电针对实验性RA关节痛镇痛作用的机理研究

[目的]探讨针刺对慢性痛(如炎性痛)的镇痛作用及其机理。[方法]以福氏完全佐剂(Freund’s complete adjuvant，FCA)作为实验性类风湿性关节炎(Rheumatoid Arthritis，RA)慢性痛模型，电针选取“太溪”和“足三里”，并在侧脑室注射孤啡肽(Orphanin FQ，OFQ)，以免疫组化、生化等为检测方法，检测其痛阈、炎性局部皮温、肿胀度、疼痛级别等指标。[结果]电针对实验性RA关节痛具有一定的治疗作用和明显的镇痛效应，电针明显提高实验性RA大鼠痛阈降低疼痛级别，具有明显的后效应。注射OFQ对抗电针提高实验性RA大鼠痛阈，对抗降低疼痛级别的效应，而且对抗电针的后效应；电针明显降低实验性RA大鼠踝部皮温和肿胀度，注射OFQ对抗电针降低踝部皮温和肿胀度不明显。[结论]本课题对深入研究针刺镇痛机理以及针刺镇痛作用规律，具有理论和实际意义，并为临床针刺治疗类风湿关节炎及痛证，提高临床疗效，增强镇痛效应，进一步探讨针刺治疗慢性痛的中枢和外周机制，提供了重要理论基础和参考价值。     

中脑导水管周围灰质内催产素对痛阈和电针镇痛效应的影响

本工作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，观察了中脑导水管周围灰质（ＰＡＧ）腹外侧区注射催产素（ＯＴ）和抗催产素血清（ＡＯＴＳ）对大鼠痛阈和电针镇痛效应的影响。结果表明，ＰＡＧ注射ＯＴ能增加大鼠痛阈和电针镇痛效应；注射ＡＯＴＳ以中和内源性的ＯＴ后，对大鼠痛阈虽克明显影响，但能显著降低电针期的停针后的电针镇痛效应。提示ＰＡＧ内生理水平的ＯＴ在电针镇痛中发挥一定作用。     

大鼠中缝大核内一氧化氮在痛觉调制和针刺镇痛中的作用

背景：L-精氨酸是内源性一氧化氮的前体物质，而一氧化氮参与外周脊髓水平和脊髓水平以上痛觉的调制。目的：探讨延髓中缝大核内一氧化氮在痛觉调制和针刺镇痛过程的作用。设计：以动物为观察对象的随机对照实验。单位：咸宁学院医学院生理教研室。材料：实验于2002-05／2003-03在咸宁学院医学院生理教研室完成。选用63只Wistar大鼠，随机分为7组，每组9只大鼠：①L-精氨酸量效关系实验分为5组：生理盐水组，L-精氨酸1，2，4，8mmol组。②L-精氨酸与电针镇痛关系实验分为两组：生理盐水＋电针组，L-精氨酸＋电针组。方法：①L-精氨酸量效关系实验：5组大鼠分别延髓中缝大核微量注射生理盐水及L-精氨酸1，2，4，8mmol，容积均为1．5μL。给药后每隔10min以（50&;#177;0．5）℃热水刺激甩尾测定痛阈，连续观察90min。②L-精氨酸与电针镇痛关系实验：两组大鼠分别延髓中缝大核微量注射生理盐水1.5μL及L-精氨酸8mmol（1．5μL），10min后电针刺激大鼠双侧后肢“足三里”穴位，频率为4～16Hz，强度按1，2，3V顺序递增电压，每一强度电针10min，共电针30min并测痛3次，停针后继续每隔10min测痛1次，直至注药后90min。主要观察指标：各组大鼠不同时间点痛阈变化。结果：63只大鼠进入结果分析。①L-精氨酸1mmol组大鼠各个时间点痛阈低于生理盐水组，但统计学分析无差异（P〉0．05），L-精氨酸2，4，8mmol组大鼠各个时间点痛阈均显著低于生理盐水组（P〈0．001），作用持续至给药后80min；且随着浓度的增加，大鼠痛阈降低的幅度增加。②L-精氨酸＋电针组大鼠给药后20～50min痛阈明显低于生理盐水＋电针组（P〈0．01）。结论：①延髓中缝大核微量注射L-精氨酸具有降低痛阈作用，其作用呈剂量依赖性。②电针能提高痛阈，L-精氨酸可削弱电针镇痛效应。③以上提示延髓中缝大核内一氧化氮参与痛和电针镇痛的病理生理过程，其含量增加明显降低痛阈。     

