中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2009年
11期
1040-1043
,共4页
哌啶类%内毒素血症%呼吸窘迫综合征%成人
哌啶類%內毒素血癥%呼吸窘迫綜閤徵%成人
고정류%내독소혈증%호흡군박종합정%성인
Piperidines%Endotoxemia%Respiratory distress syndrome%adult
目的 探讨瑞芬太尼对兔内毒素性急性肺损伤(Au)的影响.方法 健康成年雄性新西兰大白兔30只,体重2.5～3.5 kg,随机分为5组(n=6):对照组(C组)、ALI组、低剂量瑞芬太尼组(LR组)、中剂量瑞芬太尼组(MR组)和高剂量瑞芬太尼组(HR组).C组经30 min静脉输注生理盐水10 ml;ALI组经30 min静脉输注大肠杆菌内毒索(LPS)0.5 mG/kg;LR组、MR组和HR组分别静脉输注瑞芬太尼0.2、0.4和0.8μg·kg~(-1)·min~(-1)至处死,输注15 min时开始给予LPS,方法同ALI组.于LPS输注前即刻(T_0)、输注结束后1、2.5、5.5 h时记录平均动脉血压(MAP)、心率(HR)和气道峰压(P_(peak),测定动脉血氧分压(PaO_2)和血浆细胞间粘附分子1(ICAM-1)浓度,称量肺组织湿重(W)和干重(D),计算W/D比,并在光镜和电镜下观察肺组织病理学结果.结果 与C组比较,ALI组MAP、HR和PaO_2,降低,W/D比、P_(peak)和血浆ICAM-1浓度升高(P<0.05);与ALI组比较,LR组、MR组和HR组MAP、HR 升高,肺组织W/D比降低,P(peak)和血浆ICAM-1浓度降低,PaO_2升高(P<0.05);与LR组比较,MR组和HR组MAP、HR、P(peak)、血浆ICAM-1浓度和肺组织W/D比降低,PaO_2升高(P<0.05);与MR组比较,HR组注肺组织W/D比降低,PaO_2升高(P<0.05).LR组、MR组和HR组肺组织病理学损伤较ALI组减轻.结论 瑞芬太尼可减轻兔内毒素性急性肺损伤,且呈剂量依赖性,其机制可能与抑制ICAM-1的表达有关.
目的 探討瑞芬太尼對兔內毒素性急性肺損傷(Au)的影響.方法 健康成年雄性新西蘭大白兔30隻,體重2.5～3.5 kg,隨機分為5組(n=6):對照組(C組)、ALI組、低劑量瑞芬太尼組(LR組)、中劑量瑞芬太尼組(MR組)和高劑量瑞芬太尼組(HR組).C組經30 min靜脈輸註生理鹽水10 ml;ALI組經30 min靜脈輸註大腸桿菌內毒索(LPS)0.5 mG/kg;LR組、MR組和HR組分彆靜脈輸註瑞芬太尼0.2、0.4和0.8μg·kg~(-1)·min~(-1)至處死,輸註15 min時開始給予LPS,方法同ALI組.于LPS輸註前即刻(T_0)、輸註結束後1、2.5、5.5 h時記錄平均動脈血壓(MAP)、心率(HR)和氣道峰壓(P_(peak),測定動脈血氧分壓(PaO_2)和血漿細胞間粘附分子1(ICAM-1)濃度,稱量肺組織濕重(W)和榦重(D),計算W/D比,併在光鏡和電鏡下觀察肺組織病理學結果.結果 與C組比較,ALI組MAP、HR和PaO_2,降低,W/D比、P_(peak)和血漿ICAM-1濃度升高(P<0.05);與ALI組比較,LR組、MR組和HR組MAP、HR 升高,肺組織W/D比降低,P(peak)和血漿ICAM-1濃度降低,PaO_2升高(P<0.05);與LR組比較,MR組和HR組MAP、HR、P(peak)、血漿ICAM-1濃度和肺組織W/D比降低,PaO_2升高(P<0.05);與MR組比較,HR組註肺組織W/D比降低,PaO_2升高(P<0.05).LR組、MR組和HR組肺組織病理學損傷較ALI組減輕.結論 瑞芬太尼可減輕兔內毒素性急性肺損傷,且呈劑量依賴性,其機製可能與抑製ICAM-1的錶達有關.
