Komatsu E, Yamaguchi I, Fukuyama H, Takahashi K, Miyazawa K
Department of Laboratory Medicine, Yamagata University School of Medicine, Japan.
Jpn Circ J. 1993 Oct;57(10):969-78. doi: 10.1253/jcj.57.969.
Myocardial ischemia interrupts neurotransmission and causes the depression of norepinephrine release. However, the effects of sympathetic nerve stimulation on neurotransmission and norepinephrine release in post-ischemic myocardium are not well defined. We measured regional myocardial length and norepinephrine (NE) release during sympathetic nerve stimulation in anesthetized dogs. Dogs were divided into 2 groups: Group 1 (n = 14); sympathetic nerve stimulation, Group 2 (n = 9); pre-treatment with alpha-blockade yohimbine hydrochloride (0.2 mg/kg) followed by sympathetic nerve stimulation. The left anterior descending artery was occluded for 15 min. Sympathetic nerve stimulation was performed before coronary occlusion and after reperfusion. In group 1, the decrease in systolic shortening in the ischemic region persisted for more than 60 min. Although sympathetic nerve stimulation caused an increase in systolic shortening, it was lower than the pre-ischemic value. NE release from the post-ischemic myocardium remained decreased for 60 min. The decrease in the post-ischemic myocardial response to sympathetic nerve stimulation was associated with diminished NE release. When the cardiac sympathetic nerve was denervated with an epicardial phenol application, NE release decreased even further. In group 2, NE release did not decrease following reperfusion. These results suggest that sympathetic nerve conduction is not completely impaired in post-ischemic myocardium and that pre-synaptic alpha -2 receptors might play an important role in diminished NE release.
心肌缺血会中断神经传递并导致去甲肾上腺素释放减少。然而，交感神经刺激对缺血后心肌神经传递和去甲肾上腺素释放的影响尚不清楚。我们在麻醉犬身上测量了交感神经刺激期间局部心肌长度和去甲肾上腺素（NE）的释放。犬被分为两组：第1组（n = 14），交感神经刺激组；第2组（n = 9），先用α受体阻滞剂盐酸育亨宾（0.2 mg/kg）预处理，然后进行交感神经刺激。左前降支动脉闭塞15分钟。在冠状动脉闭塞前和再灌注后进行交感神经刺激。在第1组中，缺血区域的收缩期缩短减少持续超过60分钟。尽管交感神经刺激导致收缩期缩短增加，但低于缺血前值。缺血后心肌的NE释放持续60分钟减少。缺血后心肌对交感神经刺激反应的降低与NE释放减少有关。当用体表苯酚去神经支配心脏交感神经时，NE释放进一步减少。在第2组中，再灌注后NE释放没有减少。这些结果表明，缺血后心肌中的交感神经传导并未完全受损，并且突触前α-2受体可能在NE释放减少中起重要作用。
