中脑导水管周围灰质内注射抗阿片肽血清对神经降压素增强电针镇痛的影响

本工作以钾离子透入引起大鼠甩尾反应作为痛反应指标,观察纳洛酮（ＮＸ）和抗阿片肽血清对大鼠中脑导水管周围灰质（ＰＡＧ）内微量注射神经降压素（ＮＴ）增强电针镇痛作用的影响。结果显示：（１）ＰＡＧ内微量注射ＮＴ后,大鼠电针镇痛效应明显提高;（２）ＰＡＧ内注射大剂量ＮＸ,可以显著减弱ＮＴ增强电针镇痛效应;（３）ＰＡＧ内微量注射抗甲脑啡肽血清和抗β内啡肽血清后,ＮＴ增强电针镇痛的作用明显降低;而ＰＡＧ内微量注射抗强啡肽Ａ１１３血清,对于ＮＴ增强电针镇痛的作用并无明显影响。提示：ＰＡＧ内ＮＴ在针刺镇痛过程中发挥重要作用,ＮＴ增强电针镇痛的作用与甲脑啡肽和β内啡肽有较密切的关系。     

中脑导水管周围灰质内注射抗阿片肽血清对神经降压素增强电针镇痛的 …

本工作以钾离子透入引起大鼠甩尾反应作为痛反应指标,观察纳洛酮（ＮＸ）和抗阿片肽血清对大鼠中脑导水管周围灰质（ＰＡＧ）内微量注射神经降压素（ＮＴ）增强电针镇痛作用的影响。     

下丘脑室旁核注射神经降压素对大鼠胃酸分泌的影响及机制探讨

本实验用乌拉坦麻醉的大鼠,探讨了下丘脑室旁核（ＰＶＮ）注射神经降压素（ＮＴ）对胃酸分泌的影响及其机制。结果表明,ＰＶＮ注射微量ＮＴ后,胃酸排出量呈剂量依赖性减少,此效应可被侧脑室内预先注射酚妥拉明所阻断,但不能被螺哌啶酮阻断、双侧颈迷走神经切断后,ＰＶＮ注射ＮＴ对胃酸排出量无明显影响。这提示,ＰＶＮ注射ＮＴ对大鼠胃酸分泌的抑制作用,可能与该处α－受体的激活有关,并通过迷走神经所中介。     

大鼠侧脑室注射神经降压素对血压的作用

雄性Ｓｐｒａｇｕｅ－Ｄａｗｌｅｙ大鼠,用乌拉坦腹腔麻醉,在侧脑室注射神经降压素（ＮＴ）（１０,２０μｇ）可引起血压升高或降低,心率减慢,预先ｉｃｖ ａ１受体阻断剂哌唑嗪,可阻断ＮＴ的中枢升压反应,预先ｉｃｖ Ｍ受体阻断剂硫酸阿托品,可阻断ＮＴ的中枢降压反应,预先ｉｃｖ Ｈ１受体阻断剂扑尔敏或Ｈ２受体阻断剂甲氰咪胍,对ＮＴ的中枢心血管效应均无明显影响。实验结果表明：脑中ＮＴ升高可使血压升高或降低;在     

一氧化氮和cGMP参与神经降压素的肝细胞保护作用

本工作在原代培养的小鼠肝细胞上观察了一氧化氮,ｃＧＭＰ和ｃＡＭＰ的变化与神经降压素肝细胞保护作用之间的关系。结果如下：向培养液中加入醋氨酚１２ｈ后,ＧＯＴ和ＧＰＴ漏出明显增加;在加醋酚之前给予神经降压素则使液氨酶漏出明显减轻。给予ＮＯ合成酶阻断剂Ｌ－ＮＡＭＥ可完全阻断神经降压素的保护作用。     

大鼠孤束核神经降压素在迷走—加压反应中的作用

采放放射免疫、核团微量注射及组织荧光分光测定等实验方法,研究了大量孤束核神经降压素对迷走－加压反应的影响,结果表明,１．不走神经向中端,孤束核神经降压素免疫活性物的含量明显增高;２．孤束核内注入抗神经降压素血清后,刺激颈迷走神经向中端,迷走－加压反应明显;３．孤束核内注入神经降压素后,刺激颈迷走神经向中端,迷走－加压反应明显减弱,４．孤束核注入神经降压素后,刺激颈迷走神经向中端,孤束核去甲腺素含量     

