Yu Qing, Hu Ling, Wu Zi-jian, Cai Rong-lin, Wang Jie, Wang Chun-hua, Liu Lei
Zhen Ci Yan Jiu. 2014 Dec;39(6):472-6.
To observe the effect of electroacupuncture (EA) stimulation of "Shenmen" (HT 7) and "Taiyuan"(LU 9) on P50 event-related potentials in rabbits with acute myocardial ischemia (AMI), so as to evaluate the specificity of function of different acupoints.
Chinchilla rabbits were randomized into normal control, model, Shenmen (HT 7) and Taiyuan (LU 9) groups (n = 10/group). AMI model was established by temporary occlusion of the descending anterior branch of the left coronary artery. EA (1 mA, 2 Hz) was applied to bilateral HT 7 and LU 9 for 15 min. The anesthetized-rabbit's heart rate (HR) was recorded by using a BIOPAC system and the latency and amplitude of auditory sensory gating potential P 50 were measured by paired clicks auditory conditioning (S 1-P 50)/testing (S 2-P 50) stimulus paradigm using a Neuroscan workstation.
In comparison with the normal control group, the HR was significantly decreased in the model group and significantly increased in the HT 7 group than in the model group (P<0. 01). Compared to the normal control group, the amplitude of S 2-P 50 and ratio of amplitude of S 2-P 50/S 1-P 50 were significantly increased in the model group (P<0. 01), and remarkably down-regulated in the HT 7 group than in the model group (P<0. 01),suggesting an inhibitory effect of EA stimulation of HT 7 on cerebral cortical auditory gating potential in AMI rabbits. No significant changes were found in the latencies of S 1-P 50, S2-P 50 potentials in both HT 7 and LU 9 groups and in the HR, amplitude of S 2-P 50 and ratio of amplitude of S 2-P 50/S 1-P 50 in the LU 9 group (P>0. 05).
EA stimulation of HT 7 can correct AMI induced decrease of HR and increase of P 50 potential amplitude in AMI rabbits, while EA of LU 9 has no this effect, suggesting a relatively specific effect of different acupoints on cortical sensory gating.
观察电针刺激“神门”（HT 7）和“太渊”（LU 9）对急性心肌缺血（AMI）家兔P50事件相关电位的影响，以评价不同穴位功能的特异性。
将青紫蓝兔随机分为正常对照组、模型组、神门（HT 7）组和太渊（LU 9）组（每组10只）。通过临时阻断左冠状动脉前降支建立AMI模型。将电针（1 mA，2 Hz）施加于双侧HT 7和LU 9，持续15分钟。使用BIOPAC系统记录麻醉兔的心率（HR），并使用Neuroscan工作站通过配对点击听觉条件刺激（S 1 - P 50）/测试（S 2 - P 50）刺激范式测量听觉感觉门控电位P 50的潜伏期和幅度。
与正常对照组相比，模型组HR显著降低，HT 7组HR较模型组显著升高（P <0.01）。与正常对照组相比，模型组S 2 - P 50的幅度和S 2 - P 50/S 1 - P 50的幅度比值显著升高（P <0.01），HT 7组较模型组显著下调（P <0.01），提示电针刺激HT 7对AMI家兔大脑皮质听觉门控电位有抑制作用。HT 7组和LU 9组S 1 - P 50、S2 - P 50电位的潜伏期以及LU 9组的HR、S 2 - P 50幅度和S 2 - P 50/S 1 - P 50幅度比值均无显著变化（P>0.05）。
电针刺激HT 7可纠正AMI诱导的家兔HR降低和P 50电位幅度升高，而电针刺激LU 9无此作用，提示不同穴位对皮质感觉门控具有相对特异性作用。
