东南大学学报（医学版）
東南大學學報（醫學版）
동남대학학보（의학판）
JOURNAL OF SOUTHEAST UNIVERSITY(MEDICAL SCIENCE EDITION)
2015年
1期
40-43
,共4页
杜成%孙思庆%王润丰%徐婷
杜成%孫思慶%王潤豐%徐婷
두성%손사경%왕윤봉%서정
哌啶类%油酸%急性肺损伤%新西兰大白兔
哌啶類%油痠%急性肺損傷%新西蘭大白兔
고정류%유산%급성폐손상%신서란대백토
piperidines%oleic acid%acute lung injury%New Zealand white rabbits
目的：：探讨瑞芬太尼对兔油酸性急性肺损伤( ALI )的影响。方法：选取健康成年雄性新西兰大白兔18只,由东南大学医学院实验动物中心提供,体质量2.5~3.5 kg,随机分为3组(n=6),即对照组、油酸组和瑞芬太尼组。对照组经30 min静脉输注生理盐水10 ml；油酸组经30 min静脉注射油酸0.1 ml·kg-1；瑞芬太尼组静脉输注瑞芬太尼0.2μg·kg-1·min-1至处死,输注15 min时开始给予油酸,方法同油酸组。各组大白兔分别在输入瑞芬太尼或生理盐水(以下简称给药)前和给药后6 h记录平均动脉血氧分压( PaO2),及ELISA法检测血浆细胞黏附分子1( ICAM-1)、TNF-α及IL-8浓度。给药6 h后处死动物并迅速剖胸取肺脏,肉眼观察肺组织病理改变,留取肺组织标本行电镜观察肺组织超微结构变化和测定湿干质量比。结果：瑞芬太尼组肺组织损伤程度逐渐减轻,明显轻于油酸组,瑞芬太尼能显著降低油酸性ALI兔血浆中ICAM-1、TNF-α及IL-8水平,改善ALI兔肺水肿,从而使PCO2和PaO2均明显改善。结论：瑞芬太尼能有效地抑制血管内皮细胞及肺泡上皮细胞的损伤和炎症细胞浸润,阻滞ALI时失控的炎症反应,其机制可能与抑制ICAM-1、TNF-α及IL-8的表达有关。
目的：：探討瑞芬太尼對兔油痠性急性肺損傷( ALI )的影響。方法：選取健康成年雄性新西蘭大白兔18隻,由東南大學醫學院實驗動物中心提供,體質量2.5~3.5 kg,隨機分為3組(n=6),即對照組、油痠組和瑞芬太尼組。對照組經30 min靜脈輸註生理鹽水10 ml；油痠組經30 min靜脈註射油痠0.1 ml·kg-1；瑞芬太尼組靜脈輸註瑞芬太尼0.2μg·kg-1·min-1至處死,輸註15 min時開始給予油痠,方法同油痠組。各組大白兔分彆在輸入瑞芬太尼或生理鹽水(以下簡稱給藥)前和給藥後6 h記錄平均動脈血氧分壓( PaO2),及ELISA法檢測血漿細胞黏附分子1( ICAM-1)、TNF-α及IL-8濃度。給藥6 h後處死動物併迅速剖胸取肺髒,肉眼觀察肺組織病理改變,留取肺組織標本行電鏡觀察肺組織超微結構變化和測定濕榦質量比。結果：瑞芬太尼組肺組織損傷程度逐漸減輕,明顯輕于油痠組,瑞芬太尼能顯著降低油痠性ALI兔血漿中ICAM-1、TNF-α及IL-8水平,改善ALI兔肺水腫,從而使PCO2和PaO2均明顯改善。結論：瑞芬太尼能有效地抑製血管內皮細胞及肺泡上皮細胞的損傷和炎癥細胞浸潤,阻滯ALI時失控的炎癥反應,其機製可能與抑製ICAM-1、TNF-α及IL-8的錶達有關。
목적：：탐토서분태니대토유산성급성폐손상( ALI )적영향。방법：선취건강성년웅성신서란대백토18지,유동남대학의학원실험동물중심제공,체질량2.5~3.5 kg,수궤분위3조(n=6),즉대조조、유산조화서분태니조。대조조경30 min정맥수주생리염수10 ml；유산조경30 min정맥주사유산0.1 ml·kg-1；서분태니조정맥수주서분태니0.2μg·kg-1·min-1지처사,수주15 min시개시급여유산,방법동유산조。각조대백토분별재수입서분태니혹생리염수(이하간칭급약)전화급약후6 h기록평균동맥혈양분압( PaO2),급ELISA법검측혈장세포점부분자1( ICAM-1)、TNF-α급IL-8농도。급약6 h후처사동물병신속부흉취폐장,육안관찰폐조직병리개변,류취폐조직표본행전경관찰폐조직초미결구변화화측정습간질량비。결과：서분태니조폐조직손상정도축점감경,명현경우유산조,서분태니능현저강저유산성ALI토혈장중ICAM-1、TNF-α급IL-8수평,개선ALI토폐수종,종이사PCO2화PaO2균명현개선。결론：서분태니능유효지억제혈관내피세포급폐포상피세포적손상화염증세포침윤,조체ALI시실공적염증반응,기궤제가능여억제ICAM-1、TNF-α급IL-8적표체유관。
Objective:To investigate the effects of remifentanil ( RF) on acute lung injury( ALI) induced by oleic acid in rabbits. Methods:Eighteen healthy male New Zealand white rabbits weighing 2. 5-3. 5 kg were randomly divided into 3 groups ( n=6 each):control group, oleic acid group and RF group. The animals were anesthetized with intravenous 3% pentobarbital sodium 30 mg·kg-1 , tracheostomized and mechanically ventilated. The carotid artery and jugular vein were cannulated for blood sampling, fluid and drug administration. Oleic acid 0. 1 ml·kg-1 in 10 ml of normal saline (NS) was infused over 30 min in oleic acid group and RF group. RF 0. 2 μg·kg-1· min-1 was infused starting from 15 min before oleic acid administration until the death of the animals. PaO2 and plasma ICAM-1,TNF-αand IL-8 concentration were measured immediately before oleic acid infusion and at 6 h after the end of oleic acid infusion. The animals were killed and the lungs were immediately removed for microscopic examination and determination of W/D lung weight ratio. Results: PaO2 were significantly decreased while W/D ratio were significantly increased in oleic group and RF group as compared with control group. Oleic acid significantly increased plasma ICAM-1,TNF-αand IL-8 concentration and damaged the structure of lung tissue. Remifentanil infusion significantly attenuated the OA-induced changes in a dose-dependent manner. Conclusion:RF has protective effect against acute lung injury induced by oleic acid and inhibition of ICAM-1,TNF-αand IL-8 expression is involved in the mechanism.
