The full extent of myocardial contractile recovery following Ischemia is delayed beyond the immediate reperfusion (R). This may be associated with delayed metabolic recovery and/or Ca2+ overload. This can be quantified in the beating heart by the scattered laser_intensity fluctuations which senses Ca oscillations (CaOs) it produces. We measured ATP, and pH NMR and SLIF, and developed pressure in isovolumic rat hearts. During the first 5 min of R there is rapid metabolic but a more gradual developed pressure and SLIF recovery. Then both gradually recover developed pressure abruptly and SLIF increases fourfold over the next 40 min mean no change in metabolic parameters. These findings suggest that delayed contractile recovery during (R) is attributable in part to an adverse effect of increased CaOs induced by Ca2+ overload during R. In additional hearts, for the first 10 min of R, perfusate Ca was 1.5mM (Group 1, n=4) or 0.08mM (Group 2, n=4). During R the early peak in SLIF was not present in Group 2. Recovery of DP was higher and cell Ca lower in Group 2 vs Group 1 at 20 min R. Thus, Ca0s during early R are modified by perfusate Ca, noninvasively index the extent of Ca loading, and predict functional recovery. Other hearts were pretreated with Amiloride 10-4 a known Na-Ca blocker during hypoxia and reoxygenation (Re02). During Re02, DP, EDP and PCr (all % baseline), and pHi recovery were improved in the Amiloride treated hearts. Cell gain during ReO2 was reduced 50% by Amiloride. These results suggest that cell Ca loading during reoxygenation is Na dependent and may be mediated in part by Na/Ca exchange.
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