褪黑素对大鼠和小鼠的镇痛作用

采用直流串单方波电刺激鼠尾部引起鼠嘶叫的电流值为动物痛阈指标,观察褪黑素（ＭＴ）对大鼠和小鼠的镇痛作用;进而观察纳络酮的拮抗作用,以探讨ＭＴ的镇痛作用与内源性阿片肽系统的关系。结果表明,ｉｐＭＴ显著提高大鼠痛阈,具有明显的量效和时效关系;ｉｐＭＴ也显著提高小鼠痛阈。表明ＭＴ对大鼠和小鼠均可产生显著的镇痛作用。纳洛酮拮抗ＭＴ对大鼠、小鼠的镇痛作用,提示ＭＴ的镇痛作用与内源性阿片肽系数有关。     

β—内啡肽基因敲除小鼠2Hz电针镇痛效果显著降低

针刺镇痛的机理研究发现,不同频率的电针刺激释放中枢内不同的阿片肽,即２Ｈｚ低频电针主要释放β－内啡肽,而１００Ｈｚ高频电针主要释放强啡肽。本实验试图在缺乏β－内啡肽（ＰＯＭＣ基因敲除）的小鼠上进一步验证这一理论。实验在缺乏β内啡肽的小鼠和相应的野性型小鼠上进行,以热辐射甩尾潜伏期测定痛阈,选定足三里和三阴交穴位,以韩氏定位神经刺激仪（ＨＡＮＳ）的恒流、方波输出进行电针刺激。实验发现：（１）与相应野     

鞘内注射抗生长抑素血清对佐剂性关节炎大鼠电针镇痛及中枢β-EP水平的影响

目的观察鞘内注射抗生长抑素血清（ASSS）对佐剂性关节炎（AA）大鼠痛阈、电针（EA）镇痛及中枢β-内啡肽（-βEP）水平的影响,探讨其可能的镇痛机制。方法以AA大鼠为炎症痛模型,以痛阈为指标观察鞘内注射ASSS对痛阈和EA镇痛的影响;以放免法测定AA大鼠下丘脑、脊髓中-βEP含量,观察鞘内注射ASSS及EA镇痛对其影响。结果鞘内注射ASSS可显著降低AA大鼠痛阈,并使EA镇痛效应明显降低;EA镇痛可提高下丘脑和脊髓-βEP含量,鞘内注射ASSS可使中枢-βEP水平进一步显著升高。结论内源性生长抑素在痛觉调制中起重要作用,有显著的镇痛效果并与增强EA镇痛作用密切相关;其镇痛机制可能与中枢-βEP水平相关。     

