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目的观察缺血预适应对SD大鼠心肌缺血/再灌注期血清中肿瘤坏死因子-α(TNF-α)和白细胞介素-8(IL-8)及心肌组织中的白细胞介素-10(IL-10)的影响,并探讨其心肌保护机制。方法36只SD大鼠随机分成3组:①缺血预适应(IPC)组:缺血5 min+再灌注5 min反复4次后,缺血60 min+再灌注120 min;②缺血/再灌注(IRI)组:大鼠开胸后,继续观察40 min,然后予以缺血60 min+再灌注120 min;③假手术组(SO):仅开胸,分离血管,不予缺血与再灌注剌激,只进行同样长时间的观察。3组实验结束取右心房血及心肌组织,批量测定血清TNF-α和IL-8及心肌组织IL-10浓度。结果IRI组血清TNF-α和IL-8含量分别为(1 009±277)和(334±187)ng/L,IPC组血清TNF-α和IL-8含量分别为(778±178)和(229±90)ng/L,较IRI组显著降低(P<0.05);IRI组心肌组织IL-10含量为(6.8±2.6)ng/g,IPC组心肌组织IL-10含量为(9.4±4.1)ng/g,较IRI组显著升高(P<0.05)。结论缺血预适应不仅可减少心肌缺血/再灌注病理过程中促炎细胞因子TNF-α和IL-8的产生,还可促进抗炎细胞因子IL-10的产生,而发挥抗炎作用,提示缺血预适应具有保护再灌注心肌抗炎作用的新机制。
Objective To observe the effect of ischemic preconditioning on the levels of tumor necrosis factor-α (TNF-α), interleukin-8 (IL-8) and interleukin-10 (IL-10), and explore its myocardial protection mechanism. Methods Thirty-six SD rats were randomly divided into 3 groups: ① ischemic preconditioning (IPC) group: ischemic 5 min + reperfusion 5 min after repeated 4 times, ischemia 60 min + reperfusion 120 min; ② ischemia / reperfusion IRI group: After the thoracotomy in rats, the rats were observed for 40 min, then 60 min of ischemia and 120 min of reperfusion; ③ Sham operation group (SO): only thoracotomy, blood vessels were separated, and ischemia and reperfusion stimulation , Only the same long period of observation. The right atrial blood and myocardial tissue were taken at the end of the experiment in three groups, and the levels of TNF-α and IL-8 in serum and the concentration of IL-10 in myocardium were determined. Results The levels of TNF-α and IL-8 in IRI group were (1009 ± 277) and (334 ± 187) ng / L, respectively. The levels of TNF-α and IL-8 in IPC group were (778 ± 178) and 229 ± 90 ng / L, which was significantly lower than IRI group (P <0.05). The content of IL-10 in myocardium of IRI group was (6.8 ± 2.6) ng / ) ng / g, which was significantly higher than IRI group (P <0.05). Conclusion Ischemia preconditioning can not only reduce the production of proinflammatory cytokines TNF-α and IL-8 during myocardial ischemia / reperfusion, but also promote anti-inflammatory cytokine IL-10 production, It is suggested that ischemic preconditioning has a new mechanism to protect myocardium from reperfusion injury.