文章摘要
瑞芬太尼后处理对大鼠心肌缺血-再灌注损伤的影响
Effects of remifentanil postconditioning after myocardial ischemia reperfusion in rats
  
DOI:
中文关键词: 瑞芬太尼  后处理  大鼠  心肌缺血-再灌注损伤
英文关键词: Remifentanil  Postconditioning  Rat  Myocardial ischemia reperfusion injury
基金项目:
作者单位E-mail
郑宏 350000,解放军福州总医院麻醉科  
林鹏焘 350000,解放军福州总医院麻醉科  
陈文华 350000,解放军福州总医院麻醉科 whc6202@163.com 
王兰兰 350000,解放军福州总医院麻醉科  
李丽珍 350000,解放军福州总医院麻醉科  
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中文摘要:
      
目的 探讨瑞芬太尼后处理对缺血-再灌注心肌的影响及其机制。
方法 清洁级健康雄性SD大鼠78只,体重200~250 g,随机分为六组:假手术组(S组)、单纯缺血-再灌注组(IR组)、纳洛酮拮抗剂组(NAL组)、瑞芬太尼5 μg·kg-1·min-1后处理组(R1组)、瑞芬太尼10 μg·kg-1·min-1后处理组(R2组)和瑞芬太尼20 μg·kg-1·min-1后处理组(R3组),每组13只。S组仅在冠状动脉左前降支处穿线,但不结扎;IR组结扎冠状动脉左前降支,缺血45 min,再灌注24 h;R1、R2和R3组在缺血35 min时,分别静脉输注瑞芬太尼5、10和20 μg·kg-1·min-1,10 min后再灌注24 h; NAL组在心肌缺血25 min时,静脉注射纳洛酮0.1 mg·kg-1,10 min后静脉输注瑞芬太尼10 μg·kg-1·min-1,10 min后再灌注24 h。观察心肌梗死面积和心肌病理学变化,同时测定血清肌钙蛋白I(cTnI)、乳酸脱氢酶(LDH)、肌酸激酶同工酶MB(CK-MB)的浓度。
结果 与S组比较,IR、NAL、R1、R2和R3组血清cTnI、LDH、CK-MB浓度明显升高,心肌梗死面积百分比明显增大(P<0.05),心肌细胞损伤增多;与IR组比较,R1、R2和R3组血清cTnI、LDH、CK-MB浓度明显降低,心肌梗死面积百分比明显减小(P<0.05),心肌细胞损伤减少(P<0.05)。
结论 瑞芬太尼后处理可减轻大鼠心肌缺血-再灌注损伤,其机制与瑞芬太尼激活阿片受体有关,此作用具有量效“封顶”效应。
英文摘要:
      
Objective To explore the effect of remifentanil postconditioning on rats subjected to ischemia reperfusion injury and the relative mechanisms.
Methods Seventy-eight Sprague-Dawley rats, weighing 200-250 g, were randomly divided into six groups (n=13): sham group (group S), ischemia/reperfusion group (group IR), naloxone group (group NAL), 5 μg·kg-1·min-1 remifentanil postconditioning group (group R1), 10 μg·kg-1·min-1remifentanil postconditioning group (group R2) and 20 μg·kg-1·min-1remifentanil postconditioning group (group R3). Group IR was given 45 min ischemia in the left descending anterior (LAD), followed by a 24-h period of reperfusion. Groups R1, R2, R3 received 10 min of remifentanil infusion of 5, 10 and 20 μg·kg-1·min-1 after 35 min ischemia followed by a 24 h period of reperfusion. Group NAL was given injection of naloxone 0.1 mg/kg at the point of 25 min myocardial ischemia, after 10 min, then remifentanil 10 μg·kg-1·min-1 for 10 min. The myocardial infarct size and pathological changes of myocardial tissue were observed, serum cTnI, LDH and CK-MB level were measured.
Results Compared with group S, serum cTnI, LDH and CK-MB and myocardial infarct size were markedly increased in groups IR, NAL, R1, R2 and R3 (P<0.05), and pathologic injury of myocardial cells were augmented. In comparison with group IR, the indexes were decreased in groups R1, R2 and R3 (P<0.05).
Conclusion Remifentanil postconditioning could protect against myocardial ischemia reperfusion injury in rats. The protection may be related to remifentanil activating the opioid receptors. There were ceiling effects of remifentanil postconditioning induced myocardial protection.
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