大鼠中缝大核内一氧化氮在痛觉调制和针刺镇痛中的作用

背景L-精氨酸是内源性一氧化氮的前体物质,而一氧化氮参与外周脊髓水平和脊髓水平以上痛觉的调制.目的探讨延髓中缝大核内一氧化氮在痛觉调制和针刺镇痛过程的作用.设计以动物为观察对象的随机对照实验.单位咸宁学院医学院生理教研室.材料实验于2002-05/2003-03在咸宁学院医学院生理教研室完成.选用63只Wistar大鼠,随机分为7组,每组9只大鼠①L-精氨酸量效关系实验分为5组生理盐水组,L-精氨酸1,2,4,8 mmol组.②L-精氨酸与电针镇痛关系实验分为两组生理盐水+电针组,L-精氨酸+电针组.方法①L-精氨酸量效关系实验5组大鼠分别延髓中缝大核微量注射生理盐水及L-精氨酸1,2,4,8 mmol,容积均为1.5 μL.给药后每隔10 min以(50 ±0.5)℃热水刺激甩尾测定痛阈,连续观察90min.②L-精氨酸与电针镇痛关系实验两组大鼠分别延髓中缝大核微量注射生理盐水1.5μL及L-精氨酸8mmol(1.5 μL),10min后电针刺激大鼠双侧后肢"足三里"穴位,频率为4～16 Hz,强度按1,2,3 V顺序递增电压,每一强度电针10 min,共电针30 min并测痛3次,停针后继续每隔10min测痛1次,直至注药后90min.主要观察指标各组大鼠不同时间点痛阈变化.结果63只大鼠进入结果分析.①L-精氨酸1 mmol组大鼠各个时间点痛阈低于生理盐水组,但统计学分析无差异(P＞0.05),L-精氨酸2,4,8 mmol组大鼠各个时间点痛阈均显著低于生理盐水组(P＜0.001),作用持续至给药后80 min;且随着浓度的增加,大鼠痛阈降低的幅度增加.②L-精氨酸+电针组大鼠给药后20～50 min痛阈明显低于生理盐水+电针组(P＜0.01).结论①延髓中缝大核微量注射L-精氨酸具有降低痛阈作用,其作用呈剂量依赖性.②电针能提高痛阈,L-精氨酸可削弱电针镇痛效应.③以上提示延髓中缝大核内一氧化氮参与痛和电针镇痛的病理生理过程,其含量增加明显降低痛阈.     

八肽胆囊收缩素对针刺镇痛的影响及其机制

目的：观察八肽胆囊收缩素对抗电针对大鼠束旁核中痛反应神经元放电和甩尾潜伏期痛阈的同时影响及其作用机制。 方法：实验于2004-06／2005-04在哈尔滨医科大学神经痛觉电生理研究室完成。选择雄性的Wistar大鼠128只，随机分4组：对照组32只，不给大鼠任何处理。电针组32只，用G．6805型治疗仪给电压6V，频率15Hz，连续的电脉冲刺激双侧“足三里”15min。电针＋八肽胆囊收缩素组32只，在电针双侧“足三里”15min后，借助自动微量推进器立即向脑室注入八肽胆囊收缩素（1．5kg／L），2min注射完毕。电针＋八肽胆囊收缩素＋L-364，718组32只，在注射八肽胆囊收缩素后2min，右侧束旁核内注入八肽胆囊收缩素-A受体拮抗剂L-364，718（100kg/L），2min注射完毕，其他操作同电针＋八肽胆囊收缩素组。以辐射热照大鼠尾部背侧下1／3处作为伤害性刺激，引导痛反应神经元的放电。以痛兴奋神经元、痛抑制神经元和甩尾潜伏期的变化作为痛阚的观察指标。当辐射热照大鼠尾开始或甩尾发生时，用SEN-3301电刺激器的电脉冲记号作为照尾和甩尾的标记．与痛兴奋神经元或痛抑制神经元的放电同时显示在VC-9示波器上，从而观察大鼠束旁核中痛反应神经元放电和甩尾潜伏期的同时变化。用GF-777型双道录音机记录这些变化，并输入DAB-1100直方图仪绘制直方图，最后用Z3．304函数记录仪打印。 结果：纳入动物128只，均进人结果分析。①辐射热照大鼠尾可使痛兴奋神经元诱发放电增加或痛抑制神经元诱发放电减少的同时发生甩尾反射，表现出辐射热致疼痛效应。（砻电针双侧“足三里”15min，可抑制痛兴备神经元的电活动或加强痛抑制神经元的电活动，同时使甩尾潜伏期延长，16个痛兴奋神经元平均净增值从电针前的（12．14&;#177;1．31）Hz减少到（3．38&;#177;1．92）Hz、同时甩尾潜伏期从（4．79&;#177;0．22）s延长到（8．65&;#177;0．34）s。9个痛抑制神经元平均抑制时程从电针前（5．3&;#177;0．56）B减少至（2．41&;#177;0．89）s，甩尾潜伏期从（4．11&;#177;0.38）s延长到（8.01&;#177;0．59）s，即呈现出电针的镇痛效应。③脑室注射八肽胆囊收缩素能同时对抗电针所引起痛兴奋神经元或痛抑制神经元和甩尾潜伏期的镇痛作用。在电针后立即，15个痛兴奋神经元的平均净增值从电针前100％减少到（17．73&;#177;3．05）％，抑制率为（82．27&;#177;5．47）％；甩尾潜伏期延长率为（72．83&;#177;3．38）％。脑室注射八肽胆囊收缩素后立即，平均净增值的抑制率下降到（15．86&;#177;1．82）％；甩尾潜伏期的延长率减少到（13．93&;#177;2．12）％。而11个痛抑制神经元平均抑制时程从电针后立即的缩短率为（64．99&;#177;8．23）％减少到（11．41&;#177;1．58）％；甩尾潜伏期延长率为（60．84&;#177;6．28）％下降到（8．63&;#177;0．92）％。（4）束旁核内注入胆囊收缩素-A受体拮抗剂L-364318能翻转八肽胆囊收缩素对抗电针的镇痛作用。 结论：八肽胆囊收缩素的抗电针镇痛作用，在中枢痛反应神经元电活动和整体行为反射水平上是协调一致的，推测该作用是通过胆囊收缩素-A受体而实现的。揭示降低脑内八肽胆囊收缩素的含量或阻断胆囊收缩素-A受体的作用均能提高临床针刺的镇痛疗效以及痛兴奋神经元和痛抑制神经元的电活动作为疼痛和镇痛指标是确实可行的。     

