardial injury characterized by the presence of scattered apoptotic myocytes and… CONTINUE READING

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