摘要
目的 探讨低温对大鼠内毒素性急性呼吸窘迫综合征 (ARDS)肺脂质过氧化的影响。方法 采用大鼠腹腔注射内毒素 (LPS ,1mg·kg- 1 ) ,16h后再气管内滴注LPS(3mg·kg- 1 )建立ARDS模型。 2 4只雄性SD大鼠被随机分为 3组 :对照组 (C组 )、ARDS组 (A组 )、低温组 (H组 )。ARDS后 3h处死动物 ,检测肺组织中丙二醛 (MDA)含量和超氧化物歧化酶 (SOD)活性。结果 3组各时间点平均动脉压 (MAP)、中心静脉压 (CVP)相比无统计学差异 (P >0 .0 5 )。A组氧合指数 (PaO2 FiO2 )在ARDS时及ARDS后 1、2、3h与C组相比显著下降 (P <0 .0 1)。A组与C组相比大鼠肺组织中MDA含量明显增高、SOD活性显著下降 (P <0 .0 5 ) ;而H组与A组相比 ,大鼠肺组织中MDA含量明显降低、SOD活性显著升高 (P <0 .0 5 ) ,但与C组相比无统计学意义 (P >0 .0 5 )。结论 低温可减轻内毒素性ARDS大鼠肺组织脂质过氧化。
Objective To investigate the effect of hypothermia on lipid peroxidation in the lung tissue of rats with acute respiratory distress syndrome (ARDS) induced by lipopolysaccharide (LPS).Methods Twenty-four male SD rats were randomly divided into a normal control group, an ARDS group and a hypothermic treatment group. The rat model of ARDS was established by intratracheal instillation of LPS (3 mg·kg -1) 16 hours after intraperitoneal administraion of LPS (1 mg·kg -1). After 4 hours of ARDS, the rats were killed by tapping the carotid artery.The malondialdehyde (MDA) content and superoxide dismutase (SOD) activity in lung tissue were then measured.Results There were no significant differences in MAP and CVP among the three groups (P>0.05). The MDA content of the lung tissu was increased and the SOD activity was decreased significantly in the ARDS group, as compared with the control group (P<0.05). The MDA content was markedly lower and the SOD activity was significantly higher in the hypothermic group than in the ARDS group (P<0.05), while there was no significant difference in MDA content and SOD activity between hypothermic group and control group (P>0.05).Conclusion Hypothermia can attenuate lipid peroxidation in lung tissue in rats with lipopolysaccharide- induced ARDS.
出处
《徐州医学院学报》
CAS
2004年第4期292-294,共3页
Acta Academiae Medicinae Xuzhou
基金
江苏省麻醉学重点实验室开放课题 (K2 0 96 )
江苏省科技厅资助项目 (BS2 0 0 0 0 2 4 )
