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

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.

Effect of remifentanil pretreatment on lipid peroxidation following acute myocardial ischemia/reperfusion in rabbits

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.