770-6 Effect of Ischemic Preconditioning and Udocaine Pretreatment on [Ca2+]i in Rat Hearts

Recent data suggest that preconditioning attenuates the increase in free intracellular calcium ([Ca2+]i), [Na+]i and [H+]i during ischemia by reducing the stimulation of Na+-H+ and Na+-Ca2+ exchange. We evaluated the effects of 3 episodes of 5 minutes global ischemia followed by 5 minutes recovery on [Ca2+]i during control perfusion (Co) and during suppression of the sodium influx (5×10-6 M lidocaine; L) with surface fluorometry in Indo-1/AM-loaded isolated ferfused rat hearts. During the first ischemia. systolic and enddiastolic [Ca2+]i were 130% higher in Co as compared to L. The lower [Ca2+]i concentration in L-treated hearts resulted in better recovery of contractile function during recovery (left ventricular developed pressure Co vs L: p=0.01). During repeated ischemia-recovery cycles peak [Ca2+]i decreased significantly in Co and remained stable in L (Fig.1). mean %±SEM; ★ : p=0.05 vs systolic [Ca2+]i during Co.ConclusionShort cycles of ischemic preconditioning resulted in less [Ca2+]i accumulation and improved hemodynamic recovery. Lidocaine pretreatment induced also calcium influx, mimicking the first episode of ischemic preconditioning