16在呼吸机相关性肺损伤兔肺组织中表达

xpression of CC16 in lung tissue of rabbits with ventilator induced lung injury

目的探讨CC16在呼吸机相关性肺损伤（ventilatorinducedlunginlury，VILI）发生机制中的作用。方法将20只健康成年雄性日本大白兔随机分为对照组（插管后不进行机械通气）及实验组（插管后机械通气：潮气量20ml／kg，频率为30次／min，吸呼比为1：3，吸人氧浓度为21％，通气时间为24h），观察实验前后动脉血氧分压变化。取左肺中央部分肺组织，制备肺组织匀浆，采用双抗体夹心EI。IsA法检测肺组织上清液中CC16含量。取左肺组织一块，石蜡包埋，HE染色，制备石蜡组织切片，在显微镜下观察肺组织病理学变化。结果两组大白兔动脉血氧分压差异无统计学意义（P〉0．05）。对照组肺组织CC16为1．108±0．072，实验组肺组织CC16为0．621±0．056，两组差异有统计学意义（P〈0．01）。实验组肺组织病理切片可见肺组织水肿。结论CC16在VILI大白兔肺组织中表达下降，CC16可能在VILI发病机制中起重要作用。

Objective To investigate the role of clara ceil secretory 16-kD protein （CC16） in mechanism of ventilator induced lung injury （VILI）. Methods 20 healthy adult male Japanese white rabbits were randomly divided into control group （without mechanical ventilation after intubation） and experimental group （mechanical ventilation after intubatiom tidal volume was 20 rnl/kg, frequency was 30 times/min, respiratory absorption ratio was 1 = 3, FiOa was 21%, ventilation time was 24 hours）. The changes of arterial pressure of oxygen before and after experiment were observed. The central part of the left lung tissue was collected, lung tissue homogenate was prepared. The level of CC16 in the supernatant of lung tissues was detected by double antibody sandwich ELISA. The left lung tissue was collected,embedded by paraffin, and stained^by HE. Lung tissue sections were prepared for biopsies. Results There was no significant difference in arterial pressure of oxygen between the two groups （ P 0.05）. The level of CC16 in lung tissues was 1. 108 ± 0. 072 in control group, 0. 621±0. 056 in experimental group, there was significant difference between the two groups （ P d0.01）. Lung tissue edema could be found in lung tissue biopsy of experimental group. Conclusions The expression of CC16 decreases in rabbits with VILI, CC16 may play an important role in the occurrence and development of VILI.