中国危重病急救医学
中國危重病急救醫學
중국위중병급구의학
CHINESE CRITICAL CARE MEDICINE
2011年
4期
236-238,后插2
,共4页
汤展宏%盘璇%胡军涛%季晓芳
湯展宏%盤璇%鬍軍濤%季曉芳
탕전굉%반선%호군도%계효방
亚低温%脂多糖%肺损伤,急性%肺泡表面活性蛋白A
亞低溫%脂多糖%肺損傷,急性%肺泡錶麵活性蛋白A
아저온%지다당%폐손상,급성%폐포표면활성단백A
Hypothermia%Lipopolysaccharide%Acute lung injury%Surfactant protein A
目的 探讨亚低温对内毒素脂多糖(LPS)诱导急性肺损伤(ALI)大鼠肺泡表面活性蛋白A(SP-A)含量的影响.方法 按随机数字表法将40只雄性Wistar大鼠分组.采用气管内滴入LPS制备ALI动物模型;对照组气管内只滴人生理盐水.模型组和对照组分别于术后1 h和8 h处死8只大鼠;亚低温组于滴入LPS 1 h后将体温降低并维持在32.5～33.0℃,8 h后处死8只大鼠.各组分别于术前及术后1 h、8 h测定动脉血气,并计算氧合指数(PaO2/FiO2);采用酶联免疫吸附法检测支气管肺泡灌洗液(BALF)中SP-A含量;光镜下观察肺组织形态结构的变化.结果 气管内滴入LPS 1 h后,大鼠PaO2/FiO2均达到ALI的诊断标准.与对照1 h组比较,模型1 h组BALF中SP-A含量(μg/L)明显降低(53.27±1.95比74.81±6.55,P＜0.01);模型8 h组和亚低温8 h组SP-A含量(4.35±2.76和51.36±2.33)均较对照8 h组(70.81±5.01)明显降低,但亚低温8 h组SP-A含量较模型8 h组明显增高(均P＜0.01).光镜下观察,对照1 h和8 h组肺泡结构基本正常;模型8 h组肺组织炎症反应最重;模型1 h组和亚低温8 h组肺组织炎症反应较模型8 h组有所减轻.结论 亚低温能延缓内毒素诱导的ALI大鼠早期肺泡内SP-A含量下降的程度,在一定程度上可减轻肺损伤.
目的 探討亞低溫對內毒素脂多糖(LPS)誘導急性肺損傷(ALI)大鼠肺泡錶麵活性蛋白A(SP-A)含量的影響.方法 按隨機數字錶法將40隻雄性Wistar大鼠分組.採用氣管內滴入LPS製備ALI動物模型;對照組氣管內隻滴人生理鹽水.模型組和對照組分彆于術後1 h和8 h處死8隻大鼠;亞低溫組于滴入LPS 1 h後將體溫降低併維持在32.5～33.0℃,8 h後處死8隻大鼠.各組分彆于術前及術後1 h、8 h測定動脈血氣,併計算氧閤指數(PaO2/FiO2);採用酶聯免疫吸附法檢測支氣管肺泡灌洗液(BALF)中SP-A含量;光鏡下觀察肺組織形態結構的變化.結果 氣管內滴入LPS 1 h後,大鼠PaO2/FiO2均達到ALI的診斷標準.與對照1 h組比較,模型1 h組BALF中SP-A含量(μg/L)明顯降低(53.27±1.95比74.81±6.55,P＜0.01);模型8 h組和亞低溫8 h組SP-A含量(4.35±2.76和51.36±2.33)均較對照8 h組(70.81±5.01)明顯降低,但亞低溫8 h組SP-A含量較模型8 h組明顯增高(均P＜0.01).光鏡下觀察,對照1 h和8 h組肺泡結構基本正常;模型8 h組肺組織炎癥反應最重;模型1 h組和亞低溫8 h組肺組織炎癥反應較模型8 h組有所減輕.結論 亞低溫能延緩內毒素誘導的ALI大鼠早期肺泡內SP-A含量下降的程度,在一定程度上可減輕肺損傷.
목적 탐토아저온대내독소지다당(LPS)유도급성폐손상(ALI)대서폐포표면활성단백A(SP-A)함량적영향.방법 안수궤수자표법장40지웅성Wistar대서분조.채용기관내적입LPS제비ALI동물모형;대조조기관내지적인생리염수.모형조화대조조분별우술후1 h화8 h처사8지대서;아저온조우적입LPS 1 h후장체온강저병유지재32.5～33.0℃,8 h후처사8지대서.각조분별우술전급술후1 h、8 h측정동맥혈기,병계산양합지수(PaO2/FiO2);채용매련면역흡부법검측지기관폐포관세액(BALF)중SP-A함량;광경하관찰폐조직형태결구적변화.결과 기관내적입LPS 1 h후,대서PaO2/FiO2균체도ALI적진단표준.여대조1 h조비교,모형1 h조BALF중SP-A함량(μg/L)명현강저(53.27±1.95비74.81±6.55,P＜0.01);모형8 h조화아저온8 h조SP-A함량(4.35±2.76화51.36±2.33)균교대조8 h조(70.81±5.01)명현강저,단아저온8 h조SP-A함량교모형8 h조명현증고(균P＜0.01).광경하관찰,대조1 h화8 h조폐포결구기본정상;모형8 h조폐조직염증반응최중;모형1 h조화아저온8 h조폐조직염증반응교모형8 h조유소감경.결론 아저온능연완내독소유도적ALI대서조기폐포내SP-A함량하강적정도,재일정정도상가감경폐손상.
Objective To investigate the effect of hypothermia (HT) on the concentration of surfactant protein A (SP-A) during lipopolysaccharide (LPS) induced acute lung injury (ALI) in rats.Methods Forty male Wistar rats were randomly divided into three groups. The ALI model was reproduced by LPS intratracheal instillation; only saline was instilled intratracheally for control group. Rats in both model group and control group were sacrificed respectively at 1 hour and 8 hours (each n= 8). In HT group the body temperature was lowered to 32. 5 - 33.0 ℃ 1 hour after LPS instillation, and 8 rats were sacrificed st 8 hours. The arterial blood gas was determined in all the groups before and 1 hour and 8 hours after instillation of saline or LPS, and the oxygenation index (PaO2/FiO2) was calculated. The concentration of SP-A in bronchoalveolar lavage fluid (BALF) was determined by enzyme linked immunosorbent assay. The morphological changes in lung tissue of rats were observed under light microscope. Results At 1 hour after intratracheal instillation of LPS, the PaO2/FiO2 of each group reached the diagnostic criterion of ALI.Compared with control 1-hour group, the SP-A (μg/L) in BALF of model 1-hour group was decreased (53. 27±1.95 vs. 74. 81±6. 55, P＜0. 01); the SP-A in model 8-hour group and HT 8-hour group (4.35±2. 76 and 51.36±2. 33) was both obviously decreased compared with control 8-hour group (70. 81±-5. 01,both P＜0. 01). Compared with model 8-hour group, the SP-A of HT 8-hour group was obviously increased (P＜0. 01). Results of light microscopic examination, it was revealed that the alveolar structure of control 1-hour group and control 8-hour group was almost normal. Inflammatory response in lung tissues in model 8-hour group was found to be most serious; compared with model 8-hour group, inflammatory response in lung tissues in model 1-hour group and HT 8-hour group was reduced in certain degree. Conclusion A certain extent of HT may reduce lung injury of early endotoxin-induced ALI rats by delaying lowering of alveolar SP-A levels.
