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. 2017 Apr 20;7:981. doi: 10.1038/s41598-017-01056-0

Figure 1.

Figure 1

Prolongation of left ventricular monophasic action potential duration (MAPD90) by Bay K 8644 in the absence and presence of ATX-II. (a) and (b) Representative recordings of MAPs recorded from the epi- (a) and endo- (b) myocardium of the left ventricular wall in serially exposed to no drug (control), ATX-II (3 nM), Bay K 8644 (200 nM), and ATX-II (3 nM) plus Bay K 8644 (200 nM). (c) and (d) Concentration-dependent increases by Bay K 8644 of left ventricular epi- (c) and endo- (d) MAPD90 in absence (n = 11) and presence (n = 7) of ATX-II. * P < 0.05 compared with 0 nM Bay K 8644 either in absence or presence of ATX-II; # P < 0.05, the increase of MAPD90 by Bay K 8644 alone vs ATX-II plus Bay K 8644 at the same concentration. Arrows indicate ventricular tachycardia (VT) occurred at or above the concentration indicated.