100Hz电针促进吗啡依赖和戒断大鼠脊髓强啡肽的释放

目的：研究在吗啡依赖和戒断大鼠１００ＨＺ电针是否仍有镇痛作用。该作用是否仍由脊髓强啡肽通过ｋ受体介导。方法：测定辐射热甩尾阈（ＴＦＬ）作为痛阈。结果：（１）给大鼠皮下注射递增量吗啡８天造成大鼠对吗啡的依赖。这时给以１００ＨＺ电针，ＴＦＬ仍有显著升高，此作用可被大剂量纳洛酮翻转，提示由ｋ阿片受体介导；（２）吗啡依赖和或断大鼠脊髓灌注液中强腓肽放免活性明显降低，１００ＨＺ电针使之显著回升。结论：在大鼠     

小鼠低频和高频电针镇痛阿片机制的探讨

探讨小鼠低频和高频电针镇痛的阿片机制。方法：采用交叉耐受和受体药理学方法,以甩尾潜伏期增加的百发数作为评判电针镇痛效果的指标。结果：（１）吗啡镇痛与２Ｈｚ电针镇痛之间存在交叉耐受。（２）２／１００Ｈｚ电针镇痛分别与２Ｈｚ、１００Ｈｚ电针镇痛存在交叉耐受;而２Ｈｚ电针镇痛与１００Ｈｚ电针镇痛不存在交叉耐受。（３）ＣＣＫ受体拮抗剂Ｌ３６５,２６０可显著加强１００Ｈｚ电针镇痛效应,对２Ｈｚ电针镇痛无明显     

