摘要
目的 探讨高碳酸血症对急性肺损伤模型的保护作用及可能的机制。方法 24只新西兰兔随机分为对照组(对照组)、治疗性高碳酸血症组(治疗组)、预防性高碳酸血症组(预防组),采用脂多糖静脉注射复制肺损伤模型,观察3组血流动力学(血压、心率),血气指标的变化,检测肺组织湿重/干重比(W/D)、肺泡损伤数比值(IQA)及光镜下评估肺脏的损伤程度,通过测定髓过氧化物酶(MPO)、丙二醛(MDA)探讨高碳酸血症对肺脏损伤保护的可能机制。结果三组在实验前后收缩压、舒张压、心率均无明显变化,治疗组、预防组组PO2、PaCO2/FiO2比对照组有明显改善。与对照组比较,治疗组、预防组组W/D、MPO、IQA和MDA水平明显降低,肺组织损伤明显减轻。治疗组与预防组组比较各指标之间无明显差异。结论 高碳酸血症对急性肺损伤具有保护作用,可能通过抑制中性粒细胞在肺脏的聚集,抑制肺脏的氧化应激反应减轻了肺脏的损伤。
Objective To explore the protective effects of hypercapnia on acute lung injury(ALI) in rabbits and the possible mechanisms. Methods Twenty-four healthy New Zealand white rabbits were randomly allocated to control group (CN group), therapeutic hypercapnia group (TH group) ,prophylactic hypercapnia group (PH group). Lipopolysaccharide (1 mg/kg) was injected intravenously to establish ALI model. Ratio of lung wet weight/dry weight (W/D),index of quantitative assessment of histologic lung injury(IQA), pathological changes under light microscope, activity of myeloperoxidase (MPO) and malondialdehyde (MDA) in lung tissue were measured. Results Systolic blood pressure, diastolic blood pressure and heart rate were not statistically different before and after experiment between three groups ( P〉0.05). In TH and PH group,PO2 and PaCO2/FiO2 were significantly higher ( P 〈 0.01), and levels of W/D, MPO, MDA, IQA and degree of lung tissue injury were significantly lower than those in CN group ( P 〈0.01). Apoptosis index of neutrophil was negatively correlated with levels of IL-8 and TNF-α in the serum and bronchoalveolar lavage fluid. All the parameters had no differences between TH and PH group. Conclusions Hypercapnia has the protective effects on ALI through possible mechanism of inhibiting the aggregation of neutrophil and oxidative stress in lung tissue.
出处
《国际呼吸杂志》
2007年第12期892-894,共3页
International Journal of Respiration
基金
云南省教育厅科学研究基金资助项目(编号:042096C)