Liu X
Institute of Acupuncture and Moxibustion, China Academy of Traditional Chinese Medicine, Beijing.
Zhen Ci Yan Jiu. 1996;21(1):4-11.
The vast research have demonstrated that the acupuncture analgesia is effected through a physiological mechanism brought about by the nervous system, particularly the central nervous system. We combined the acupuncture effects and theory of channels and collaterals with the new advance of pain neurophysiology, and centred attention on nucleus raphe magnus (NRM), that is one of the origins of the important descending inhibitory pathways of the intrinsic analgesic systems in brain. The unit discharges of NRM neurons and their nociceptors/ph responses were recorded extracellularly with glass microelectrode at 1495 neurons on 634 wastar rats. The modulation of cerebral cortex, the head of N. caudatum (NCa), N. Accumbens (N. Ac), N lateral habenular (NHa) and Periaquaeductal gray matter (PAG) on NRM and their role in acupuncture analgesia were studied by central locational stimulation, lesion and microinjection. The result were as follows: 1. The most NRM neurons could respond to noxious stimulation of tail tip with increasing or decreasing firing rate. Electroacupuncture (EA) at "Zusanli" could activate the NRM neuron, increasing discharges, and inhibit their nociceptive responses, producing analgesia. 2. The activity of NRM neuron was modulated by PAG, NAc, and NCa. Stimulation at one of them can activate neuron of NRM, increasing firing rate, and induce analgesia. When the lesion or microinjection naloxone were made in PAG, NAc or NCa, EA analgesia could be weakened or lost, even the nociceptive responses might be increased. It is suggest that the nuclei participated in EA analgesia with their endogenous opiate like substance, and were playing an important role. It is also indicated that the electroacupuncture was used on the patients with some nuclei lesion or pathological changes should be careful to avoid making patients feel more painful. 3. Somatosensory area II (Sm II) of cerebral cortex participated in EA analgesia. The analgesic effects of EA at "Zusanli" were reduced after lesion of Sm II. The nociceptive responses could be inhibited by stimulation of Sm II. We have further demonstrated that analgesic effects of Sm II stimulation were achieved by the modulation of Sm II on NRM, via NAc and NHa closely related to limbic-midbrain system, and with NRM descending inhibitory pathways through dorsal lateral fasciculus (DLF) in the level of spinal cord. 4. The sensorimotor area (SM) of cerebral cortex seems was not necessary structure for EA analgesia. Either of hindlimb areas or larger range of bilateral SM were resected, the analgesic effects of EA at "Zusanli" were not obviously influenced. The stimulation of somatosensory area I (Sm I) of SM could inhibit the nociceptive responses of NRM neurons. It was also demonstrated the Sm I could modulate NRM by mediation of NCa of extrapyramidal system enhancing EA analgesia. Stimulation of Sm I could directly inhibit the nociceptive responses through pyramidal system in the level of spinal cord, producing analgesia. But the information of electroacupuncture was noxious stimulation, so it could be also inhibited by Sm I stimulation, playing an antagonism to EA analgesia. Thus when patient's emotion was very nervous or physical exercise was very strong, EA analgesic effects would be decreased. Therefore, in order to guarantee EA analgesic effects, it is necessary that patients should take a rest and calm down before electroacupuncture. The contrary action between pyramidal and extrapyramidal systems in EA analgesia may be the one of mechanisms of that EA analgesia to be not full and changeful.
大量研究表明,针刺镇痛是通过神经系统,特别是中枢神经系统所产生的一种生理机制来实现的。我们将针刺效应和经络理论与疼痛神经生理学的新进展相结合,并将注意力集中在中缝大核(NRM)上,它是脑内固有镇痛系统重要下行抑制通路的起源之一。用玻璃微电极在634只Wistar大鼠的1495个神经元上,细胞外记录了NRM神经元的单位放电及其对伤害性刺激的反应。通过中枢定位刺激、损毁和微量注射等方法,研究了大脑皮层、尾状核头部(NCa)、伏隔核(N. Ac)、外侧缰核(NHa)和导水管周围灰质(PAG)对NRM的调制及其在针刺镇痛中的作用。结果如下:1. 大多数NRM神经元对尾尖的伤害性刺激能产生放电频率增加或减少的反应。电针“足三里”能激活NRM神经元,使其放电增加,并抑制其伤害性反应,产生镇痛作用。2. NRM神经元的活动受PAG、NAc和NCa的调制。刺激其中之一能激活NRM神经元,使其放电频率增加,并诱导镇痛。当在PAG、NAc或NCa进行损毁或微量注射纳洛酮时,电针镇痛作用减弱或消失,甚至伤害性反应可能增强。提示这些核团通过其内源性阿片样物质参与电针镇痛,并发挥重要作用。这也表明,对某些核团有病变或病理改变的患者使用电针时应谨慎,以免使患者感觉更痛。3. 大脑皮层体感区II(Sm II)参与电针镇痛。损毁Sm II后,电针“足三里”的镇痛作用减弱。刺激Sm II能抑制伤害性反应。我们进一步证明Sm II刺激的镇痛作用是通过Sm II对NRM的调制实现的,经由与边缘-中脑系统密切相关的NAc和NHa,并通过脊髓水平的背外侧束(DLF)与NRM下行抑制通路相连。4. 大脑皮层感觉运动区(SM)似乎不是电针镇痛的必要结构。切除后肢区或双侧较大范围的SM,电针“足三里”的镇痛作用无明显影响。刺激SM的体感区I(Sm I)能抑制NRM神经元的伤害性反应。还证明Sm I可通过锥体外系的NCa介导调制NRM,增强电针镇痛。刺激Sm I可通过脊髓水平的锥体系统直接抑制伤害性反应,产生镇痛。但电针信息属于伤害性刺激,故也可被Sm I刺激抑制,对电针镇痛起拮抗作用。因此,当患者情绪非常紧张或体力活动非常剧烈时,电针镇痛效果会降低。所以,为保证电针镇痛效果,患者在电针前应休息并平静下来。电针镇痛中锥体系统与锥体外系的相反作用可能是电针镇痛不充分且多变的机制之一。