Vagal stimulation suppresses ischemia-induced myocardial interstitial myoglobin release
Vagal stimulation suppresses ischemia-induced myocardial interstitial myoglobin release
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DOI：
10.1016/j.lfs.2008.07.013
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发表时间：
2008-09-26
期刊：
影响因子：
6.1
通讯作者：
Sugimachi, Masaru
中科院分区：
文献类型：
--
作者：
Kawada, Tbru;Yamazaki, Toji;Sugimachi, Masaru
目的：评价迷走神经刺激介导的心肌保护作用对缺血和再灌注在体内缺血myocardial.Main方法：我们测量了心肌间质肌红蛋白水平在缺血区域使用心脏微透析技术在麻醉和迷走神经切断猫。VX组（n =6）：结扎左前降支（LAD）60 min，再灌注60 min。双侧迷走神经刺激（10 V，5 Hz，1 ms脉冲持续时间），立即启动后，LAD闭塞的影响，进行了检查（VS组，n=6）。为了检查磷脂酰肌醇3-激酶（PI 3 K）的参与，在用PI 3 K抑制剂渥曼青霉素（0.6mg/kg，i. v.）(VS-W n=6）。为检测心动过缓的作用，采用固定频率心室起搏进行迷走神经刺激（VS-P组，n =6）。关键发现：缺血期间VX组的平均肌红蛋白水平为1170 ± 141（ng/ml，平均值± SE），VS组显著降低（466 ± 87，P
Aims: To evaluate vagal stimulation-mediated myocardial protection against ischemia and reperfusion in in vivo ischemic myocardium.Main methods: We measured myocardial interstitial myoglobin levels in the ischernic region using a cardiac microdialysis technique in anesthetized and vagotomized cats. We occluded the left anterior descending coronary artery (LAD) for 60 min and reperfused it for 60 min (VX group, n =6). The effects of bilateral vagal stimulation (10 V, 5 Hz, 1-ms pulse duration), initiated immediately after LAD occlusion, were examined (VS group, n=6). To examine the involvement of phosphatidylinositol 3-kinase (PI3K), vagal stimulation was performed after pretreatment with a PI3K inhibitor wortmannin (0.6 mg/kg, i.v.) (VS-W group, n=6). To examine the contribution of bradycardia, vagal stimulation was performed with fixed-rate ventricular pacing (VS-P group, n =6).Key findings: The average myoglobin level during the ischernic period was 1170 +/- 141 in VX (in ng/ml, mean +/- SE), which was significantly attenuated in VS (466 +/- 87, P