摘要
目的 探讨胰岛素不同目标血糖管理对脓毒症心肌损伤的保护作用及其可能机制.方法 SD大鼠40只随机分为五组（n=8）：假手术组（sham组）、CLP组、控制A组、控制B组和控制C组.盲肠结扎穿孔（CLP）术后12 h处死,双抗夹心ELISA法检测血清心肌肌钙蛋白I（cTnI）的含量;光镜及电镜观察左室心肌组织形态学变化并行组织病理积分及线粒体损伤评分分析.结果.CLP组cTnI浓度、病理积分及线粒体损伤评分均明显高于sham组及各控制组（P均〈0.05）;控制A组较B、C组明显降低（P均〈0.05）;B组低于C组,但P〉0.05.CLP组线粒体损伤评分与cTnI水平及病理积分均有显著正相关（P均〈0.01）.光镜及电镜可见各控制组较CLP组心肌形态及细胞超微结构改变均明显减轻.结论.不同水平的胰岛素强化血糖控制都可改善脓毒症心肌损伤,其机制可能为抑制心肌线粒体损伤而实现.与6.1～8.3 mmol/L及8.3～10.0 mmol/L相比,血糖控制在4.4～6.1 mmol/L对脓毒症大鼠心肌损伤的保护作用最为明显.
Objective To investigate the protective effects of different levels intensive glycemic control and the possible mechanism on septic myocardial damage. Methods The sepsis model of rat was reproduced by cecal ligation and puncture. Forty Sprague - Dawley rats were randomly divided into five groups （ n = 8 ） ： sham operation group, sepsis group, glycemie control A group, glycemic control B group, and glycemic control C group. The myocardial tissue was obtained after CLP 12 hours. Serum levels of cardiac trbponin （cTn） I was detected by euzymelinked immunosorbent assay （ELISA）. The histopathologic changes of myocardial tissue were observed and the myocardial histopathologic score was counted by optical microscope, and the uhramicrostrueture of myocardial cell was examined and the degree of myocardial mitochondrion injury was analyzed by electron microscope. Results The serum concentration of cTnI, myocardial bistopatbologic score, and semiquantitative evaluation of myocardial mitochondrion in group CLP was higher than them in group sham, group A, group B, and group C （ P 〈 0.05, respectively）. Compared with group B and C, they were degraded in group A （P 〈 0.05, respectively）. By correlation analysis, in group CLP there exists positive correlation respectively between semiquantitative evaluation of myocardial mitochondrion and cTnI, myocardial histopathologic score, with statistical significance（P 〈 0.01, respectively）. The histopathologie changes of myocardial tissue and the lesion of ultrastructure were significantly lessened in group A, B and C, comparing with those in group CLP. Conclusion Different levels intensive glycemic control could decrease myocardial damage produced in septic rats. The mechanism might be that different levels intensive glycemic control could protect septic myocardial damage through relieving the lesion of myocardial mitochondrion. The level of blood glucose in 4.4 - 6.1 mmol/L could significantly alleviate myocardial damage in comparison with it in the 6.1
出处
《中国急救医学》
CAS
CSCD
北大核心
2012年第2期112-114,I0003,共4页
Chinese Journal of Critical Care Medicine
