中缝大核内催产素在电针镇痛中的作用

目的 :探讨中缝大核 (NRM )内催产素 (OT)在电针镇痛中的作用 ,及其和内源性 5 HT在电针镇痛中的关系。方法 :以钾离子透入法引起大鼠甩尾反应的电流强度为痛行为反应指标 ,测定动物痛阈 ,观察NRM内注射催产素和噻庚啶对电针镇痛的影响。结果 :向大鼠NRM内微量注入催产素后 ,能明显增加电针镇痛的效应 ;而向NRM内注入噻庚啶后 ,可阻断催产素增加电针镇痛的效应。结论 :NRM内的催产素在电针镇痛的复杂过程中发挥着一定作用 ,且其效应可能是通过内源性 5 HT系统中介的。     

中脑导水管周围灰质内催产素参与电针镇痛

以钾离子透入法引起大鼠甩尾反应的电流强度（ｍＡ）为痛反应指标，通过向中脑导水管周围灰质（ＰＡＧ）内注射催产素（ＯＴ），抗催产素血清（ＡＯＴＳ）和纳洛酮（Ｎｘ），观察了ＰＡＧ内ＯＴ对动物电针镇痛的影响。结果表明，ＰＡＧ内生理水平的ＯＴ参与电针镇痛的过程，并且其作用不依赖于内源性阿片肽系统。     

催产素与八肽胆囊收素对电针镇痛的影响

<正> 近年来国内外文献报道,中枢神经系统的催产素(OT)在痛觉调制过程中发挥着一定的作用,我们最近的工作也表明,脑和脊髓内的OT不仅可以提高大鼠的痛阈,而且能明显增强电针镇痛效应。为进     

中脑导水管周围灰质内催产素在电针镇痛中的作用及机制的实验研究

我们以往的工作表明 ,侧脑室和脊髓蛛网膜下腔内注射催产素 (ＯＴ)能明显提高大鼠电针镇痛效应 ,注射抗催产素血清 (ＡＯＴＳ)则能显著降低电针镇痛效应。提示 ,中枢神经系统内的催产素在电针镇痛的复杂过程中发挥着一定作用。中脑导水管周围灰质 (ＰＡＧ)是电针镇痛的关键部位 ,其内含有丰富的ＯＴ、ＯＴ神经末梢及ＯＴ受体 ,但中枢ＯＴ在电针镇痛中的作用是否与之有关 ,作用机制怎样 ?是一个引人关注的问题。本工作以钾离子透入法 ,以甩尾法作为疼痛指标 ,测定大鼠痛阈 ,观察ＰＡＧ注射ＯＴ、ＡＯＴＳ、纳洛酮 (Ｎｘ)、抗 β 内啡肽血清 (…     

脊髓小胶质细胞激活与电针镇痛效应研究

既有研究表明脊髓小胶质细胞的激活不仅与异常性疼痛、痛敏的产生和维持有关,而且与慢性疼痛持续状态有密切关系。脊髓小胶质细胞激活后,释放大量的细胞因子、炎症介质和神经活性物质,从而使脊髓小胶质细胞扩大疼痛反应。而目前电针镇痛研究则表明针刺效应不仅具有即刻效应,同时其镇痛后效应也较为突出。文章通过文献回顾,分析电针镇痛是否通过抑制了小胶质细胞的活化而实现其远期效应,探讨脊髓水平的电针镇痛作用机制与胶质细胞之间的相关性。     

电针镇痛脊髓中枢机制实验研究进展

电针对于各种急慢性疼痛(如癌痛、神经痛、炎性痛等)具有良好的镇痛作用,其中对脊髓的作用机制仍在进行深入研究,本文综述近年来电针镇痛的脊髓中枢机制,为今后科研及临床研究提供理论基础。     

