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. 2008 Oct 6;155(8):1185–1194. doi: 10.1038/bjp.2008.354

Figure 2.

Figure 2

(a) Representative monophasic action potential (MAP) recordings during baseline and after the combined administration of veratridine (125 nM), dofetilide (7.5 or 10 nM) and with or without HMR 1556 (100 nM) in perfused rabbit hearts. Endocardial MAP signals were obtained from the left ventricular apex. Amplitude of the MAP recordings was rescaled for the figure. The variability in MAP morphology and amplitude can be caused by changes in contact pressure between the MAP catheter and tissue, and do not necessarily reflect changes in specific ionic currents. Such variability is consistent with the known reported feature of MAP (Franz, 1999). (b) Effects of combined administration of veratridine (125 nM), dofetilide (7.5 or 10 nM) and with or without HMR 1556 (100 nM) on MAP duration at 90% repolarization (MAPD90) at pacing cycle length of 500 ms. Mean±s.d., n=6. *P<0.05 vs 125 nM veratridine+7.5 nM dofetilide or 125 nM veratridine+7.5 nM dofetlide+100 nM HMR 1556.