中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2010年
10期
1204-1207
,共4页
曹译匀%孟尽海%廖红%屈伸
曹譯勻%孟儘海%廖紅%屈伸
조역균%맹진해%료홍%굴신
哌啶类%脂质过氧化作用%心肌再灌注损伤
哌啶類%脂質過氧化作用%心肌再灌註損傷
고정류%지질과양화작용%심기재관주손상
Piperidines%Lipid peroxidation%Myocardial reperfusion injury
目的 评价瑞芬太尼预先给药对兔心肌缺血再灌注时脂质过氧化反应的影响.方法 家兔40只,雌雄不拘,体重1.5~2.5 kg,随机分为5组(n=8),Ⅱ组、Ⅲ组和V组采用静脉注射垂体后叶素2.5 U/kg的方法制备急性心肌缺血模型,Ⅰ组和Ⅳ组给予等容量生理盐水.Ⅲ组静脉注射吗啡3.3 mg/kg后30 min给予垂体后叶素前;Ⅳ组静脉输注瑞芬太尼3.3μg·kg-1·min-130 min时给予生理盐水;V组静脉输注瑞芬太尼3.3μg·kg-1·min-1 30 min时给予垂体后叶素.于给予垂体后叶素前即刻(T1)、给予垂体后叶素后24 h(T2)、48 h(T3)时采集颈内静脉血样,测定血清心肌肌钙蛋白I(cTnI)浓度.取心肌组织,测定超氧化物歧化酶(SOD)活性及丙二醛(MDA)含量.电镜下观察心肌组织超微结构.结果 与Ⅰ组比较,Ⅱ组血清cTnI浓度和心肌组织MDA含量升高,心肌组织SOD活性降低(P<0.01);与Ⅱ组比较,Ⅲ组及V组血清cTnI浓度和MDA含量降低,心肌组织SOD活性升高(P<0.05或0.01).电镜下Ⅴ组心肌损伤程度轻于Ⅱ组.结论瑞芬太尼预先给药可抑制脂质过氧化反应,从而减轻兔心肌缺血再灌注损伤.
目的 評價瑞芬太尼預先給藥對兔心肌缺血再灌註時脂質過氧化反應的影響.方法 傢兔40隻,雌雄不拘,體重1.5~2.5 kg,隨機分為5組(n=8),Ⅱ組、Ⅲ組和V組採用靜脈註射垂體後葉素2.5 U/kg的方法製備急性心肌缺血模型,Ⅰ組和Ⅳ組給予等容量生理鹽水.Ⅲ組靜脈註射嗎啡3.3 mg/kg後30 min給予垂體後葉素前;Ⅳ組靜脈輸註瑞芬太尼3.3μg·kg-1·min-130 min時給予生理鹽水;V組靜脈輸註瑞芬太尼3.3μg·kg-1·min-1 30 min時給予垂體後葉素.于給予垂體後葉素前即刻(T1)、給予垂體後葉素後24 h(T2)、48 h(T3)時採集頸內靜脈血樣,測定血清心肌肌鈣蛋白I(cTnI)濃度.取心肌組織,測定超氧化物歧化酶(SOD)活性及丙二醛(MDA)含量.電鏡下觀察心肌組織超微結構.結果 與Ⅰ組比較,Ⅱ組血清cTnI濃度和心肌組織MDA含量升高,心肌組織SOD活性降低(P<0.01);與Ⅱ組比較,Ⅲ組及V組血清cTnI濃度和MDA含量降低,心肌組織SOD活性升高(P<0.05或0.01).電鏡下Ⅴ組心肌損傷程度輕于Ⅱ組.結論瑞芬太尼預先給藥可抑製脂質過氧化反應,從而減輕兔心肌缺血再灌註損傷.
목적 평개서분태니예선급약대토심기결혈재관주시지질과양화반응적영향.방법 가토40지,자웅불구,체중1.5~2.5 kg,수궤분위5조(n=8),Ⅱ조、Ⅲ조화V조채용정맥주사수체후협소2.5 U/kg적방법제비급성심기결혈모형,Ⅰ조화Ⅳ조급여등용량생리염수.Ⅲ조정맥주사마배3.3 mg/kg후30 min급여수체후협소전;Ⅳ조정맥수주서분태니3.3μg·kg-1·min-130 min시급여생리염수;V조정맥수주서분태니3.3μg·kg-1·min-1 30 min시급여수체후협소.우급여수체후협소전즉각(T1)、급여수체후협소후24 h(T2)、48 h(T3)시채집경내정맥혈양,측정혈청심기기개단백I(cTnI)농도.취심기조직,측정초양화물기화매(SOD)활성급병이철(MDA)함량.전경하관찰심기조직초미결구.결과 여Ⅰ조비교,Ⅱ조혈청cTnI농도화심기조직MDA함량승고,심기조직SOD활성강저(P<0.01);여Ⅱ조비교,Ⅲ조급V조혈청cTnI농도화MDA함량강저,심기조직SOD활성승고(P<0.05혹0.01).전경하Ⅴ조심기손상정도경우Ⅱ조.결론서분태니예선급약가억제지질과양화반응,종이감경토심기결혈재관주손상.
Objective To investigate the effect of remifentanil pretreatment on lipid peroxidation following acute myocardial ischemia/reperfusion (1/R) in rabbits. Methods Forty healthy adult rabbits of both sexes weighing 1.5-2.5 kg were randomly divided into 5 groups (n = 8 each): group control (group Ⅰ ); group I/R(group Ⅱ ); group morphine pretreatment + I/R (group Ⅲ ); group remifentanil (group Ⅳ ) and group remifentanil pretreatment + I/R (group Ⅴ ). The animals were anesthetized with intraperitoneal 2% pentobarbital 45 mg/kg and were mechanically ventilated after tracheal intubation. PET CO2 was maintained between 35-45 mm Hg. Myocardial I/R was induced by iv pituitrin 2.5 U/kg in group Ⅱ , Ⅲ and Ⅴ. In group Ⅰ and Ⅳ normal saline 0.3 ml/kg was injected iv instead of pituitrin. In group Ⅲ morphine 3.3 mg/kg was injected iv at 30 min before iv pituitrin. In group Ⅳ and V remifentanil was infused at 3.3 μg· kg-1 ·min-1 for 30 min before iv normal saline and pituitrin.Venous blood samples were taken before (baseline) and at 24 h and 48 h after iv pituitrin for determination of serum cTnI concentration. The myocardial specimens were taken at T3 after blood sampling for microscopic examination and determination of SOD activity and MDA content. Results Intravenous pituitrin 2.5 U/kg significantly increased serum cTnI concentration and myocardial MDA content and decreased myocardial SOD activity in group Ⅱas compared with group Ⅰ . Morphine or remifentanil preatment significantly attenuated the myocardial I/R-induced changes mentioned above. Microscopic examination showed that myocardial tissue damages were ameliorated in group V as compared with group Ⅱ . Conclusion Remifentanil pretreament can attenuate acute myocardial ischemic injury by inhibiting lipid peroxidation.