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. 2008 Jul 16;105(29):10256–10261. doi: 10.1073/pnas.0801336105

Fig. 2.

Fig. 2.

Nitrite-induced formation of NO-heme complexes during ischemia and reperfusion. (A) Experimental protocol. (B Upper) EPR spectrum of the mitochondrial ubiquinone radical signal formed in a postischemic reperfused myoglobin wild-type (+/+) heart loaded with Krebs-Henseleit buffer. (B Lower) EPR spectrum of nitrosylated myoglobin formed in a postischemic reperfused myoglobin+/+ heart loaded with 50 μM [15N]nitrite. (C) Graph of the time courses of cardiac NO-heme levels in hearts loaded with 50 μM [15N]nitrite before, during, and after ischemia (n = 3). The levels of NO-heme complexes formed in myoglobin+/+ hearts were quite high after 30 min of ischemia and 5 min of reperfusion compared with the concentrations of NO-heme in myoglobin−/− hearts. (D) EPR spectra of the Mb[15N]NO complexes formed in nitrite-treated myoglobin+/+ and myoglobin−/− hearts (50 μM) before, during, and after global ischemia. The highest level of MbNO formation was observed 5 min after reperfusion.