中国小儿急救医学
中國小兒急救醫學
중국소인급구의학
CHINESE PEDIATRIC EMERGENCY MEDICINE
2010年
6期
526-528,后插2
,共4页
刘薇%张慧%黄敬孚%常诚%林书祥%赵津生%郑捷%马继军%康杰
劉薇%張慧%黃敬孚%常誠%林書祥%趙津生%鄭捷%馬繼軍%康傑
류미%장혜%황경부%상성%림서상%조진생%정첩%마계군%강걸
急性肺损伤%弹性蛋白酶%肺表面活性物质蛋白A%抗氧化剂%大鼠
急性肺損傷%彈性蛋白酶%肺錶麵活性物質蛋白A%抗氧化劑%大鼠
급성폐손상%탄성단백매%폐표면활성물질단백A%항양화제%대서
Acute lung injury%Neutrophil elastase%Pulmonary surfactant protein A%Anti-oxidant%Rat
目的 探讨急性肺损伤(ALI)时血中中性粒细胞弹性蛋白酶(NE)、肺组织肺表面活性物质蛋白A(SP-A)的变化及抗氧化剂的影响效应.方法 健康、成熟Wistar大鼠60只随机均分为2组,模型组和治疗组,2组均以大肠杆菌腹腔注射建立ALI动物模型.治疗组在注射大肠杆菌30 min后,经大鼠尾静脉注射还原型谷胱甘肽.分别于注射大肠杆菌后3、6、12 h测定血中NE及肺组织SP-A的变化.结果 模型组注射大肠杆菌后3 h出现ALI症状,6 h更为明显,12 h口吐粉红色分泌物.肺组织大体病理检查可见双肺有明显水肿及出血点.治疗组3h无明显变化,6h呼吸稍促,12h肺组织仅轻度水肿.治疗组3、6、12 h测得血中NE水平低于模型组,在6、12 h差异有显著性(P<0.05);3、6、12 h测得肺组织SP-A阳性表达细胞数均高于模型组,差异均有显著性(P<0.05).结论 ALI时肺表面活性物质功能失常是继发性变化,其中原因之一就是SP-A被降解,应用抗氧化剂--还原型谷胱甘肽后可有效抑制NE分解细胞外基层弹性蛋白、破坏表面活性蛋白的作用,对ALI具有保护效应.
目的 探討急性肺損傷(ALI)時血中中性粒細胞彈性蛋白酶(NE)、肺組織肺錶麵活性物質蛋白A(SP-A)的變化及抗氧化劑的影響效應.方法 健康、成熟Wistar大鼠60隻隨機均分為2組,模型組和治療組,2組均以大腸桿菌腹腔註射建立ALI動物模型.治療組在註射大腸桿菌30 min後,經大鼠尾靜脈註射還原型穀胱甘肽.分彆于註射大腸桿菌後3、6、12 h測定血中NE及肺組織SP-A的變化.結果 模型組註射大腸桿菌後3 h齣現ALI癥狀,6 h更為明顯,12 h口吐粉紅色分泌物.肺組織大體病理檢查可見雙肺有明顯水腫及齣血點.治療組3h無明顯變化,6h呼吸稍促,12h肺組織僅輕度水腫.治療組3、6、12 h測得血中NE水平低于模型組,在6、12 h差異有顯著性(P<0.05);3、6、12 h測得肺組織SP-A暘性錶達細胞數均高于模型組,差異均有顯著性(P<0.05).結論 ALI時肺錶麵活性物質功能失常是繼髮性變化,其中原因之一就是SP-A被降解,應用抗氧化劑--還原型穀胱甘肽後可有效抑製NE分解細胞外基層彈性蛋白、破壞錶麵活性蛋白的作用,對ALI具有保護效應.
목적 탐토급성폐손상(ALI)시혈중중성립세포탄성단백매(NE)、폐조직폐표면활성물질단백A(SP-A)적변화급항양화제적영향효응.방법 건강、성숙Wistar대서60지수궤균분위2조,모형조화치료조,2조균이대장간균복강주사건립ALI동물모형.치료조재주사대장간균30 min후,경대서미정맥주사환원형곡광감태.분별우주사대장간균후3、6、12 h측정혈중NE급폐조직SP-A적변화.결과 모형조주사대장간균후3 h출현ALI증상,6 h경위명현,12 h구토분홍색분비물.폐조직대체병리검사가견쌍폐유명현수종급출혈점.치료조3h무명현변화,6h호흡초촉,12h폐조직부경도수종.치료조3、6、12 h측득혈중NE수평저우모형조,재6、12 h차이유현저성(P<0.05);3、6、12 h측득폐조직SP-A양성표체세포수균고우모형조,차이균유현저성(P<0.05).결론 ALI시폐표면활성물질공능실상시계발성변화,기중원인지일취시SP-A피강해,응용항양화제--환원형곡광감태후가유효억제NE분해세포외기층탄성단백、파배표면활성단백적작용,대ALI구유보호효응.
Objective To explore the changes of neutrophil elastase (NE) and surfactant protein A (SP-A) in acute lung injury(ALI) rats,and the effect of antioxidant. Methods Sixty healthy mature Wister rats were divided into 2 groups, the control group and treatment group. The rats in two groups all received peritoneal injection of E. coli to establish the ALI animal model. 30 minutes after injection of E. coli,the rats in treatment group were injected reduced glutathione from vena caudalis. The levels of NE in blood and expressions of SP-A in lung tissue were detected at 3,6 and 12 hours after injection of E. coli. Results ALI symptom appeared 3 hours after injection of E. coli in the control group, obvious after 6 hours, the rats vomi-ted pink secretion after 12 hours. Lung edema and bleeding were found by pathologic examination. No obvious symptom was found in treatment group after 3 hours, slight tachypnea after 6 hours, slight edema in pulmonary tissue after 12 hours. After administration of reduced glutathione,levels of NE at 3,6 and 12 hours in the treatment group were lower than those in the control group,and indicated statistical significance in 6 and 12 hours(P <0. 05) ;Levels of SP-A in 3,6 and 12 hours in the treatment group were higher than those in the control group, and indicated statistical significance in 3,6 and 12 hours (P < 0. 05). Conclusion Dysfunction of pulmonary surfactant is secondary in ALI, degradation of SP-A is the one of reasons, the application of reduced glutathione as antioxidant, could effectively suppress NE to decompose basosexine elastin of cells and destroy surface active protein, has protective effect on ALI.