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Peroxynitrite‐mediated oxidation of dihydrorhodamine 123 occurs in early stages of endotoxic and hemorrhagic shock and ischemia‐reperfusion injury
Author(s) -
Szabó Csaba,
Salzman Andrew L.,
Ischiropoulos Harry
Publication year - 1995
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(95)00984-h
Subject(s) - peroxynitrite , hemorrhagic shock , endotoxic shock , reperfusion injury , ischemia , pharmacology , shock (circulatory) , chemistry , medicine , cardiology , biochemistry , superoxide , enzyme
To quantify peroxynitrite production during shock, we measured oxidation of dihydrorhodamine 123 in rats. In endotoxic and hemorrhagic shock and splanchic ischemia‐reperfusion, dihydrorhodamine oxidation rapidly increased, which was prevented by inhibition of endothelial nitric oxide (·NO) synthase (ecNOS). Thus, peroxynitrite is already formed at early stages of shock from ecNOS‐derived ·NO. Overproduction of ·NO by the inducible NOS at late shock was not associated with additional increases in dihydrorhodamine oxidation. ecNOS inhibition enhanced dihydrorhodamine oxidation in control rats. These latter findings may be explained by ·NO‐mediated inhibition of peroxynitrite‐induced dihydrorhodamine oxidation, a phenomenon also observed in vitro.