CAJ | 학술논문

目的观察内毒素(革兰阴性菌细胞壁的脂多糖成分)对大鼠膈肌收缩功能及线粒体超微结构的影响,为探索呼吸衰竭发生机制提供新思路.方法将28只SD大鼠按随机数字表法分为:(1)对照组(10只)气管内灌注生理盐水;(2)实验组气管内灌注内毒素,浓度为200 ?g/ml,剂量为0.5 ml/kg,制备急性肺损伤(acute lung injury,ALI)动物模型,再分为观察4 h(内毒素4 h组,9只)及24 h(内毒素24 h组,9只)2组.然后,取膈肌肌条,用体外电生理方法测定膈肌的最大收缩力、颤搐收缩峰值及疲劳指数.另外取膈肌标本固定后做电镜检测.采用SPSS 15.0统计软件分析数据,组间比较用单因素方差分析及q检验.计量资料以x-±s表示.结果 (1)内毒素4 h组膈肌的收缩力及颤搐收缩峰值[(3.4 ±1.9)及(0.9±0.4)N/cm2,经肌肉横截面积校正]均明显低于对照组[(6.7±4.3)及(2.2±1.7)N/cm2,F值分别为3.59、3.78,P＜0.05];内毒素24 h组膈肌的收缩力及颤搐收缩峰值[(4.1±1.2)和(1.2±0.7)N/cm2]较内毒素4 h组明显恢复.(2)膈肌的疲劳指数在内毒素4 h及24 h组(分别为0.07±0.06和0.12±0.07)均较对照组(0.26±0.14)明显下降(F=9.27,P＜0.01).(3)内毒素4 h组及24 h组电镜下显示膈肌间线粒体肿胀、嵴减少,外膜模糊、变形,部分溶解破坏等超微结构的改变.结论内毒素可导致ALI大鼠膈肌的收缩力下降并易于疲劳,这可能是导致呼吸功能衰竭的原因之一.
목적 관찰내독소(혁란음성균세포벽적지다당성분)대대서격기수축공능급선립체초미결구적영향,위탐색호흡쇠갈발생궤제제공신사로.방법 장28지SD대서안수궤수자표법분위:(1)대조조(10지)기관내관주생리염수;(2)실험조기관내관주내독소,농도위200 ?g/ml,제량위0.5 ml/kg,제비급성폐손상(acute lung injury,ALI)동물모형,재분위관찰4 h(내독소4 h조,9지)급24 h(내독소24 h조,9지)2조.연후,취격기기조,용체외전생리방법측정격기적최대수축력、전휵수축봉치급피로지수.령외취격기표본고정후주전경검측.채용SPSS 15.0통계연건분석수거,조간비교용단인소방차분석급q검험.계량자료이x-±s표시.결과 (1)내독소4 h조격기적수축력급전휵수축봉치[(3.4 ±1.9)급(0.9±0.4)N/cm2,경기육횡절면적교정]균명현저우대조조[(6.7±4.3)급(2.2±1.7)N/cm2,F치분별위3.59、3.78,P＜0.05];내독소24 h조격기적수축력급전휵수축봉치[(4.1±1.2)화(1.2±0.7)N/cm2]교내독소4 h조명현회복.(2)격기적피로지수재내독소4 h급24 h조(분별위0.07±0.06화0.12±0.07)균교대조조(0.26±0.14)명현하강(F=9.27,P＜0.01).(3)내독소4 h조급24 h조전경하현시격기간선립체종창、척감소,외막모호、변형,부분용해파배등초미결구적개변.결론 내독소가도치ALI대서격기적수축력하강병역우피로,저가능시도치호흡공능쇠갈적원인지일.
Objective To investigate the diaphragmatic contractile function and mitochondrial ultrastructure in rats with acute lung injury.Methods Twenty-eight Sprague-Dawley (SD) rats were allocated randomly into three groups:a control group (n=10),a lipopolysaccharide(LPS,endotoxins)4 h group (n=9) and a LPS 24 h group(n=9).Diaphragmatic samples were taken at 4 h and 24 h after 100 ?g/kg LPS was instilled into the trachea of the rats.Normal saline (0.5 ml/kg) was instilled in the control group.Then the contractile function of the diaphragmatic samples,including the peak twitch tension,frequency depended force and fatigue index (FI),was tested in vitro.The diaphragmatic ultrastructare was also measured by electron microscopy.SPSS version 15.0 was used for statistical analysis.Data were presented as -x±s.and means were compared with analysis of variance.Results The diaphragmatic forcegenerating capacity and peak twitch tension in LPS 4 h group [(3.4±1.9);(0.9±0.4)N/cm2] decreased significantly compared to the control group [(6.7±4.3);(2.2 ±1.7)N/cm2,F=3.59 and 3.78 respectively,P＜0.05],but a marked recovery was observed in LPS 24 h group[(4.1±1.2)and(1.2±0.7)N/cm2),P＜0.05].The F1 was also reduced remarkably in LPS 4 h and LPs 24 h group(0.07±0.06;0.12±0.07) compared to the control group (0.26±0.14,F=9.27,P＜0.01.Ultrastructural examination showed mitochondria derangement at LPS 4 h and LPS 24 h groups.including swollen mitochondria with abnormal cristae, and disrupted external membrane of mitochondria. Conclusion Diaphragmatic contractile force-generating capacity decreased remarkably in rats treated with 100 ?g/kg LPS,and the diaphragm was susceptible to developing fatigue.These changes may result in respiratory failure.