Sodium/hydrogen exchanger inhibition reduces myocardial reperfusion edema after normothermic cardioplegia.
OBJECTIVE
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.


CONCLUSIONS
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.
Tritto
F P
FP
Laboratorio de Cardiologia Experimental B. Servicio de Cardiologia, Hospital General Universitari Vall d'Hebron, Barcelona, Spain.
Inserte
J
J
Garcia-Dorado
D
D
Ruiz-Meana
M
M
Soler-Soler
J
J
D000818:Animals; D004489:Edema, Cardiac / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D006146:Guanidines / Q000494:pharmacology*; D006324:Heart Arrest, Induced; D006439:Hemodynamics; D066298:In Vitro Techniques; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D015428:Myocardial Reperfusion Injury / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D051381:Rats; D017207:Rats, Sprague-Dawley; D017923:Sodium-Hydrogen Exchangers / Q000037:antagonists & inhibitors*; D013450:Sulfones / Q000494:pharmacology*; D016277:Ventricular Function, Left
D006146:Guanidines; D017923:Sodium-Hydrogen Exchangers; D013450:Sulfones; C093373:cariporide; D007770:L-Lactate Dehydrogenase