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. 2016 Sep 26;5(9):e003774. doi: 10.1161/JAHA.116.003774

Figure 2.

Figure 2

TRPV1 regulates mitochondrial membrane potential and infarct size. A, Representative images (at BL and 30 minutes after drug application) for assessment of mitochondrial membrane potential by TMRE for primary neonatal cardiomyocytes treated with vehicle (dimethyl sulfoxide) or CAP (0.1, 1, or 10 μmol/L). B, TMRE fluorescence measurements (relative to each BL measurement set at 1) for vehicle or CAP (0.1, 1.0, or 10 μmol/L). CAP dose‐dependently caused changes in mitochondrial membrane potential over 30 minutes, as assessed by TMRE (3 biological replicates per group, + P<0.05 vs CON, *P<0.01 vs CON). C, Experimental protocol for myocardial ISC–REP studies. Arrow indicates time of treatment for either CON or CAP. D, Change in heart rate after CAP administration. CAP logarithmically increased heart rate in a dose‐dependent fashion (n=6 per group, *P<0.01). E, CAP maximally decreased infarct size at 0.3 mg/kg, with partial effects at 0.1 and 1.0 mg/kg. Individual infarct size for each experiment is presented (n=6 per group, *P<0.01 vs vehicle). BL indicates baseline; CAP, capsaicin; CON, control; ISC, ischemia; REP, reperfusion; RX, treatment; TMRE, tetramethylrhodamine, ethyl ester; TRPV1, transient receptor potential vanilloid 1.