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作 者:单琦[1] 程青虹[1] 田培刚[1] 何永来[1] 李建华[1]
机构地区:[1]石河子大学医学院第一附属医院重症医学科,新疆维吾尔自治区石河子市832008
出 处:《中华实用诊断与治疗杂志》2012年第3期238-240,共3页Journal of Chinese Practical Diagnosis and Therapy
基 金:国家自然科学基金(30960355)
摘 要:目的探讨胰岛素控制不同目标血糖水平对脓毒症大鼠心肌线粒体损伤的保护作用及机制。方法 40只SD大鼠随机分为5组各8只:假手术组、脓毒症组及血糖控制A组(控制血糖为>4.4~6.1mmol/L)、B组(控制血糖为>6.1~8.3mmol/L)、C组(控制血糖为>8.3~10.0mmol/L)。盲肠结扎穿孔术后12h处死,比色法检测心肌线粒体超氧化物歧化酶及丙二醛水平;电镜观察心肌线粒体形态学变化,并进行线粒体损伤评分分析。结果脓毒症组线粒体氧化应激水平及线粒体损伤评分均明显高于假手术组及各控制组(P均<0.05),A组较B,C组明显降低(P均<0.05),B组低于C组,但差异无统计学意义(P>0.05);脓毒症组线粒体超氧化物歧化酶活力及丙二醛含量分别与线粒体损伤评分呈负相关(r=-0.918,P<0.01)及正相关(r=0.872,P<0.05);A,B,C组心肌细胞超微结构改变较脓毒症组明显减轻。结论血糖控制为>4.4~6.1mmol/L对脓毒症大鼠心肌线粒体损伤保护作用最明显。Objective To investigate the protective effect of different target blood glucose control on septic myocardial damage and its mechanism. Methods Forty SD rats were randomly divided into sham operation group, sepsis group, group A(glucose was controlled at 4.4 to 6.1retool/L), group B(glucose was controlled at 6.1 to 8.3 mmol/L), and group C(glucose was controlled at 8. 3 to 10.0 mmol/L), with 8 rats in each group. The myocardial tissue was obtained 12 hours after cecal ligation and puncture. Superoxide dismutase and malondialdehyde levels in myocardial mitochondrion were detected with colorimetric technique. The ultramicrostructure of myocardial cell was examined under electron microscope and the degree of myocardial mitochondrion injury was analyzed. Results The oxidative stress and semiquantitative evaluation of myocardial mitochondrion were higher in sepsis group than those in the other four groups (P〈0.05), were lower in group A than those in group B and C(P〈0.05), and were lower in group B than that in group C(P〉0.05). Superoxide dismutase activity was positively correlated (r=-0. 918, P-(0.01) and malondialdehyde level was negatively correlated (r 0. 872, P〈0.05) with myocardial mitochondrion damage. The ultrastructure change was significantly lighter in group A, B and C than that in sepsis group. Conclusion The level of glucose at 4.4 to 6.1 mmol/ L can significantly alleviate myocardial mitochondrial damage in rats with sepsis.
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