极小剂量纳洛酮增强电针的镇痛作用但不影响电针对吗啡戒断症状的抑制作用

目的:纳洛酮(naloxone,NX)是一种阿片受体拮抗剂,应用于大鼠,在1～10mg/kg范围内能对抗吗啡镇痛和电针(electroacupuncture,EA)镇痛。但有人报道,极小剂量NX可加强吗啡镇痛。本工作观察极小剂量NX是否能加强大鼠电针镇痛,及电针对大鼠吗啡戒断的抑制作用。方法:选用成年雄性SD大鼠,分两批进行实验。第一批以辐射热甩尾阈(TFL)作为大鼠痛阈指标,检测腹腔注射(i.p.)NX10ng/kg对2Hz EA和100Hz EA镇痛效应的影响。第二批在慢性吗啡依赖大鼠模型上,以体重丢失作为吗啡戒断反应指标,观察i.p NX 10 ng/kg对 2Hz EA和 100Hz EA抑制 NX(lmg/kg,i.p.)诱发的体重丢失的影响。结果:(1)EA之前10分钟 i.p. NX 10 ng/kg,不仅能显著增强2Hz EA的镇痛作用(P<0.05),而且可使其镇痛效应延长至120分钟;同样剂量NX对100 Hz EA的镇痛效应无明显影响(P>0.05)。(2)EA之前10分钟i.p. NX 10 ng/kg,对两种频率EA抑制吗啡戒断大鼠体重丢失的效应均无显著影响。结论:极小剂量的NX能增强和延长2Hz EA的镇痛作用,该发现可能具有临床应用意义。极小剂量的NX未能影响EA抑制吗啡戒断大鼠体重丢失的作用,这可能与吗啡戒断状态下阿片受体的功能改变有关。     

100Hz电针和脊髓鞘内注射强啡肽A引起大鼠镇痛作用的性别差异

目的：比较１００Ｈｚ电针对雌性与雄性大鼠的镇痛作用,以及脊髓蛛网膜下腔（ｉ．ｔ．）注射阿片κ受体激动剂强啡肽Ａ１１７（ＤｙｎＡ）对雌、雄大鼠镇痛的差异性。方法：用辐射热甩尾法测痛。为避免强啡肽的致瘫作用,本实验采用小剂量（５μｇ或２．３ｎｍｏｌ,１０μｌ）ｉ．ｔ．注射,并以斜板试验观察大鼠运动功能的变化。结果：雌性大鼠１００Ｈｚ电针的镇痛作用强于雄性大鼠,这种差异以电针２０ｍｉｎ时最为显著。ｉ．ｔ．注射ＤｙｎＡ２．３ｎｍｏｌ后１０ｍｉｎ雌鼠有镇痛作用,而雄鼠在给药后６０ｍｉｎ内均未表现镇痛作用。结论：１００Ｈｚ电针对雌性大鼠的镇痛作用强于雄性,这种性别差异可能与脊髓水平强啡肽镇痛的性别差异有关。     

The effect of genotype on sensitivity to electroacupuncture analgesia

Individual differences in sensitivity to pain and analgesia are well appreciated, and increasing evidence has pointed towards a role of inherited genetic factors in explaining some proportion of such variability. It has long been known by practitioners of acupuncture, an ancient modality of analgesia, that some patients are 'responders' and others 'non-responders.' The present research was aimed at defining the inherited genetic influence on acupuncture analgesia in the mouse, using 10 common inbred strains. Two pairs of metallic needles were inserted into acupoints ST 36 and SP 6, fixed in situ and then connected to the output channel of an electric pulse generator. Electroacupuncture (EA) parameters were set as constant current output (intensity: 1.0-1.5-2.0 mA, 10 min each; frequency: 2 or 100 Hz) with alteration of a positive and negative square wave, 0.3 ms in pulse width. Tail-flick latencies evoked by radiant heat were measured before, during and after EA stimulation. Narrow-sense heritability estimates of 2 and 100 Hz EA were 0.37 and 0.16, respectively. We found that the C57BL/10 strain was the most sensitive, and the SM strain was the least sensitive to both 2 and 100 Hz EA. However, the relative sensitivities of other strains to these two EA frequencies suggested some genetic dissociation between them as well. These results demonstrate a role of inherited genetic factors in EA sensitivity in the mouse, although the low-to-moderate heritability estimates suggest that environmental factors may be of greater importance in predicting who will benefit from this analgesic modality.     

