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. 2015 Nov 23;109(1):174–184. doi: 10.1093/cvr/cvv254

Figure 1.

Figure 1

OA-NO2 treatment attenuates elevated vulnerability for atrial fibrillation and restores electrical homogeneity in AngII-treated mice. AngII and OA-NO2 were administered over a period of 2 weeks via osmotic minipumps (Alzet), and afterwards, the mice underwent an electrophysiological study with right atrial stimulation. (A) Representative figures of ECGs with and without fibrillation episodes. (B) AngII treatment leads to a distinct elevation of the number of AF episodes in AngII(+)/OA-NO2(−) mice (n = 14), whereas notably in AngII(+)/OA-NO2(+) mice (n = 7), the number of AF episodes is comparable to the control group [AngII(−)/OA-NO2(−) mice] (n = 19). (C) The total time of AF episodes was calculated and the prolonged time of AF episodes was significantly reduced in AngII(+)/OA-NO2(+) (n = 7) compared with AngII(+)/OA-NO2(−) mice (n = 14). Data are expressed as mean ± SEM. **P < 0.01 and ***P < 0.001.