Lymbury Robyn, Venardos Kylie, Perkins Anthony V
Heart Foundation Research Centre, School of Medical Science, Griffith University Gold Coast Campus, Southport, QLD, 9726. Australia.
Biol Trace Elem Res. 2006 Winter;114(1-3):197-206. doi: 10.1385/BTER:114:1:197.
Cardiac surgery often generates oxidative stress leading to ischemia reperfusion injury (I-R). Antioxidants have been shown to prevent this injury and have been added to cardioplegic solutions to assist in recovery. In this study, we tested the effectiveness of sodium selenite in protecting against ischemia reperfusion injury and investigated the mechanisms behind this protection. Hearts from male Wistar rats were subjected to ischemia reperfusion using the Langendorf model. Krebs-Henseleit perfusion solutions were supplemented with 0, 0.1, 0.5, 1.0, and 10 microM sodium selenite. Hearts were perfused for 30 min and then subjected to 22.5 min of global ischemia followed by 45 min reperfusion. Heart rate, ischemic contracture, end diastolic pressure, and developed ventricular pressure were monitored. At the completion of the experiment, hearts were homogenized and tissue extracts were assayed for glutathione peroxidase (GSH-Px) and thioredoxin reductase (Thx-Red) activity. Sodium selenite, at a concentration of 0.5 microM, demonstrated a protective effect on the recovery of cardiac function following I-R, as evidenced by a lower end diastolic pressure and enhanced recovery of rate pressure product. There was no beneficial effect observed in hearts perfused with 0.1 microM sodium selenite-supplemented buffer, whereas poorer functional recovery was observed in hearts perfused with 10 microM sodium selenite-supplemented buffer. The beneficial effect of sodium selenite was not mediated through increased activity of GSH-Px or Thx-Red. This study demonstrates that the addition of sodium selenite to reperfusion solutions, at an optimal concentration of 0.5 microM, assists in cardiac recovery following ischemia reperfusion.
心脏手术常引发氧化应激，导致缺血再灌注损伤（I-R）。抗氧化剂已被证明可预防这种损伤，并已被添加到心脏停搏液中以辅助恢复。在本研究中，我们测试了亚硒酸钠预防缺血再灌注损伤的有效性，并研究了这种保护作用背后的机制。使用Langendorf模型对雄性Wistar大鼠的心脏进行缺血再灌注。Krebs-Henseleit灌注液中添加0、0.1、0.5、1.0和10微摩尔亚硒酸钠。心脏灌注30分钟，然后进行22.5分钟全心缺血，随后再灌注45分钟。监测心率、缺血性挛缩、舒张末期压力和心室发育压力。实验结束时，将心脏匀浆，并检测组织提取物中的谷胱甘肽过氧化物酶（GSH-Px）和硫氧还蛋白还原酶（Thx-Red）活性。浓度为0.5微摩尔的亚硒酸钠对I-R后心脏功能的恢复具有保护作用，表现为较低的舒张末期压力和心率压力乘积的恢复增强。在灌注含0.1微摩尔亚硒酸钠缓冲液的心脏中未观察到有益作用，而在灌注含10微摩尔亚硒酸钠缓冲液的心脏中观察到功能恢复较差。亚硒酸钠的有益作用不是通过增加GSH-Px或Thx-Red的活性介导的。本研究表明，在再灌注溶液中添加最佳浓度为0.5微摩尔的亚硒酸钠有助于缺血再灌注后的心脏恢复。
