前言：電針刺激合谷穴位(Hoku acupoint) 可以透過體-交感神經反射(somaticsympatheticreflex) 來影響不同臟器功能，本研究想探討電針刺激合谷穴所引發體-交感神經反射，對骨盆神經-尿道外括約肌反射塑性所產生之影響。方法：以麻醉大白鼠為實驗動物進行以下實驗(1) 電刺激骨盆神經：頻率分別為0.003Hz (為測試刺激) 與1 Hz (為反複性刺激)；(2) 在骨盆神經刺激時，同時對合谷穴(Li-4) 施予2 Hz 與20 Hz 兩種頻率之電針刺激[固定刺激強度為20xT (T 為能引起肌肉收縮之最小電流閾值)]，觀察並比較外尿道括約肌肌動作電位數之變化。結果： 測試刺激所產生之動作電位數(spike number) 平均為1.00±0.26spikes╱stimulation (n=20)，反複性刺激誘導出一逐漸增強之神經塑性增益現象，大約在刺激後90 秒達一穩定的動作電位數，其最終所達到一個穩定的動作電位數目為16.50±1.62 spikes╱stimulation（n=15）。脊髓腔內分別給予NMDA 接受器之拮抗劑(APV) 和AMPA 接受器之拮抗劑(NBQX)，則會完全阻斷(16.50±1.62 to 1.20±0.20spikes╱stimulation P<0.01 n=5)，或部份阻斷(16.50±1.62 to 9.01±0.71 spikes╱stimulationP<0.01 n=5) 由重複性電刺激引發的增益現象。另外，以2Hz 刺激合谷穴，動物血壓及心率持續增加至電針刺激結束才恢復正常，20 Hz 刺激合谷穴位使平均血壓迅速增加，隨後血壓在3~4 分鐘後逐漸恢復正常。骨盆神經給予測試性或重複性電刺激時，同時在合谷穴給予2 或20 Hz 的電針刺激：結果重複性電刺激仍可引發反射增益現象；合谷穴之電針刺激亦可產生增壓反應，但兩種刺激並沒有互相加成的效果，亦即藉由功能性電針刺激調整自主神經活動的方式可能對骨盆-尿道反射之塑性增益作用無顯著影響。 Introduction: Recent studies in our laboratory have shown that electroacupuncture (Ea) at Hoku acupoint may modulate autonomic nerve activity influencing visceral function via somatic-sympathetic reflex in urethane-anesthetized rats. The reflex plasticity between pelvic afferent and pudendal efferent nerve fibers is physiologically important inurine continence during the storage phase of voiding cycles. To perform the Ea stimulation at Hoku acupoint to examine the effect of Ea on the plasticity of the pelvic nerve-to-urethral sphincter reflex (PPR) is the interesting aim of this study. Method：External urethral sphincter electromyogram (EUSE) of anesthetized rats response to pelvic afferent test stimulation (TS, 1╱30 Hz) or repetitive stimulation (RS, 1 Hz) were recorded synchronized with╱without Ea at Hoku acupoint [2 Hz: the low frequency Ea (LFEa) and 20 Hz with intensity of 20 times of motor threshold for 10 min), and╱or intrathecal administration 10 .mu.L of (1)2,3-dihydroxy-6-nitro -7-sulfamoyl-benzo (F) quinoxaline (NBQX, 100 .mu.M), (2) D-2-amino-5-phosphonoraleric acid (APV, 100.mu.M). Results：RS-induced potentiation of the pelvic-to-pudendal reflex was abolished by a selective Nmethyl-D-aspartate (NMDA) receptor antagonist (16.50 +- 1.62 to 1.20 +- 0.20 spikes╱stimulation P<0.01 n＝5) and attenuated by a non-NMDA excitatory amino acid receptor antagonist (16.50 +- 1.62 to 9.01 +- 0.71 spikes╱stimulation P<0.01 n＝5), suggesting the RS-induced PUR should be mediated by glutamatergic transmission. In addition, Ea stimulation at the Hoku point elicit chronotropic and pressor effects. The pattern of response induced by thebLFEa was different from that by the HFEa, i.e. a tonic effect was elicited by the LFEa, while a phasic one was induced by the HFEa. However, synchronized Ea stimulation at the Hoku acupoints didn't significantly affect the PUR activity. All the results in this study implicated that: (1) The mechanisms of RS-induced PUR are glutamatergic transmission involved; (2) Ea at Hoku may activate the sympathetic nerve to induce chronotropic and pressor effects; (3) Ea at Hoku with different stimulation frequencies may elicit distinct mechanism to induce therapeutic effect; (4) The mechanisms of RS-induced PUR maybe distinct from Ea-induced pressor response.
