芪丹通脉片对急性缺血／再灌注大鼠心肌一氧化氮合酶系统的影响

目的观察芪丹通脉片对缺血／再灌注大鼠心肌一氧化氮合酶（nitric oxide synthase，NOS）的影响。方法将雄性SD大鼠随机分为假手术组、缺血／再灌注模型组、芪丹通脉片＋缺血／再灌注Ⅰ组、芪丹通脉片＋缺血／再灌注Ⅱ组。大鼠麻醉开胸，结扎冠状动脉前降支40mim，再灌注4h。TUNEL法测定大鼠心肌组织的细胞凋亡，化学比色法检测心肌组织中总的一氧化氮合酶（NOS）、诱导型一氧化氮合酶（iNOS）活性，并计算出结构型一氧化氮合酶（cNOS）的活性。结果不同剂量的芪丹通脉片预处理抑制缺血／再灌注大鼠心肌细胞凋亡，其凋亡指数与模型组比较均存在显著差异（P〈0．05，P〈0．01）。与假手术组比较，模型组心肌组织iNOS的活性增加（P〈0．05），cNOS活性降低（P〈0．01）。不同剂量的芪丹通脉片能够抑制心肌缺血／再灌注大鼠iNOS的活性（P〈0．05），增加cNOS活性（P〈0．05，P〈0．01）。结论芪丹通脉片能够抑制缺血／再灌注大鼠心肌细胞凋亡可能与调节心肌组织中NOS的活性有关。

Effect of Qidan Tongmai Tablet on Nitric Oxide Synthase of Ischemia/Reperfusion Myocardium in Rats

Objective To investigate the effect of Qidan Tongmai tablet （QDTMT） on apoptosis and nitric oxide synthase （NOS） of ischemia/reperfusion myocardium in rats. Methods Male Sprague-Dawley （SD） rats were divided randomly into 4 groups： Sham, ischemia/reperfusion （control）, QDTMT-Ⅰ （1.08 g/kg） treatment and QDTMT-Ⅱ （3.24 g/kg） treatment. Anesthetized and the open-chest animals were subjected to 40 min of myocardium ischemia followed by 4 h-reperfusion. The cardiomyocyte apoptosis was determined by terminal deoxynucleotidyl transfease-mediated dUTP nick-end labeling （TUNEL） method. The activity of NOS in heart tissue was assessed by chemical assay. Results Pretreatment with QDTMT at different doses reduced cardiomyocyte apoptosis indexes significantly compared with the control （P〈0.05, P〈0.01）. The preconditioning of QDTMT could decrease the activity of iNOS （P〈0.05） and increase the activity of cNOS （P〈0.05, P〈0.01）. Conclusion QDTMT treatment could inhibit myocardial apoptosis, which is possibly related to the changes of the activities of NOS.