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Received for publication February 27, 2006.
Revised April 12, 2006.
Accepted for publication April 12, 2006.
Ranolazine is an inhibitor of the late sodium channel, and via this mechanism decreases sodiumdependent intracellular calcium overload during ischemia and reperfusion. Ranolazine reduces angina, but there is little information on its effects in acute myocardial infarction. The aim of this study was to test the effects of ranolazine on left ventricular (LV) function and myocardial infarct size after ischemia/reperfusion in rabbits. Ten minutes before coronary artery occlusion (CAO), anesthetized rabbits were assigned to vehicle (n=15) or ranolazine (2 mg/kg I.V. bolus plus 60 µg/kg/min I.V. infusion, n=15). Hearts received 60 min of CAO and 3 hours reperfusion. CAO caused LV dysfunction associated with necrosis. However at the end of reperfusion, rabbits treated with ranolazine had better global LV ejection fraction (0.42±0.02 vs. 0.33±0.02, p<0.007) and stroke volume (1.05±0.08 ml vs. 0.78±0.07 ml, p<0.01) compared with vehicle. The fraction of the LV wall that was akinetic or dyskinetic was significantly less in the ranolazine group at 0.23±0.033 vs. 0.34±0.03 in vehicle treated, p<0.02. The ischemic risk region was similar in both groups; however infarct size was significantly smaller in the treated group (44±5 vs. 57±4% vehicle, p<0.04). There were no significant differences between groups in heart rate, arterial pressure, LVEDP or maximum positive or negative dP/dt. In conclusion, the results of this study show that ranolazine provides protection during acute myocardial infarction in this rabbit model of ischemia/reperfusion. Ranolazine treatment led to better ejection fraction, stroke volume and less wall motion abnormality after reperfusion, and less myocardial necrosis.
Key words:
late sodium channel inhibitor, left ventricular global function, left ventricular wall motion, myocardial infarction, rabbit, ranolazine
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