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. Author manuscript; available in PMC: 2009 Aug 1.
Published in final edited form as: J Cardiovasc Pharmacol. 2008 Aug;52(2):121–128. doi: 10.1097/FJC.0b013e31817618eb

Figure 6.

Figure 6

Ranolazine suppresses AF and/or prevents its induction in 2 experimental models involving isolated arterially perfused right atria. A, Ranolazine (10 μM) prevents rapid-pacing induction of AF following pretreatment with acetylcholine (ACh; 0.5 μM). Effective refractory period (ERP) is 140 ms at a cycle length (CL) of 500 ms (left panel). Acceleration of pacing rate from a CL of 500 to 200 ms permits a 1:1 response only during the first 7 beats (right panel). B, Persistent AF induced following pretreatment with ACh (0.5 μM) is suppressed by ranolazine (10 μM). AF is initially converted to flutter (within 17 min) and then to sinus rhythm (17 sec later). C, Rapid-pacing induced nonsustained AF (48-sec duration) induced following ischemia/reperfusion and isoproterenol (ISO, 0.2 μM) (left panel) and the effect of ranolazine to prevent the electrical induction of AF (right panel). In both models, ranolazine causes prominent use-dependent depression of excitability and induction of post-repolarization refractoriness. ECG, pseudoelectrocardiogram; AP, action potential. From Burashnikov et al7 with permission.