The hypothesis was that Na+/H+ exchange occurring during normothermic cardioplegia contributes to the development of myocardial edema during subsequent reperfusion and impairs functional recovery.Methods:
Rat hearts were perfused in a Langendorff apparatus and submitted to 60 minutes of normothermic cardioplegia and 90 minutes of reperfusion. Hearts were allocated to one of four groups (n = 8): inhibition of Na+/H+ exchanger with HOE642 throughout the whole experiment (HOE group), only during cardioplegia (HOE-C) or during reperfusion (HOE-R), and a control group.Results:
In HOE and HOE-C groups, myocardial water content at the end of reperfusion was lower than in the HOE-R and control groups (526 ± 19 and 533 ± 18 ml/100 gm dry tissue vs 632 ± 25 and 634 ± 17 ml/100 gm dry tissue, respectively, p = 0.001), left ventricular end-diastolic pressure increased less after reperfusion (46.6 ± 9.7 and 63.2 ± 10.0 mm Hg vs 75.1 ± 4.3 mm Hg and 85.7 ± 8.9 mm Hg, respectively, p = 0.006), and recovery of left ventricular developed pressure was better (46.7% and 45.8% vs 4.5% and 9.8%, p = 0.048). Relative to the control group, total lactate dehydrogenase release during reperfusion was reduced by 80.2%, 69.3% and 36% in HOE, HOE-C, and HOE-R groups, respectively.Conclusion:
Inhibition of the Na+/H+ exchange during normothermic cardioplegia reduces myocardial edema and necrosis during subsequent reperfusion, improving functional recovery. Inhibition of Na+/H+ exchange during reperfusion only has a much smaller effect.