CO_2气腹对慢性肺功能不全兔肺组织氧化应激反应影响的实验研究

Oxidative stress in lung tissue induced by CO_2 pneumoperitoneum in rabbits with emphysema

目的探讨CO2气腹对慢性肺功能不全兔肺组织氧化应激反应的损伤机制。方法兔肺气肿模型稳定后,施加CO2气腹2h,压力为10mmHg和15mmHg。分别于气腹解除即时、2h、6h和18h各时间点测定肺组织中SOD、GSHPX、MPO、CAT活力和MDA、GSH含量。结果在气腹作用后即时肺组织中SOD、CAT、GSHPX活力和GSH含量开始下降,至气腹2h后达最低,后开始增高,但18h后仍未恢复到气腹前水平。而MDA含量和MPO活力变化则相反。在15mmHg压力下上述指标变化更为显著。结论在CO2气腹条件下肺组织缺血、缺氧,活性氧自由基生成增加,氧化应激反应增强,导致了肺功能的损伤。气腹压力越高,损伤程度越显著。

Objective To examine oxidative stress markers in lung tissue induced by CO_2 pneumoperitoneum in the rabbits with emphysema and investigate the possible mechanism of these changes. Methods After the model of emphysema was established in rabbits, the abdominal cavity of the rabbits was gradually insufflated with CO_2 gas to inflict CO_2 pneumoperitoneum. Then the pneumoperitoneum was maintained at the pressure of 10 mmHg and 15 mmHg, respectively, for 2 h. The levels of SOD, GSH-PX, MPO, CAT, MDA and GSH in lung tissue homogenates were determined at 0h, 2h, 6h and 18h after laparoscopy. Results The levels of SOD, GSH-PX, CAT and GSH were decreased while those of MDA and MPO increased at 0h and 2h after the laparoscopy. However, the levels of SOD, GSH-PX, CAT and GSH were increased but those of MDA and MPO decreased at 6h and 18h after the laparoscopy. These changes were more significant in the rabbits receiving CO_2 at the pressure of 10 mmHg than in those at the pressure of 15 mmHg. Conclusions The blood and oxygen decrease but free radical increases in lung tissue of rabbits with CO_2 pneumoperitoneum, which aggregate the oxidative stress. This results in impairment of pulmonary function. The severity of lung damage is increased along with increase in CO_2 pressure.