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目的观察胺碘酮对兔心肌缺血再灌注炎症因子水平的影响。方法 30只新西兰大白兔随机分为模型对照组、胺碘酮组和假手术组,每组10只。模型对照组和胺碘酮组建立缺血再灌注无复流模型,分别于再灌注后120min取血,采用酶联免疫吸附法(ELISA)测定兔血清超敏C反应蛋白(hs-CRP)、血栓素A2(TXA2)、5-羟色胺(5-HT)水平,并进行组间比较。结果在缺血范围差异无统计学意义的条件下,胺碘酮组无复流面积明显小于模型对照组[(50.44±5.36)%vs.(78.91±3.35),P<0.01]。胺碘酮组血清hsCRP、TXA2、5-HT水平(2.80±0.18)μg/L、(3.27±0.54)mg/L、(2.63±0.73)ng/L明显低于模型对照组(3.05±0.29)μg/L、(4.57±0.78)mg/L、(3.84±0.93)ng/L,差异均有统计学意义(P<0.05)。结论胺碘酮可抑制兔急性缺血再灌注后炎症反应,减轻心肌无复流损伤程度。
Objective To observe the effect of amiodarone on the level of inflammatory cytokines in myocardial ischemia-reperfusion injury in rabbits. Methods Thirty New Zealand white rabbits were randomly divided into model control group, amiodarone group and sham operation group, 10 rats in each group. The model control group and amiodarone group were established ischemia-reperfusion no-reflow model, blood was collected at 120 min after reperfusion, and the serum hs-CRP was detected by enzyme-linked immunosorbent assay (ELISA) Thromboxane A2 (TXA2) and 5-hydroxytryptamine (5-HT) levels, and compared between groups. Results The area of no-reflow in the amiodarone group was significantly lower than that in the model control group [(50.44 ± 5.36)% vs (78.91 ± 3.35), P <0.01] when the range of ischemia was not significantly different. The levels of hsCRP, TXA2 and 5-HT in amiodarone group were significantly lower than those in model group (3.05 ± 0.29) (2.80 ± 0.18) μg / L and (3.27 ± 0.54) mg / L, (4.57 ± 0.78) mg / L and (3.84 ± 0.93) ng / L, respectively (all P <0.05). Conclusions Amiodarone can inhibit the inflammation reaction after acute ischemia-reperfusion in rabbits and reduce the degree of myocardial damage caused by no-reflow.