摘要
目的 :观察在缺血预处理期间抑制一氧化氮合酶对 2 4h后 5′-核苷酸酶活性的影响和对缺血预处理第二保护窗的影响。方法 :阻断兔冠脉 5 m in,再灌注 10 min,重复 4次 ,造成缺血预处理。在缺血预处理期间静脉注射一氧化氮合酶抑制剂 NG-硝基 - L-精氨酸甲酯 (L- NAME) ,缺血预处理后 2 4h,提取心肌标本测量 5′-核苷酸酶活性 ,或阻断冠脉 30 m in再灌注 12 0 min,测量心肌梗死面积。结果 :缺血预处理 2 4h后 ,心肌细胞膜和胞浆 5′-核苷酸酶活性均较假手术对照组明显升高。静脉注射 L- NAME阻断了缺血预处理所致的细胞膜和胞浆 5′-核苷酸酶活性的升高。缺血预处理组心梗面积明显小于对照组 ,而 L- NAME阻断了这种保护作用。结论 :一氧化氮参与了缺血预处理所致的 5′-核苷酸酶活性的延迟升高。延迟升高的 5′-核苷酸酶活性可能参与了缺血预处理的第二保护窗。
AIM: To examine the inhibition of nitric oxide (NO) synthesis during ischemic preconditioning (IP) on the activity of myocardial 5'-nucleotidase (5'-N) 24 h after IP and infarct size-limiting effect of the second window of cardioprotection of IP. METHODS: Rabbits were subjected to 4 cycles of 5-min of coronary artery occlusion separated by 10-min reperfusion, or received a sham operation. During this procedure, we injected 10 mg·kg -1 of N G-nitro-L-arginine methyl ester (L-NAME, an inhibitor of NO synthase) intravenously 5 min before IP followed by its continuous infusion (1.5 mg·kg -1·min -1). 24 h after IP or the sham operation, the hearts were rapidly excised for measuring myocardial 5'-N activity or were subjected to 30-min coronary artery occlusion followed by 120-min reperfusion and then measured infarct size (IS). RESULTS: 24 h after IP or the sham operation, there was no difference in heart rate and mean arterial pressure between groups. Both ectosolic-5'-N activity [80.8±7.0 nmol·(mg protein) -1·min -1] and cytosolic-5'-N activity [12.2±0.9 nmol·(mg protein) -1·min -1] increased, compared with that in sham-operated control group [54.6±4.0 and 8.4±0.6 nmol·(mg protein) -1·min -1, respectively, P<0.01], which was blocked by L-NAME [57.2±6.2 and 8.8±0.5 nmol·(mg protein) -1·min -1]. Pretreatment with L-NAME alone did not change the activity of ecto- and cytosolic 5'-N [53.1±4.9 and 8.7±0.5 nmol·(mg protein) -1·min -1], In the IP rabbits, IS was reduced compared with sham-operated control rabbits [ (30.3±3.3)% vs (50.4±4.4)%, P<0.01], and which was blunted by L-NAME [ (49.8±5.0)% ]. L-NAME alone did not affect IS [ (48.8±4.6)% ]. CONCLUSION: NO is involved in the delayed activation of 5'-N, which may be attributable to the second window of cardioprotection of IP.
出处
《心脏杂志》
CAS
2002年第3期189-191,194,共4页
Chinese Heart Journal