Amitriptyline prolongs the antihyperalgesic effect of 2‐ or 100‐Hz electro‐acupuncture in a rat model of post‐incision pain

The mechanisms through which electro‐acupuncture (EA) and tricyclic antidepressants produce analgesia seem to be complementary: EA inhibits the transmission of noxious messages by activating supraspinal serotonergic and noradrenergic neurons that project to the spinal cord, whereas tricyclic antidepressants affect pain transmission by inhibiting the reuptake of norepinephrine and serotonin at the spinal level. This study utilized the tail‐flick test and a model of post‐incision pain to compare the antihyperalgesic effects of EA at frequencies of 2 or 100 Hz in rats treated with intraperitoneal or intrathecal amitriptyline (a tricyclic antidepressant). A gradual increase in the tail‐flick latency (TFL) occurred during a 20‐min period of EA. A strong and long‐lasting reduction in post‐incision hyperalgesia was observed after stimulation; the effect after 2 Hz lasting longer than after 100‐Hz EA. Intraperitoneal or intrathecal amitriptyline potentiated the increase in TFL in the early moments of 2‐ or 100‐Hz EA, and the intensity of the antihyperalgesic effect of 100‐Hz EA in both the incised and non‐incised paw. In contrast, it did not significantly change the intensity of the antihyperalgesic effect of 2‐Hz EA. The EA‐induced antihyperalgesic effects lasted longer after intraperitoneal or intrathecal amitriptyline than after saline, with this effect of amitriptyline being more evident after 100‐ than after 2‐Hz EA. The synergetic effect of amitriptyline and EA against post‐incision pain shown here may therefore represent an alternative for prolonging the efficacy of EA in the management of post‐surgical clinical pain.     

A minimal stress model for the assessment of electroacupuncture analgesia in rats under halothane.

The use of anesthetics in acupuncture analgesia is controversial. We evaluate a steady-state light anesthesia model to test whether minimal stress manipulation and reliable measurement of analgesia could be simultaneously achieved during electroacupuncture (EA) in animals. A series of experiments were performed. Firstly, EA compliance and tail-flick latencies (TFL) were compared in rats under 0.1%, 0.3%, 0.5%, 0.7%, or 1.1% halothane for 120min. Under 0.5% halothane, TFL were then measured in groups receiving EA at intensity of 3, 10 or 20 volt (V), 1 or 2mg/kg morphine, 20V EA plus naloxone, or control. Subsequently, the effect of EA on formalin-induced hyperalgesia was tested and c-fos expression in the spinal dorsal horn was analyzed. Rats exhibited profound irritable behaviors and highly variable TFL under 0.1% or 0.3% halothane, as well as a time-dependent increase of TFL under 0.7% or 1.1% halothane. TFL remained constant at 0.5% halothane, and needle insertion and electrical stimulation were well tolerated. Under 0.5% halothane, EA increased TFL and suppressed formalin-induced hyperalgesia in an intensity-dependent and naloxone-reversible manner. EA of 20V prolonged TFL by 74%, suppressed formalin-induced hyperalgesia by 32.6% and decreased c-fos expression by 29.7% at the superficial and deep dorsal horn with statistically significant difference. In conclusion, 0.5% halothane provides a steady-state anesthetic level which enables the humane application of EA stimulus with the least interference on analgesic assessment. This condition serves as a minimal stress EA model in animals devoid of stress-induced analgesia while maintaining physiological and biochemical response in the experiment.     

Endogenous orphanin FQ/nociceptin is involved in the development of morphine tolerance