催产素与加压素在针刺镇痛中的作用（之三）下丘脑室旁核参与电针镇痛

本工作采用损毁、刺激PVH，结合行为测痛(钾离子透入—甩尾区应)及AVP和OT的放射免疫测定(RIA)，初步探讨PVH参与痛觉调制和电针镇痛的机制。     

针刺治疗脊髓损伤作用机制的研究进展

脊髓损伤（SCI）是一种严重的神经创伤类疾病，脊髓损伤后会出现运动障碍、感觉障碍及二便障碍等后遗症，一直是医学界治疗难点。脊髓损伤的病理机制包括炎症反应、氧化应激、细胞凋亡及轴突再生等，各病理过程相互影响、错综复杂。针刺治疗脊髓损伤具有多角度、多靶点的治疗优势，能明显改善脊髓损伤后遗症的临床症状。本文综述了近年来针刺治疗脊髓损伤的作用机制，发现针刺可通过抑制脊髓损伤后炎症反应、改善氧化应激、减少细胞凋亡、促进轴突再生等方面促进神经功能恢复。     

针刺对继发性脊髓损伤的作用机制研究进展

继发性脊髓损伤是一种严重的中枢神经系统损伤性疾病,针刺治疗对于继发性脊髓损伤所造成截瘫的恢复有肯定的促进作用,同时在改善神经源性膀胱与减轻截瘫性疼痛等合并症方面也有较好的疗效。随着实验技术的发展,研究人员在动物实验中发现针刺对脊髓的结构及功能的影响是多方面的,进一步从神经和生化方面揭示了针刺治疗继发性脊髓损伤的作用机制。对近10年来针刺对继发性脊髓损伤的治疗现状和作用机制进行综述。     

针灸治疗脊髓损伤机制研究进展

脊髓损伤是多种外伤所致中枢神经系统损伤的一种疾病,针灸可有效治疗脊髓损伤造成的一系列并发症.随着实验技术的发展,研究人员发现部分针灸治疗脊髓损伤的机制,但尚不明确.文章总结了近年来针灸疗法治疗该病的机制研究文献,通过抑制神经细胞凋亡、改善脊髓损伤区域微环境、促进轴突细胞延伸及神经纤维再生等作用机制对针灸治疗脊髓损伤的机...     

Treatment of uroschesis due to spinal cord injury by acupuncture in 32 cases

Treated uroschesis due to spinal cord injury in 32 cases with acupuncture therapy (acupuncture group) and compared with Neostigmine injection (control group). In acupucture group, 10 cases got clinical recovery, 17 efficacy and 5 inefficacy, with an effective rate of 84.4%; among 32 cases in control group, 3 cases got clinical recovery, 15 efficacy and 14 inefficacy, the effective rate was 56.2%. Author: Huang Zhi-gang (1967-), male, attending physician     

电针对大鼠脊髓中抑制性生长因子的影响

目的通过电针对坐骨神经损伤大鼠脊髓中髓鞘相关糖蛋白（myelinassociated glycoprotein,MAG）表达影响的实验研究,进一步探讨电针治疗周围神经损伤的修复机理,为临床治疗提供理论支持。方法采用神经夹持损伤的方式建立大鼠坐骨神经损伤模型,通过坐骨神经功能指数（sciatic nerve function index,SFI）及热痛阈检测观察大鼠的行为学变化;通过免疫组织化学染色观察大鼠脊髓内MAG表达情况,进而统计分析各组间的差异。结果行为学检测结果显示,在基本功能改善方面,与模型组及模型对照组比较,电针治疗组（P〈0.05）大鼠右后腿感觉及运动功能明显改善。免疫组化结果显示模型组、模型对照组及电针组MAG表达均比正常组高（P〈0.05）,但电针组治疗1、2个疗程后,MAG表达明显降低,越来越接近正常组。结论通过本实验研究发现,电针能改善坐骨神经损伤大鼠的一般状况,电针组大鼠脊髓中MAG的表达明显降低,说明电针能抑制脊髓中抑制性生长因子的释放,促进周围神经损伤再生修复。     

针刺镇痛在肠镜检查中的应用

目的:评估针刺镇痛在减轻患者肠镜检查中不适的效果。方法:将80例门诊结肠镜检查患者随机分为电针组和对照组各40例。电针组在镜检前30min于右侧足三里、上巨虚,左侧阴陵泉、三阴交以电针刺激持续至镜检结束,同时针刺合谷;对照组不予任何防治措施。连续监测患者血压、心率的变化;分别观察两组患者结肠镜插镜时,过乙状结肠、脾区、肝区时的疼痛级别;记录插镜至回盲部时间、术后不良反应以及检查后患者满意度。结果:80例患者全部完成了肠镜检查,电针组患者在结肠镜插镜时、过乙状结肠以及脾区时其疼痛评分显著低于对照组(P<0.01);同时电针组患者插镜至回盲部的时间为(9.58±3.86)min,亦显著快于对照组的(12.96±6.4)min(P<0.05);电针组患者术后满意度亦显著高于对照组(P<0.05)。2组患者血压、心率并无显著差异。结论:针刺镇痛能够有效地缓解患者结肠镜检查的不适感,同时缩短肠镜检查时间,患者满意度高。     

