Vardenafil protects isolated rat hearts at reperfusion dependent on GC and PKG
Vardenafil protects isolated rat hearts at reperfusion dependent on GC and PKG
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DOI：
10.1038/bjp.2008.71
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发表时间：
2008-05-01
影响因子：
7.3
通讯作者：
Krieg, T.
中科院分区：
文献类型：
--
作者：
Maas, O.;Donat, U.;Krieg, T.
背景和目的：当在动物模型中再灌注时应用5型PDE抑制剂伐地那非时，在缺血/再灌注后原位减少心肌梗死面积。对潜在的保护信号知之甚少。在这里，我们测试伐地那非是否是保护大鼠离体心脏和在细胞模型的钙stress.Experimental方法：在大鼠离体心脏的心肌体积进行了测量后，30分钟的区域缺血和120分钟的再灌注。在再灌注期间输注伐地那非（1 nM-1 μ M）。用四甲基罗丹明乙酯（TMRE），一种线粒体膜电位（cm）的荧光标记物负载HL-1心肌细胞。关键结果：伐地那非在再灌注时使梗死面积占缺血区的百分比从对照心脏的45.8 ± 2.0%减少到26.2 ± 2.7%（P
Background and purpose: The type-5 PDE inhibitor vardenafil reduces myocardial infarct size in situ, following ischemia/reperfusion, when applied at reperfusion in animal models. Little is known about the underlying protective signaling. Here, we test whether vardenafil is protective in rat isolated hearts and in a cell model of calcium stress.Experimental approach: Infarct size in rat isolated hearts was measured after a 30 min regional ischemia and 120 min reperfusion. Vardenafil (1 nM-1 mu M) was infused during reperfusion. HL-1 cardiomyocytes were loaded with tetramethylrhodamine ethyl ester (TMRE), a fluorescent marker of mitochondrial membrane potential (cm).Key results: Vardenafil at reperfusion reduced infarct size as percentage of the ischemic zone from 45.8 +/- 2.0% in control hearts to 26.2 +/- 2.7% (P