The neuropeptide orphanin FQ/nociceptin (OFQ/N) has been shown to counteract several effects of endogenous and exogenous opioids, and it has been proposed as an opioid-modulating agent involved in the development of morphine tolerance and dependence. However, conflicting results have been obtained from animal models using different protocols to induce morphine tolerance. Here, we report that both genetic and pharmacological blockade of OFQ/N signaling can effectively prevent development of morphine tolerance. OFQ/N knockout mice injected daily with low doses of morphine (10 mg/kg) fail to develop tolerance even after 3 weeks of treatment, whereas their wild-type litter mates show profound tolerance starting after 10 days. Likewise, coadministration of morphine together with the synthetic N/OFQ peptide antagonist, J-113397 (1-[(3R,4R)-1-cyclooctylmethyl-3-hydroxymethyl-4-piperidyl]-3-ethyl-1,3-dihydro-2H-benzimidazol-2-one), is able to block tolerance development in normal mice. These data indicate that release of endogenous OFQ/N after morphine administration might produce a gradual decline of analgesic potency, i.e., tolerance. Interestingly, tolerant and nontolerant groups of mice receiving repeated daily low morphine doses did not differ in their withdrawal behavior after naloxone injection. In contrast, mice receiving escalating doses of morphine developed analgesic tolerance independent of their OFQ/N genotype, whereas withdrawal symptoms were attenuated in OFQ/N-deficient animals. These results indicate that the endogenous OFQ/N system is differentially involved in morphine tolerance development and establishment of opiate dependence, depending on the specific morphine dosage regimen. Furthermore, it suggests that OFQ/N antagonists could provide a novel therapeutic strategy to attenuate morphine tolerance development.     

大鼠电针镇痛的个体差异性及其与基础痛阈的关系

电针镇痛具有个体差异性。我们采用聚类分析的统计学方法,以１００Ｈｚ电针３０分钟内辐射热甩尾潜伏期升高百分数之平均值为指标,将１６８例大鼠分为优针效和劣地效两个群体,其针效至少在两之内保持相对稳定。电针镇痛效果与基础痛阈呈显著正相关。即优针效鼠的基础痛阈显著高于劣针效鼠。     

Electroacupuncture analgesia,stress responses,and variations in sensitivity in rats anesthetized with different sub‐MAC anesthetics

The use of anesthetics to stabilize animals for the purpose of electroacupuncture (EA) analgesic studies can be problematic because of the interference of differential physiological responses to EA and pain. In this study, EA‐induced physiological profiles were surveyed under a sub‐minimal alveolar concentration (sub‐MAC) of two different anesthetics in a previously proposed minimal stress model. First, to select an adequate concentration, compliance with EA and tail‐flick stimulation was evaluated under various concentrations of halothane and isoflurane. Second, using the chosen concentrations, low‐ (4‐Hz) and high‐frequency (100‐Hz) EA were conducted on the right hind limb. The EA effects of the two gases were compared by tail‐flick latency (TFL), hemodynamic variables, and individual variations in analgesic sensitivity. The optimal concentrations for halothane and isoflurane were 0.5% and 0.75%, respectively. TFLs were stable under these anesthetic levels, but rats under 0.75% isoflurane had better compliance than those under 0.5% halothane. EA inhibited TFLs with distinct analgesic patterns when comparing high‐ and low‐frequency EA, but TFL suppression did not differ between the two gases. Heart rate and blood pressure showed temporal and differential responses to low‐ vs. high‐frequency EA, but were comparable between groups under the two anesthetics. The ratios of EA non‐responders in the isoflurane and halothane groups were 32.4% and 26.7%, respectively, without statistical difference. We concluded that sub‐MAC halothane and isoflurane provide optimal conditions for the study of EA‐induced analgesia in rats. In this model, 0.75% isoflurane appears to be a better choice than 0.5% halothane in terms of EA compliance.     

电针抑制iGluRs激动剂鞘内给药易化的大鼠脊髓背角突触传递LTP

目的:观察电针对离子型谷氨酸受体(iGluRs)激动剂易化脊髓背角神经元而形成的长时程增强(LTP)的抑制作用,并探讨其机制.方法:大鼠脊髓L4/L5节段细胞外记录脊髓背角C-纤维诱发场电位的LTP.iGluRs激动剂NMDA或[±]-AMPA HBr 40pg鞘内给药(i.t.)易化脊髓背角神经元;对照组i.t.生理盐水2μl.2 Hz,1 mA电针(EA)环跳和委中穴.观察电针对iGluRs激动剂i.t.易化的LTP的抑制作用.结果:对照组低强度强直刺激(HFS)前、后脊髓背角LTP)的变化率无统计学差异;i.t.NMDA或[±]-AMPA HBr后低强度HFS,可引起显著的LTP,与对照组比较P相似文献