The electrogenic cardiac sodium bicarbonate co-transporter (NBCe1) contributes to reperfusion injury.

JC FANTINELLI; A ORLOWSKI; A AIELLO; SM MOSCA

CARDIOVASCULAR PATHOLOGY

ELSEVIER SCIENCE INC

Lugar: Amsterdam; Año: 2014

1054-8807

Abstract Background: We have recently demonstrated that selective antibodies against extracellular loop domain 3 (a-L3) and 4 (a-L4) of the electrogenic sodium/bicarbonate cotransporter isoform (NBCe1) have opposite effects on the transporter function. Methods: The objective of the present study was to assess the role of a-L3 and a-L4 in the infarct size (IS) and myocardial dysfunction produced by ischemia and reperfusion. Isolated rat hearts were isovolumically perfused and submitted to 40 min of coronary occlusion and 1 hour of reperfusion. a-L3, a-L4 or S0859 -the selective inhibitor of NBC- were administered during the initial 10 min of reperfusion. IS was measured by TTC staining technique. Left ventricular developed pressure (LVDP) and left ventricular end diastolic pressure (LVEDP) were used to determine the systolic and diastolic function, respectively. Results: a-L3 and S0859 treatments decreased significantly the IS (16 ± 3 % for a-L3 vs. 32 ± 5% in ischemic control hearts treated with non-immune serum, and 19 ± 3 % for S0859 vs. 39 ± 2 % in ischemic control non-treated hearts). LVDP significantly increased and LVEDP decreased after a-L3 but not after S0859 treatment during reperfusion. The infusion of a-L4 did not modify neither the IS nor myocardial dysfunction detected in hearts treated with non-immune serum. Conclusions: These data show that the NBCe1 plays an important role in the reperfusion injury and that its blockade only during reperfusion exerts cardioprotective effect.