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目的探讨吗啡延迟预处理对兔心肌缺血再灌注损伤的保护机制。方法 30只健康新西兰雄性大白兔随机分成3组:假手术组(C组)、缺血再灌注组(I/R组)、吗啡预处理组(M组),每组10只。C组仅行左冠状动脉套线而不阻断160min;I/R组行左冠状动脉阻断40min,再灌注120min;M组在静注吗啡1.0mg/kg24h后处理同I/R组。各组分别于左冠状动脉前降支阻断前20min(T1)、左冠状动脉前降支阻断20min(T2)、左冠状动脉前降支阻断40min(T3)、心肌再灌注1h(T4)、心肌再灌注2h(T5)5个时点抽取颈内动脉血测定血清中TNF-α含量。再灌注120min后,免疫印迹法测心肌p38丝裂原活化蛋白激酶(P38MAPK)活性水平,同时测心肌梗死面积。结果与I/R组比,M组TNF-α含量降低,p38MAPK活性降低,心肌梗死面积减少[M组(21.5%±2.4)%,I/R组(37.8%±1.7)%]。上述差异均有统计学意义(均P<0.05)。结论吗啡延迟预处理对心肌缺血再灌注损伤的保护作用可能通过抑制心肌p38MAPK的活性、减少TNF-α生成来实现。
Objective To investigate the protective effect of morphine delayed preconditioning on myocardial ischemia-reperfusion injury in rabbits. Methods Thirty healthy male New Zealand white rabbits were randomly divided into three groups: sham operation group (C group), ischemia reperfusion group (I / R group) and morphine preconditioning group (M group). In group C, only the left coronary artery was sutured without interruption for 160 min. Left coronary artery occlusion was performed in I / R group for 40 min and reperfusion for 120 min. M group was treated with morphine 1.0 mg / kg for 24 h followed by I / R group. The left coronary artery occlusion of the left anterior descending coronary artery 20 minutes (T1), left anterior descending coronary artery 20 minutes (T2), left anterior descending artery occlusion 40 minutes (T3), myocardial reperfusion 1 hour (T4) ), 2h after myocardial reperfusion (T5), the carotid artery blood was taken for determination of the content of TNF-α in serum. After 120 min of reperfusion, the activity of p38 mitogen-activated protein kinase (P38MAPK) was detected by immunoblotting and myocardial infarct size was measured at the same time. Results Compared with I / R group, the content of TNF-α in M group decreased, the activity of p38MAPK decreased and the area of myocardial infarction decreased [M group (21.5% ± 2.4)%, I / R group, 37.8% ± 1.7%]. The above differences were statistically significant (all P <0.05). Conclusion The protective effects of morphine delayed preconditioning on myocardial ischemia-reperfusion injury may be achieved by inhibiting the activity of p38 MAPK and decreasing the production of TNF-α.