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. Author manuscript; available in PMC: 2017 Sep 27.
Published in final edited form as: Circulation. 2016 Aug 31;134(13):961–977. doi: 10.1161/CIRCULATIONAHA.116.021618

FIGURE 7. Cardiac arrest hearts demonstrated increased myocardial O2•– generation, which can be inhibited by Alda-1.

FIGURE 7

A. Myocardial O2•– production, measured by lucigenin, was mildly increased in hearts treated with epinephrine, but markedly elevated after cardiac arrest (†P < 0.01). The NADPH oxidase inhibitor DPI and the NOS inhibitor L-NMMA did not change O2•– generation compared to uninhibited controls, however the ALDH2 inhibitor Alda-1 did inhibit O2•– (*P < 0.01). B. Dihydroethidium (DHE) fluorescence microscopy allowed topographic assessment of O2•– production in the ventricular wall, and showed mild increase in O2•– production with epinephrine infusion, compared with marked increase after cardiac arrest (†P < 0.01). Alda-1 inhibited O2•– generation. Mito-TEMPO, used as the mitochondria-targeted antioxidant with superoxide and alkyl scavenging properties, confirmed that the majority of O2•– being generated was from mitochondria (compared to uninhibited *P < 0.01). Myocytes exhibited green autofluorescence. White arrows denoted endothelial O2•– producing cells. Scale bar: 5 μm.