CAJ | 학술논문

目的探讨大肠杆菌导致的肺内源性急性肺损伤(ALI)模型大鼠肾上腺皮质功能的变化.方法 Wistar大鼠气管注射3 ml/kg大肠杆菌混悬液[(4.4～5.6)×10~(12) CFU/L],制作大鼠肺内源性ALl/急性呼吸窘迫综合征(ARDS)模型,存活大鼠随机分为三组,于滴人大肠杆菌混悬液术后6 h(η=10)、24 h(η=10)、36 h(η=10)3个时间点进行观察.每个时间点各8只大鼠作为对照(NS组,气管注射0.9%盐水3 mL/kg).各组分别于术后6、24、36 h 3个时间点经气管切开插管机械通气,颈总动脉插管监测其血压、血气,取血,PaO_2/FiO_2<300 mmHg(39.9 kPa)为ALI,PaO_2/FiO_2<200 mmHg(26.6 kPa)为ARDS,符合上述标准的模型大鼠纳入实验.给予小剂量ACTH作ACTH刺激试验,应用ELISA法测定血清中皮质酮、ACTH含量.结果血浆ACTH水平在模型组大鼠各时间点均高于对照组(P均<0.01),24 h达峰值(P<0.01).模型组6 h、24 h时间点皮质酮较对照组明显升高(P<0.01,P<0.05),36 h模型大鼠皮质酮低于对照组(P<0.05).模型组6 h皮质酮达峰值,高于24 h时间点皮质酮水平(P<0.05).模型组大鼠在ACTH刺激后皮质酮于各时间点上升的幅度均低于对照组(6 h,P<0.05;24 h、36 h,P均<0.01).结论 ALI大鼠早期即可存在肾上腺皮质功能不全(AI),随着病情进展,肾上腺储备功能下降,肾上腺对ACTH反应程度降低,存在AI的大鼠比例增加,通过小剂量ACTH刺激试验可评价ALI大鼠肾上腺皮质功能.
목적 탐토대장간균도치적폐내원성급성폐손상(ALI)모형대서신상선피질공능적변화.방법 Wistar대서기관주사3 ml/kg대장간균혼현액[(4.4～5.6)×10~(12) CFU/L],제작대서폐내원성ALl/급성호흡군박종합정(ARDS)모형,존활대서수궤분위삼조,우적인대장간균혼현액술후6 h(η=10)、24 h(η=10)、36 h(η=10)3개시간점진행관찰.매개시간점각8지대서작위대조(NS조,기관주사0.9%염수3 mL/kg).각조분별우술후6、24、36 h 3개시간점경기관절개삽관궤계통기,경총동맥삽관감측기혈압、혈기,취혈,PaO_2/FiO_2<300 mmHg(39.9 kPa)위ALI,PaO_2/FiO_2<200 mmHg(26.6 kPa)위ARDS,부합상술표준적모형대서납입실험.급여소제량ACTH작ACTH자격시험,응용ELISA법측정혈청중피질동、ACTH함량.결과혈장ACTH수평재모형조대서각시간점균고우대조조(P균<0.01),24 h체봉치(P<0.01).모형조6 h、24 h시간점피질동교대조조명현승고(P<0.01,P<0.05),36 h모형대서피질동저우대조조(P<0.05).모형조6 h피질동체봉치,고우24 h시간점피질동수평(P<0.05).모형조대서재ACTH자격후피질동우각시간점상승적폭도균저우대조조(6 h,P<0.05;24 h、36 h,P균<0.01).결론 ALI대서조기즉가존재신상선피질공능불전(AI),수착병정진전,신상선저비공능하강,신상선대ACTH반응정도강저,존재AI적대서비례증가,통과소제량ACTH자격시험가평개ALI대서신상선피질공능.
Objective To study the adrenal function in rats with pulmonary acute lung injury (ALI) induced by Escherichia coli (0111B4) . Methods ALI rat model was induced by intratracheal injection of E.coli (3 ml/kg,0111B4,(4.4-5.6) x 10~(12) CFU/L).ALI rats were then randomly divided into three groups,and each group had 10 rats.Mechanical ventilation was applied at three time points,6 hours,24 hours,and 36 hours after injection At each time point 8 rats were used as control with saline administered intratracheally.The plasma ACTH and corticosterone levels were measured after stimulated by 100 μg porcine ACTH.Results Compared with control group,the model group had a higher level of plasma ACTH at each time point (P < 0.01).The plasma ACTH level reached the peak at 24 hours.The model group had a higher level of plasma corticosterone at 6 hours (P < 0.01) and 24 hours (P <0.05),but had a lower level of plasma corticosterone at 36 hours (P < 0.05).The plasma corticosterone level reached the peak at 6 hours in model group,which was higher than 24 hours (P < 0.05).After stimulated by ACTH,the increased levels of corticosterone were lower in model group than those in control group (6 hours,P < 0.05; 24 hours and 36 hours,P < 0.01).Conclusions Adrenal dysfunction may occur at early stage of ALI in rats.With the disease developed,adrenal response to ACTH decreased.Low dose corticotrophin-stimulated test could evaluate adrenal function in rats with pulmonary ALI induced by Escherichia coli (O111B4).