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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 effects and mechanisms of insulin on blood glucose levels in myocardial mitochondria of septic rats. Methods Forty Sprague - Dawley rats were randomly divided into five groups: sham operation group, sepsis group and A group (blood glucose> 4.4-6.1 mmol / L), B group (control blood glucose> 8.3mmol / L), C group (control blood sugar> 8.3 ~ 10.0mmol / L). The cecal ligation and puncture were performed 12h after operation. The myocardial mitochondrial superoxide dismutase and malondialdehyde levels were detected by colorimetric method. The mitochondrial morphological changes were observed by electron microscopy and the mitochondrial damage score was analyzed. Results The levels of mitochondrial oxidative stress and mitochondrial damage in sepsis group were significantly higher than those in sham group and control group (all P <0.05), and were significantly lower in group A than those in group B and C (all P <0.05) (P> 0.05). The activity of mitochondrial superoxide dismutase and the content of malondialdehyde in sepsis group were negatively correlated with the mitochondrial damage score (r = -0.918, P <0.01), but the difference was not statistically significant ) And positive correlation (r = 0.872, P <0.05). The ultrastructural changes of myocardial cells in groups A, B and C were significantly reduced compared with those in sepsis group. Conclusion The glycemic control of> 4.4 ~ 6.1mmol / L has the most obvious protective effects on myocardial mitochondrial injury in septic rats.