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作 者:赵宁军[1] 许铁[1] 叶英[1] 燕宪亮[1] 梁高永[1] 刘蓓[1]
机构地区:[1]徐州医学院急救医学教研室,江苏徐州221002
出 处:《徐州医学院学报》2009年第12期804-806,共3页Acta Academiae Medicinae Xuzhou
摘 要:目的观察左旋卡尼汀(L-CN)预处理对离体兔心缺血/再灌注致心肌损伤及丙二醛(MDA)、超氧化物歧化酶(SOD)的影响。方法采用离体兔心Langendorff灌注实验模型,离体兔心12只随机分成缺血/再灌注组(I/R组)和L-CN预处理组,每组6只。I/R组灌注K-H液25 min,(兔心)4℃标准St.Thomas停搏液(K+16 mmol/L)至心脏停搏,45 min后恢复K-H液灌注20 min;L-CN预处理组灌注K-H液10 min,再予L-CN续灌15 min,余步骤同I/R组。测定再灌注末心肌组织中MDA、SOD的活性;2,3,5-三苯基氯化四氮唑(TTC)染色测定心肌存活面积百分比。结果L-CN预处理组SOD活性明显高于I/R组(P<0.01),MDA含量明显低于I/R组(P<0.05)。L-CN预处理组心肌存活面积百分比高于I/R组(P<0.05)。结论L-CN预处理对高钾停搏离体兔缺血/再灌注心脏具有抑制氧化应激、提高抗氧化能力的作用,可减轻心肌损伤。Objective To investigate the effects of L-carnitine(L-CN) preconditioning on levels of superoxide dismutase(SOD) and malondialdehyde(MDA) against ischemia/reperfusion-induced myocardial injury in isolated rabbit hearts.Methods The experiment was performed on isolated rabbit hearts perfused on Langendorff apparatus.12 rabbit hearts were randomized into ischemia/reperfusion group(I/R group) and L-CN preconditioning group(n=6 each).The I/R group was firstly perfused with Krebs-Henseleit buffer(K-H) solution at 4℃ for 25 min,followed by St.Thomas Ⅱ solutions(K+ 16 mmol/L) until cardiac arrest for 45 min and then reperfused with K-H solution for 20 min.The treatment of L-CN preconditioning group was similar to that of the I/R group,except that this group was initially perfused with K-H solution for 10 min and then perfused with L-CN.At the end of reperfusion,the contents of MDA,the activity of SOD were measured.The percentage of survival areas of myocardium was measured by using 2,3,5-triphenyltetrazolium chloride(TTC) stain.Results In contrast to the findings in the I/R group,the percentages of surviving myocardium areas in the L-CN preconditioning group were higher(P〈0.05).SOD content in L-CN preconditioning group was significant higher than that in I/R group(P〈0.01).MDA content in L-CN preconditioning group was significantly lower than that in I/R group(P〈0.05).Conclusion L-CN preconditioning can attenuate the myocardium injury by inhibiting oxidative stress and increasing the anti-oxidative capacity to the isolated rabbit heart undergoing cardiac ischemia due to high potassium-induced cardiac arrest and reperfusion.
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