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首页> 外文期刊>Journal of receptor and signal transduction research >Environmentally persistent free radicals decrease cardiac function before and after ischemia/reperfusion injury in vivo
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Environmentally persistent free radicals decrease cardiac function before and after ischemia/reperfusion injury in vivo

机译：体内环境持久性自由基会降低体内缺血/再灌注损伤前后的心脏功能

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摘要

Exposure to airborne particles is associated with increased cardiovascular morbidity and mortality. During the combustion of chlorine-containing hazardous materials and fuels, chlorinated hydrocarbons chemisorb to the surface of transition metal-oxide-containing particles, reduce the metal, and form an organic free radical. These radical-particle systems can survive in the environment for days and are called environmentally persistent free radicals (EPFRs). This study determined whether EPFRs could decrease left ventricular function before and after ischemia and reperfusion (I/R) in vivo. Male Brown-Norway rats were dosed (8mg/kg, intratracheal) 24h prior to testing with particles containing the EPFR of 1, 2-dichlorobenzene (DCB230). DCB230 treatment decreased systolic and diastolic function. DCB230 also produced pulmonary and cardiac inflammation. After ischemia, systolic, but not diastolic function was significantly decreased in DCB230-treated rats. Ventricular function was not affected by I/R in control rats. There was greater oxidative stress in the heart and increased 8-isoprostane (biomarker of oxidative stress) in the plasma of treated vs. control rats after I/R. These data demonstrate for the first time that DCB230 can produce inflammation and significantly decrease cardiac function at baseline and after I/R in vivo. Furthermore, these data suggest that EPFRs may be a risk factor for cardiac toxicity in healthy individuals and individuals with ischemic heart disease. Potential mechanisms involving cytokines/chemokines and/or oxidative stress are discussed.
机译：暴露于空气中的颗粒物会增加心血管疾病的发病率和死亡率。在含氯有害物质和燃料的燃烧过程中，氯化碳氢化合物会化学吸附到含过渡金属氧化物的颗粒表面，还原金属并形成有机自由基。这些自由基-粒子系统可以在环境中存活数天，被称为环境持久性自由基（EPFR）。这项研究确定EPFRs是否可以在体内缺血和再灌注（I / R）前后降低左心室功能。在测试前24小时给雄性Brown-Norway大鼠（8mg / kg，气管内）给药，其中含有1，2-二氯苯（2B）的EPFR。 DCB230治疗降低了收缩和舒张功能。 DCB230还产生了肺部和心脏炎症。缺血后，DCB230治疗的大鼠的收缩功能（而非舒张功能）显着降低。对照大鼠的心室功能不受心室功能的影响。 I / R后，治疗组和对照组大鼠的心脏中存在更大的氧化应激，而血浆中的8-异前列腺素含量升高。这些数据首次证明DCB230可以在基线和体内I / R后产生炎症并显着降低心脏功能。此外，这些数据表明，EPFR可能是健康个体和缺血性心脏病个体心脏毒性的危险因素。讨论了涉及细胞因子/趋化因子和/或氧化应激的潜在机制。

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