The Na+/HCO3- cotransporter and the cardiac carbonic anhydrase contribute to myocardial reperfusion injury.

FANTINELLI JC; ORLOWSKI A; ALVAREZ BV; AIELLO EA; MOSCA MS

Congreso; 1st Panamerican Congress of Physiological Sciences.; 2014

We previously demonstrated in rat cardiomyocytes that the electrogenic isoform of Na+/HCO3- co-transporter (NBCe1) and carbonic anhydrase (CA) are co-localized in surface and t-tubule membrane. To study the contribution of both entities to infarct size (IS) and postischemic myocardial dysfunction isolated rats hearts were submitted to 40 min of regional ischemia (I) and 60 min of reperfusion (R). Other hearts were treated with a selective inhibitor of NBC, S0859 (10 µM), the antibody against the extracellular loop 3 of NBCe1 (a-L3, 10 µM) or CA inhibitor, benzolamide (BZ, 5 µM). Myocardial function was assessed by the left ventricular developed pressure (LVDP) and left ventricular end diastolic pressure (LVEDP). S0859, a-L3 and BZ significantly reduced the IS (19±1%, 16±3% and 6.0±0.4% respectively vs 39±2% in non-treated hearts). Systolic function improved after a-L3 and BZ (LVDP= 70±6% and 80±3% for a-L3 and BZ, respectively vs. 46 ± 5 % in non-treated hearts).LVEDP increased after I/R and it was attenuated by a-L3 and BZL. S0859 did not modify the postischemic myocardial dysfunction. These data demonstrate that the blockade of NBC and CA exerts a cardioprotective effect indicating that both entities are involved in the irreversible injury and contractile alterations subsequent to I/R