Guo Jialong, Zhang Jun, Luo Xiangyu, Luo Weimin, Lin Chengyi, Zhang Kailun, Ji Yanmei
Department of Cardiothoracic Surgery, Taihe Hospital Affiliated to Hubei Medical College, Shiyan, Hubei 442000, P.R. China.
Department of Cardiovascular Surgery, Union Hospital, Huazhong University of Science and Technology, Wuhan, Hubei 430022, P.R. China.
Exp Ther Med. 2014 May;7(5):1197-1202. doi: 10.3892/etm.2014.1581. Epub 2014 Feb 24.
The present study used an model of cold cardioplegia in isolated working rat hearts to evaluate the possible role of ethyl pyruvate (EP) in promoting cardiac function and preventing apoptosis. Two groups of rats were evaluated; the EP (2 mM EP; n=8) and control (n=8) groups. Isolated rat hearts were perfused with Krebs-Henseleit buffer (KHB) for 30 min, arrested with cardioplegic solution and stored for 4 h in B21 solution at 4°C. The hearts were reperfused with KHB for 45 min. EP was added to the cardioplegic and storage solutions and also to KHB for reperfusion. Cardiac parameters of the heart rate, including left ventricular systolic pressure, left ventricular end-diastolic pressure, left ventricular developed pressure and maximal rise rate of the left ventricular pressure, were monitored. In addition, coronary flow, adenosine triphosphate (ATP) levels and malondialdehyde (MDA) content were recorded and apoptotic cell determination was detected. The functional parameters in the EP group were significantly higher compared with those in the control group during the reperfusion period (P<0.05). In addition, ATP levels were higher in the EP group than in the control group and the content of MDA was lower in the EP group than in the control group. A concentration of 2 mM EP significantly reduced the number of apoptotic cells in the EP group compared with that of the control group (P<0.05). Therefore, EP significantly preserved cardiac function, enhanced tissue ATP levels, attenuated myocardial oxidative injury and markedly reduced apoptosis following myocardial ischemia in an model of 4 h of cold cardioplegia and reperfusion.
本研究采用离体工作大鼠心脏冷停搏模型，以评估丙酮酸乙酯（EP）在促进心脏功能和预防细胞凋亡方面的可能作用。评估了两组大鼠；EP组（2 mM EP；n = 8）和对照组（n = 8）。将离体大鼠心脏用 Krebs-Henseleit 缓冲液（KHB）灌注30分钟，用心脏停搏液使其停搏，并在4℃的B21溶液中保存4小时。心脏再用KHB灌注45分钟。将EP添加到心脏停搏液和保存液中，也添加到用于再灌注的KHB中。监测心率的心脏参数，包括左心室收缩压、左心室舒张末期压力、左心室发展压力和左心室压力最大上升速率。此外，记录冠状动脉流量、三磷酸腺苷（ATP）水平和丙二醛（MDA）含量，并检测凋亡细胞测定。再灌注期间，EP组的功能参数明显高于对照组（P<0.05）。此外，EP组的ATP水平高于对照组，EP组的MDA含量低于对照组。与对照组相比，2 mM EP浓度显著降低了EP组的凋亡细胞数量（P<0.05）。因此，在4小时冷停搏和再灌注模型中，EP显著保留了心脏功能，提高了组织ATP水平，减轻了心肌氧化损伤，并显著减少了心肌缺血后的细胞凋亡。
