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- W2017135085 abstract "Although the participation of the electrogenic sodium/bicarbonate cotransporter (NBCe1) in the recovery from an intracellular acid load is recognized, its role in ischemia–reperfusion is still unclear. Our objective was to assess the role of NBCe1 in reperfusion injury. We use selective functional antibodies against extracellular loop 3 (a-L3) and loop 4 (a-L4) of NBCe1. a-L3 inhibits and a-L4 stimulates NBCe1 activity. Isolated rat hearts were submitted to 40 min of coronary occlusion and 1 h of reperfusion. a-L3, a-L4 or S0859 — selective Na+-HCO3- co-transport inhibitor — were administered during the initial 10 min of reperfusion. The infarct size (IS) was measured by triphenyltetrazolium chloride staining technique. Postischemic systolic and diastolic functions were also assessed. a-L3 and S0859 treatments decreased significantly (P<.05) the IS (16±3% for a-L3 vs. 32±5% in hearts treated with control nonimmune serum and 19±3% for S0859 vs. 39±2% in untreated hearts). Myocardial function during reperfusion improved after a-L3 treatment, but it was not modified by S0859. The infusion of a-L4 did not modify neither the IS nor myocardial function. The NBCe1 hyperactivity during reperfusion leads to Na+ and Ca2+ loading, conducing to Ca2+ overload and myocardial damage. Consistently, we have shown herein that the selective NBCe1 blockade with a-L3 exerted cardioprotection. This beneficial action strongly suggests that NBCe1 could be a potential target for the treatment of coronary disease." @default.
- W2017135085 created "2016-06-24" @default.
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- W2017135085 date "2014-07-01" @default.
- W2017135085 modified "2023-10-09" @default.
- W2017135085 title "The electrogenic cardiac sodium bicarbonate co-transporter (NBCe1) contributes to the reperfusion injury" @default.
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- W2017135085 doi "https://doi.org/10.1016/j.carpath.2014.03.003" @default.
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