Komuro Issei, Ohtsuka Masashi
Department of Cardiovascular Science and Medicine, Chiba University Graduate School of Medicine, Inohana, Chuo-ku, Japan.
J Pharmacol Sci. 2004 Sep;96(1):23-6. doi: 10.1254/jphs.fmj04002x5. Epub 2004 Sep 10.
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.
我们使用钠钙交换体(NCX)基因敲除小鼠来评估NCX在缺血/再灌注损伤后对心脏功能和梗死面积的影响。缺血/再灌注后,NCX基因敲除小鼠心脏的收缩功能明显优于野生型(WT)小鼠心脏,且与WT小鼠心脏相比,NCX基因敲除小鼠心脏的梗死面积明显更小。NCX在缺血/再灌注诱导的心肌损伤发展过程中起关键作用,因此抑制NCX功能可能有助于对缺血/再灌注损伤的心脏保护。