针灸治疗脊髓损伤神经原性膀胱功能障碍概况

介绍近年来国内外针灸治疗脊髓损伤后神经原性膀胱功能障碍的情况。分别从体针、电针、点穴推拿、穴位注射、穴位贴敷及其他疗法等几方面对针灸治疗此类疾病的方法进行归类分析。针灸治疗脊髓损伤后神经原性膀胱功能障碍常用腧穴为八、三阴交、中极、关元等;刺激方式为针刺、电针、点穴推拿、穴位注射等。针灸治疗脊髓损伤后神经原性膀胱功能障碍的其他评价指标的有效性,尚需要更多的设计严谨、方法科学的高质量随机对照试验来证实。     

Scientific bases of acupuncture analgesia

The present paper was to review the physiological bases of acupuncture analgesia (AA) on normal subjects, patients, and animals. Effect of acupuncture on pain perception in normal subjects was studied and compared with sham acupuncture. It was shown that the analgesic effect of acupuncture has its physiological basis. Using neurophysiological, neuropharmacological, neurobiochemical and neuromorphological methods, the neurohumoral mechanism of AA was studied from the peripheral neural pathway of acupuncture sensation (De-Qi sensation in Chinese traditional medicine) to the central neuromodulatory effect of AA. It was indicated that needling of acupuncture point could activate the afferent fibers of peripheral nerves to elicit De-Qi sensation, then ascended mainly through the ventro-lateral funiculi, which conducted pain and temperature sensation upward to the brain, activated the antinociceptive system including certain brain nuclei. modulators (opioid peptides), neurotransmitters, through the descending inhibitory pathway resulting in analgesia. Especially the clinical and laboratory results indicated that the endogenous opiate peptides (EOP) participated in AA from the presynaptic level to the receptor sites, which provided a scientific basis for understanding the mechanism of AA. Substantial evidences have been accumulated that acupuncture has prominent analgesic effect; but it fails to give sufficient analgesia during operation. Some effective measures to improve the therapeutic effect of acupuncture, such as the combination of acupuncture with drugs, the selection of suitable EA parameters and optimal time spacing should be adopted.     

Differentiation of acupuncture and nonacupuncture points by difference of associated opioids in the spinal cord in production of analgesia by acupuncture and nonacupuncture point stimulation, and relations between sodium and those opioids

Antiserum of methionine-enkephalin (Met-Enk) applied intrathecally abolished acupuncture analgesia (AA) caused by low frequency stimulation of an acupuncture point (tibial muscle, APS) of rats, but antisera of leucine-enkephalin (Leu-Enk) and dynorphin (Dyn) did not. Antiserum of Dyn applied intrathecally abolished analgesia (NAA) produced by stimulation of a nonacupuncture point (NAPS) which was revealed by lesion in the analgesia inhibitory system (AIS), whereas antisera of Met-Enk and Leu-Enk did not. NAA was antagonized by the kappa-receptor antagonist, Mr2266, and analgesia was produced by the kappa-agonist, U50-488H, in the AIS lesioned rats. Potentials in the dorsal periaqueductal central gray (D-PAG) evoked by APS were antagonized by naloxone and antiserum of Met-Enk, and those in the lateral PAG (L-PAG) evoked by NAPS were antagonized by Mr2266 and antiserum of Dyn. After adrenalectomy, AA, potentials in the D-PAG, and analgesia caused by stimulation (SPA) of the D-PAG were abolished 12 hour; and NAA, potentials in the L-PAG, and SPA of the L-PAG were abolished in 24 hour. All were then restored one hour after intravenous application of 1 ml of 5% NaCl solution. AA and NAA which were augmented for several hours before their abolition after adrenalectomy were not antagonized by naloxone nor M 2266, respectively. However naloxone and Mr2266 did antagonize AA and NAA, respectively, one hour after treatment with 1 ml of 5% NaCl solution.