不同压力及时间机械通气对大鼠血清白细胞介素8、白细胞介素10水平和肺组织形态学的影响

目的 探讨不同压力及时间机械通气对大鼠血清白细胞介素8（IL-8）、IL-10水平及肺组织形态学的影响.方法 成年雄性SD大鼠30只,随机分为空白对照组（C组）、低气道压力2 h组L2组,压力为15 cm H2O（1 cm H2O=0.098 kPa）,通气时间为2 h]、低气道压力4 h组（L4组,压力为15 cmH2O,通气时间为4 h）和高气道压力2 h组（H2组,压力为25 cm H2O,通气时间为2 h）、高气道压力4 h组（H4组,压力为25 cm H2O,通气时间为4 h）,每组6只.连接呼吸机,设定呼吸频率为40次/min,按既定压力及时间进行机械通气,分别于机械通气2、4 h后血处死大鼠,检测血清中IL-8、IL-10的含量,并取肺组织,光镜及电镜下观察组织损伤的病理改变.结果 与C组相比,L2、L4、H2、H4组血清中IL-8、IL-10的含量均明显增加,且随通气时间的延长而升高,L4组高于L2组IL-8：（71.5±7.6）ng/L比（38.4±6.3）ng,L,IL-10：（364.5±18.6）ng/L比（271.6±21.3）ng/L,P〈0.05],H4组高于H2组IL-8：（140.7±23.5）ng/L比（76.4±9.2）ng/L,IL-10：（472.8±22.5）ng/L比（357.6±20.4）ng/L,P〈0.05];相同通气时间下,高气道压力组血清中IL-8、IL-10的含量较低气道压力组明显增多,H2组高于L2组,H4组高于L4组（P〈0.05）.光镜及电镜下组织学检查显示与C组比较,其余各组肺组织均出现不同程度的炎性细胞浸润、肺气肿、线粒体肿胀、内质网扩张、细胞核质间隙增宽等炎性反应改变,且随时问及气道压力的增加而加重.结论 通气压力及时间的增加能够刺激大鼠血清中炎性反应因子IL-8、IL-10水平的升高,加重肺组织的损伤.有效控制通气的压力及时间可以减轻肺组织炎性反应和损伤.

Effects of mechanical ventilation with different pressure and duration on plasma interleukin-8, interleukin-10 and lung ultrastructure in rats

Objective To investigate the effects of mechanical ventilation with different pressure and duration on plasma IL-8 , IL-10 and lung ultrastructure in rats. Methods Thirty adult male SD rats weighting 200-220 g were randomly divided into 5 groups （ n=6 each ）：control group （ group C ） , 2 h low airway pressure group （group L2, ventilated for 2 h at 15 cm H2O ） , 4 h low airway pressure group （ group L4, ventilated for 4 h at 15 cm H2O ） , 2 h high airway pressure group （ group H2, ventilated for 2 h at 25 cm H2O ） and 4 h high airway pressure group （ group H4 , ventilated for 4 h at 25 cm H2O）.Mechanical ventilation was given at a rate of 40 tpm, at specified pressures for designed duration. The rats were sacrificed at 2 h or 4 h after ventilation. Blood samples were then collected and tested for levels of IL-8 and IL-10. Changes in lung ultrastructure was observed under light and electronic microscopes respectively. Results Compared with group C,the levels of IL-8 and IL-10 were significantly higher in groups L2, Lt, H2 and H4. Moreover, these levels appeared increasing along with longer duration of ventilation, with higher values in group L4 vs group L2 IL-8： （71.5±7.6） ng/L vs （38.4±6.3） ng/L,IL-10：（364.5±18.6） ng/Lvs （271.6＋21.3） ng/L, P〈0.05], and in group H4 vs group H2 IL-8： （140.7±23.5） ng/L vs （76.4±9.2） ng/L, IL-10： （472.8±22.5） ng/L vs （357.6±20.4） ng/L, P〈0.05]. Over the same duration, levels of IL-8 and IL-10 were significantly greater with higher pressure used, namely, higher values in group H2 vs group L2, and in group H4 vs group L4 （P〈0.05）. Compared with group C, various degrees of inflammatory infiltration, emphysema, mitochondrial edema, dilated endoplama reticulum and expanded perinuclear space of lung ultrastructure existed in the other groups as shown by both light and electronic microscopes, which appeared to deteriorate along with longer ventilation time and higher pressure. Conclusions Higher pressure and longer duration for mechanical ventilation may induce IL-8 and IL-10, and also deteriorate lung tissue injury. Effective control of ventilation pressure and duration may ameliorate inflammation and injury of lung tissue.