CAJ | 학술논문

目的建立大鼠肺内源性急性肺损伤/急性呼吸窘迫综合征(ALI/ARDS)模型.方法大肠杆菌[O111B4,(4.0～6.0)×1012 CFU/L]3 ml/kg气管注射制作大鼠肺内源性ALI模型.分别于注射大肠杆菌后12、24、36、48、72 h共5个时间点给予机械通气,监测氧合指数(PaO_2/FiO_2)及胸肺动态顺应性(Cdyn).肺组织常规固定进行病理学检查.结果 12、24、36、48、72 h大鼠PaO_2/FiO_2分别为(30.71±7.95)kPa、(21.66±5.34)kPa、(21.09±4.75)kPa、(25.01±8.78)kPa、(33.82±8.02)kPa.均低于正常组(63.82±3.03)kPa(P＜0.01).12、24、36、48、72 h大鼠Cdyn分别为(4.23±0.13)ml/(kg·kPa)、(4.19±0.96)ml/(kg·kPa)、(4.28±0.69)ml/(kg·kPa)、(4.44±0.62)ml/(kg·kPa)、(4.58±0.35)ml/(kg·kPa),均低于正常组(8.16±0.78)ml/(kg·kPa)(P＜0.01).12、24、36、48、72 h大鼠ALI发生率分别为71.4%、100%、100%、83.3%、57.1%;ARDS发生率分别为28.6%、85.7%、83.3%、66.7%、14.3%.病理学改变方面,随着感染时间延长,由肺内少量渗出液到肺泡壁明显水肿.肺泡腔内出现大量渗出液和炎症细胞,可见透明膜形成以及严重肺泡萎陷,但在72 h炎症已明显减轻.结论本实验经气管滴入大肠杆菌建立了肺内源性ALI/ARDS动物模型,分时间点观察了病情演变,为有效利用动物模型提供了资料.
목적 건립대서폐내원성급성폐손상/급성호흡군박종합정(ALI/ARDS)모형.방법 대장간균[O111B4,(4.0～6.0)×1012 CFU/L]3 ml/kg기관주사제작대서폐내원성ALI모형.분별우주사대장간균후12、24、36、48、72 h공5개시간점급여궤계통기,감측양합지수(PaO_2/FiO_2)급흉폐동태순응성(Cdyn).폐조직상규고정진행병이학검사.결과 12、24、36、48、72 h대서PaO_2/FiO_2분별위(30.71±7.95)kPa、(21.66±5.34)kPa、(21.09±4.75)kPa、(25.01±8.78)kPa、(33.82±8.02)kPa.균저우정상조(63.82±3.03)kPa(P＜0.01).12、24、36、48、72 h대서Cdyn분별위(4.23±0.13)ml/(kg·kPa)、(4.19±0.96)ml/(kg·kPa)、(4.28±0.69)ml/(kg·kPa)、(4.44±0.62)ml/(kg·kPa)、(4.58±0.35)ml/(kg·kPa),균저우정상조(8.16±0.78)ml/(kg·kPa)(P＜0.01).12、24、36、48、72 h대서ALI발생솔분별위71.4%、100%、100%、83.3%、57.1%;ARDS발생솔분별위28.6%、85.7%、83.3%、66.7%、14.3%.병이학개변방면,수착감염시간연장,유폐내소량삼출액도폐포벽명현수종.폐포강내출현대량삼출액화염증세포,가견투명막형성이급엄중폐포위함,단재72 h염증이명현감경.결론 본실험경기관적입대장간균건립료폐내원성ALI/ARDS동물모형,분시간점관찰료병정연변,위유효이용동물모형제공료자료.
Objective To establish pulmonary acute lung injury(ALI)model in rats.Methods ALI model was induced in rats by intratracheal Escherichia coli injection[3 ml/kg,O111B4,(4.0～6.0)×1012 CFU/L].Mechanical ventilation was applied 12,24,36,48 and 72 h after Escherichia coli injection,PaO_2/FiO_2 and dynamic compliance were recorded,and the normal control group was also subjected to mechanical ventilation.After the experiment,lungs were fixed with formalin to perform pathological examination.Results At 12,24,36,48 and 72 h,the PaO_2/FiO_2 were(30.71±7.95)kPa,(21.66±5.34)kPa,(21.09±4.75)kPa,(25.01±8.78)kPa and(33.82±8.02)kPa,respectively,which were significantly lower than that in the normal control group(63.82±3.03)kPa(P＜0.01).At 12,24,36,48 and 72 h,the Cdyn were(4.23±0.13)ml/(kg·kPa),(4.19±0.96)ml/(kg·kPa),(4.28±0.69)ml/(kg·kPa),(4.44±0.62)ml/(kg·kPa)and(4.58±0.35)ml/(kg·kPa)respectively,which were significantly lower than that in the normal control group(8.16±0.78)mL/(kg·kPa)(P＜0.01).At 12,24,36,48 and 72,the percentage of ALI was 71.4%,100.0%,100.0%,83.3%and 57.1%respectively,and the percentage of ARDS was 28.6%,85.7%,83.3%,66.7%,14.3%respectively.As for pathological examinations,predominance of alveolar collapse,fibrinous exudates,alveolar wall edema and neutrophil recruitment into the alveolar space was observed.Hyaline membrane formation was found.At 72 h,inflammation was relieved.Conclusion We successfully established pulmonary ALI/ARDS model in rats induced by intratracheal Escherichia coli injection,and acquired some useful information by observing the lung function and morphological changes at different time points.