中华小儿外科杂志
中華小兒外科雜誌
중화소인외과잡지
CHINESE JOURNAL OF PEDIATRIC SURGERY
2001年
1期
48-51
,共4页
郑珊%张文颍%孙波%朱列伟
鄭珊%張文潁%孫波%硃列偉
정산%장문영%손파%주렬위
肺表面活性剂%小肠%再灌注损伤
肺錶麵活性劑%小腸%再灌註損傷
폐표면활성제%소장%재관주손상
目的 了解外源性肺表面活性物质(PS)对小肠缺血再灌注所致肺损伤的治疗效果。方法 正常雄性SD大鼠27只,腹腔麻醉后随机分为3组(n=9),A组:钳夹肠系膜上动脉10s作为对照;B组:阻断动脉1h后,去除阻断,形成再灌注2h;C组:模型制作同B组,PS以100mg/kg气道滴入。所有动物再机械通气2h。监测动脉血气(PaO2)、肺顺应性(Cdyn)和气道阻力(R)和病理改变。结果 血气分析B组PaO2进行性降低(B组与A组比较,P<0.05),C组PS治疗后PaO2较为稳定,不表现为进行性下降,120min时较病变组差异有显著性意义(C组与B组比较,P<0.05),肺功能表现为B组Cdyn降低、R升高,治疗后Cdyn稳定,120min时略有升高(C组与B组比较,P<0.05),病理观察:B组肺水肿、间质出血、炎性细胞浸润及部分肺不张,C组治疗后病变减轻。结论 外源性肺表面活性物质在这种模型的肺损伤治疗中可明显改善肺功能。
目的 瞭解外源性肺錶麵活性物質(PS)對小腸缺血再灌註所緻肺損傷的治療效果。方法 正常雄性SD大鼠27隻,腹腔痳醉後隨機分為3組(n=9),A組:鉗夾腸繫膜上動脈10s作為對照;B組:阻斷動脈1h後,去除阻斷,形成再灌註2h;C組:模型製作同B組,PS以100mg/kg氣道滴入。所有動物再機械通氣2h。鑑測動脈血氣(PaO2)、肺順應性(Cdyn)和氣道阻力(R)和病理改變。結果 血氣分析B組PaO2進行性降低(B組與A組比較,P<0.05),C組PS治療後PaO2較為穩定,不錶現為進行性下降,120min時較病變組差異有顯著性意義(C組與B組比較,P<0.05),肺功能錶現為B組Cdyn降低、R升高,治療後Cdyn穩定,120min時略有升高(C組與B組比較,P<0.05),病理觀察:B組肺水腫、間質齣血、炎性細胞浸潤及部分肺不張,C組治療後病變減輕。結論 外源性肺錶麵活性物質在這種模型的肺損傷治療中可明顯改善肺功能。
목적 료해외원성폐표면활성물질(PS)대소장결혈재관주소치폐손상적치료효과。방법 정상웅성SD대서27지,복강마취후수궤분위3조(n=9),A조:겸협장계막상동맥10s작위대조;B조:조단동맥1h후,거제조단,형성재관주2h;C조:모형제작동B조,PS이100mg/kg기도적입。소유동물재궤계통기2h。감측동맥혈기(PaO2)、폐순응성(Cdyn)화기도조력(R)화병리개변。결과 혈기분석B조PaO2진행성강저(B조여A조비교,P<0.05),C조PS치료후PaO2교위은정,불표현위진행성하강,120min시교병변조차이유현저성의의(C조여B조비교,P<0.05),폐공능표현위B조Cdyn강저、R승고,치료후Cdyn은정,120min시략유승고(C조여B조비교,P<0.05),병리관찰:B조폐수종、간질출혈、염성세포침윤급부분폐불장,C조치료후병변감경。결론 외원성폐표면활성물질재저충모형적폐손상치료중가명현개선폐공능。
Objective To study the effects of exogenous pulmonarysurfactant(PS) on acute lung injury induced by intestinal ischemia-reperfusion in mice.Methods Twenty-seven healthy SD mice were anesthetized and divided equally into 3 groups at random, namely : Group A transient occlusion of mesenteric artery for 10 seconds as sham control; Group B occlusion of the artery for 1h followed by 2h reperfusion ; Group C intratracheal injection of PS (100mg/kg). All mice were tracheotomized and ventilated mechanically after the initial 3h, pH, dynamic compliance(Cdyn), and resistance(R) were measured simultaneously. Results 1. Pathological examination showed that the lung edema, hemorrhage and partial atelectasis were found in group B. All of these features were reversed by PS in group C;2. The gas exchange function was damaged in group B ( lower PaO2 and higher PaCO2, B vs A, P<0.05). After using PS, PaO2 was improved and PaCO2 decreased (C vs B, P<0.05); 3. The lung function of group B also showed decreasing in Cdyn and increasing in R. Cdyn in group C was obvious better than that in group B. Conclusion PS is an effective therapy in animal models of acute lung injury.