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 ([Ca 2+ ] i ), [Na + ] i and [H + ] i during ischemia by reducing the stimulation of Na + -H + and Na + -Ca 2+ exchange. We evaluated the effects of 3 episodes of 5 minutes global ischemia followed by 5 minutes recovery on [Ca 2+ ] 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 [Ca 2+ ] i were 130% higher in Co as compared to L. The lower [Ca 2+ ] 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 [Ca 2+ ] i decreased significantly in Co and remained stable in L (Fig.1). mean % ± SEM; ★ : p = 0.05 vs systolic [Ca 2+ ] i during Co. Download high-res image (100KB) Download full-size image Conclusion Short cycles of ischemic preconditioning resulted in less [Ca 2+ ] i accumulation and improved hemodynamic recovery. Lidocaine pretreatment induced also calcium influx, mimicking the first episode of ischemic preconditioning.