脓毒症大鼠不同时期炎症因子水平与心功能关系的研究

目的探讨脓毒症大鼠炎症因子与心功能之间的关系及其可能机制。 方法采用盲肠结扎穿孔法制备腹腔感染脓毒症动物模型。将120只大鼠分为对照组60只、脓毒症组60只，再按照造模后不同时点分成6个亚组（造模后3、6、12、24、48、72 h），每个亚组10只大鼠。监测各亚组动物心功能指标左室舒张末压（LVEDP）、左室发展压（LVDP）、左室最大收缩速率（＋dP／dt max）及左室最大舒张速率（＋dp／dt max），血清炎症因子肿瘤坏死因子α（TNF-α）、白介素6（IL-6）及IL-10，心肌酶谱心肌肌钙蛋白I（cTn I）、肌酸激酶（CK）、肌酸激酶同工酶（CK-MB）。同时电镜下观察心肌超微结构的变化情况。结果与对照组相比较，脓毒症组±dp／dt max、LVDP水平从3 h开始出现下降，至12 h下降最明显（P均〈0．05），而脓毒症组LVEDP水平于造模后12～48 h与对照组比较均显著升高（P均〈0．05）。脓毒症组TNF—α、IL-6水平于3 h后与对照组比较出现升高（P均〈0．05），而IL-10在6～72 h后与对照组比较差异均具有统计学意义（P均〈0．05）。同时脓毒症组cTn I、CK、CK．MB水平在不同时间点较对照组均显著增加（P均〈0．05）。此外，电镜观察脓毒症组大鼠心肌超微结构损伤明显至24 h病变最为严重。 结论脓毒症不同时期促炎因子与抗炎因子失衡，可能是导致脓毒症心功能改变的重要因素之-。

Relationship between inflammatory factor and cardiac function at different periods in septic rats

Objective To observe the relationship and underlying mechanisms between cardiac function and inflammatory factor in septic rats. Methods Male adult rats were subjected to sepsis by cecal ligation and puncture. Total of 120 rats were randomly divided into the control group （60 rats） and sepsis group （60 rats）. The rats were further divided into 3, 6, 12, 24, 48, and 72 h subgroups, 10 rats in each subgroup. The left ventricular end diastolic pressure （LVEDP）, left ventricular developed pressure （LVDP）, maximal velocity increase of left ventricular pressure per second （＋dP/ dt max）, maximal velocity decrease of left ventricular pressure per second （-dP/dt max）, tumor necrosis factor-alpha （TNF-α）, intedeukin-6 （IL-6）, IL- l0, cardiac troponin I （cTn I ）, creatine kinase （CK） and creatine kinase-MB （CK-MB） were detected. The changes of myocardial ultrastructural were examined by electron microscope. Results The levels of ＋dp/dt max and LVDP in the sepsis group were lower after 3 h, and were much lower at 12h （all P〈0.05）, and the LVEDP at 12-48hwere all higher than those in the control group （all P〈 0.05）. Compared with the control group, the levels of TNF-α and IL-6 in the sepsis group increased markedly after 3 h （all P 〈 0.05）, and the IL-10 at 6-72 h all showed significant differences as compared with those in the control group （all P 〈 0.05）. Meanwhile, the cTn I, CK and CK-MB in the sepsis group at different time points were all higher than those in the control group （all P 〈 0.05）. Under electron microscope, the myocardial uhrastructure in the sepsis group were damaged and destroyed, especially at 24 h. Conclusion The imbalance of proinflammatory factor and anti-inflammatory factor is an important factor leading to cardiac dysfunction at different periods in septic rats.