Key result
Heterozygous knockout of the Na+/Ca2+ exchanger significantly reduced myocardial infarct size to 32% compared to 68% in wild type mice following ischemia/reperfusion injury.
Why the study?
Does heterozygous knockout of Na+/Ca2+ exchanger improve contractile function and reduce infarct size after ischemia/reperfusion injury in mice?
Does heterozygous knockout of Na+/Ca2+ exchanger improve contractile function and reduce infarct size after ischemia/reperfusion injury in mice?
Heterozygous knockout of the Na+/Ca2+ exchanger in mice reduces infarct size and improves contractile function following ischemia/reperfusion injury, suggesting NCX inhibition as a potential cardioprotective strategy.
We used Na+/Ca2+ exchanger (NCX) knockout mice to evaluate the effects of NCX in cardiac function and the infarct size after ischemia/reperfusion injury. The contractile function in NCX KO mice hearts was significantly better than that in wild type (WT) mouse hearts after ischemia/reperfusion and the infracted size was significantly smaller in NCX KO mice hearts compared with that in WT mice hearts. NCX is critically involved in the development of ischemia/reperfusion-induced myocardial injury, and therefore the inhibition of NCX function may contribute to cardioprotection against ischemia/reperfusion injury.
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Komuro et al. (2004) studied Myocardial ischemia/reperfusion injury (n=33). Na+/Ca2+ exchanger (NCX) knockout vs. Wild type (WT) mice was evaluated on Myocardial infarct size as a percentage of the total heart (p=<0.05). Heterozygous knockout of the Na+/Ca2+ exchanger significantly reduced myocardial infarct size to 32% compared to 68% in wild type mice following ischemia/reperfusion injury.
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