목적 탐토서분태니대토내독소성급성폐손상(Au)적영향.방법 건강성년웅성신서란대백토30지,체중2.5～3.5 kg,수궤분위5조(n=6):대조조(C조)、ALI조、저제량서분태니조(LR조)、중제량서분태니조(MR조)화고제량서분태니조(HR조).C조경30 min정맥수주생리염수10 ml;ALI조경30 min정맥수주대장간균내독색(LPS)0.5 mG/kg;LR조、MR조화HR조분별정맥수주서분태니0.2、0.4화0.8μg·kg~(-1)·min~(-1)지처사,수주15 min시개시급여LPS,방법동ALI조.우LPS수주전즉각(T_0)、수주결속후1、2.5、5.5 h시기록평균동맥혈압(MAP)、심솔(HR)화기도봉압(P_(peak),측정동맥혈양분압(PaO_2)화혈장세포간점부분자1(ICAM-1)농도,칭량폐조직습중(W)화간중(D),계산W/D비,병재광경화전경하관찰폐조직병이학결과.결과 여C조비교,ALI조MAP、HR화PaO_2,강저,W/D비、P_(peak)화혈장ICAM-1농도승고(P<0.05);여ALI조비교,LR조、MR조화HR조MAP、HR 승고,폐조직W/D비강저,P(peak)화혈장ICAM-1농도강저,PaO_2승고(P<0.05);여LR조비교,MR조화HR조MAP、HR、P(peak)、혈장ICAM-1농도화폐조직W/D비강저,PaO_2승고(P<0.05);여MR조비교,HR조주폐조직W/D비강저,PaO_2승고(P<0.05).LR조、MR조화HR조폐조직병이학손상교ALI조감경.결론 서분태니가감경토내독소성급성폐손상,차정제량의뢰성,기궤제가능여억제ICAM-1적표체유관.
Objective To investigate the effects of remifentanil on lipopolysaccharide ( LPS)-induced acute lung injury (ALI) in rabbits.Methods Thirty healthy male New Zealand white rabbits weighing 2.5-3.5 kg were randomly divided into 5 groups ( n = 6 each) : group Ⅰ control (group C) ;group Ⅱ ALI;group Ⅲ, Ⅳ, Ⅴ low, median and high dose RF + LPS (group LR, MR, HR) . The animals were anesthetized with intravenous 3% pentobarbital sodium 30 mg/kg, tracheostomized and mechanically ventilated. The carotid artery and jugular vein were cannulated for MAP and HR monitoring, blood sampling, and fluid and drug administration. LPS 0.5 mg/kg in 10 ml of normal saline (NS) was infused over 30 min in group Ⅱ-Ⅴ. Remifentanil 0.2, 0.4 or 0.8 μg·kg~(-1)·min~(-1) was infused starting from 15 min before LPS administration until the death of the animals. MAP, HR, peak airway pressure (P_(peak) ), PaO_2 and plasma intercellular adhesion molecule 1 (ICAM-1) concentration were measured immediately before LPS infusion (T_0, baseline) and at 1, 2.5 and 5.5 h after the end of LPS infusion. The animals were killed and the lungs were immediately removed for microscopic examination and determination of W/D lung weight ratio. Results MAP, HR and PaO_2 were significantly decreased while W/D ratio and P_(peak) were significantly increased after iv LPS infusion as compared with control group. LPS significantly increased plasma ICAM-1 concentration and damaged the structure of lung tissue. Remifentanil infusion significantly attenuated the LPS-induced changes in a dose-dependent manner. Conclusion RF has protective effect against LPS-induced ALI and inhibition of ICAM-1 expression is involved in the mechanism.