大鼠蓝斑核区神经降压素对迷走—加压反应的影响

本文应用放射免疫、核团微量注射及组织荧光分光测定等实验方法,研究大鼠蓝斑核区神经降压素对迷走-加压反应的影响。结果表明:1.电刺激颈迷走神经向中端,孤束核、蓝斑核区和下丘脑中神经降压素免疫活性物的含量明显增高(p<0.05)。2.蓝斑核区注入神经降压素后,刺激颈迷走神经向中端,迷走-加压反应明显减弱(P<0.01),并呈明显的量效依赖关系。3.蓝斑核区注入抗神经降压素血清,迷走-加压反应明显加强(p<0.01)。4.蓝斑核区注入神经降压素后,刺激颈迷走神经向中端,该区去甲肾上腺素含量明显增高(p<0.05)。以上结果提示:内源与外源性神经降压素参与迷走-加压反应的调节过程,并可能与神经降压素引起蓝斑核区去甲肾上腺素含量增加有关。     

神经降压素对刺激下丘脑减压区所致减压反应的影响

大鼠下丘脑前部一侧减压区,采用直流方波或化学刺激、注射微量神经降压素及其抗血清和放射免疫分析等方法,探讨了神经降压素对刺激该减压区所致减压反应的影响。结果表明：（１）电或化学刺激该减压区,可出现同其它哺乳动物相似的减压反应;（２）该减压区注射微量神经降压素,可使电刺激该减压区所致的减压反应明显增强;反之,注射抗神经降压素血清,该减压反应明显抑制;（３）电刺激该减压区,可使下丘脑和血浆中的神经降压素免疫活性物含量明显增高。结果提示,神经降压素可能参与电刺激该减压区所致的减压反应过程。     

中枢催产素在电针镇痛中的作用

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,观察了侧脑室注射催产素(OT)及抗催产素血清(AOTS)对大鼠痛阈和电针镇痛效应的影响。注射50 ngOT 后80min 内,大鼠痛阈比注药前增加20—38%。与注射生理盐水组的痛阈相比有非常明显的增高(p<0.01—0.001),侧脑室注射 OT 后电针期内,痛阈增加139—234%,与生理盐水电针组相比,有显著差异(P<0.05—0.01)。OT 的剂量在25—100ng 范围内,其增强电针镇痛效应有明显的剂量-效应关系。注射 AOTS 后,电针镇痛应明显低于注射正常兔血清(NRS)组(p<0.05—0.01)。上述结果表明,侧脑室注射 OT,既可提高痛阈又可明显地增强电针镇痛效应,而用 AOTS消除内源性 OT 的作用后,电针镇痛效应明显降低。这提示,中枢神经系统内的 OT 在电针镇痛过程中,发挥一定的作用     

神经激肽A注入大鼠外侧网状核或中缝大核产生的镇痛效应

本工作采用核团内微量注射的方法,以甩尾反射潜伏期（ＴＦＬ）为痛阈指标,在浅麻状态下的大鼠上,对神经激肽Ａ（ＮＫＡ）在外侧网状核（ＬＲＮ）和中缝大核（ＮＲＭ）中的作用作了探讨。研究结果表明,ＮＫＡ（０．５μｇ／０．５μｌ）注入ＬＲＮ后的１０ｍｉｎ内大鼠ＴＦＬ明显延长（ｎ＝１２,Ｐ＜０．００１）,同样剂量ＮＫＡ注入ＮＲＭ后的５ｍｉｎ内,ＴＦＬ也明显延长（ｎ＝１３,Ｐ＜０．００１）,提示ＮＫＡ可能是ＬＲＮ和ＮＲＭ内参与痛觉的一种神经调质。     

大鼠侧脑室注射精氨酸加压素对针刺镇痛的影响

以钾离子透入法引起大鼠甩尾反应为指标,测定动物的痛阈。由侧脑室注射精氮酸加压素(AVP)后,大鼠痛阈升高33.6％～68.5％,针刺镇痛效应明显加强,痛阈提高202.4％～302.7％。脑室注射抗精氨酸加压素血清,动物痛阈虽无明显变化,但针刺镇痛效应明显削弱,痛阈仅增加41.6％～71.0％。注射抗β-内啡肽血清和抗强啡肽A血清并不阻断AVP增强针刺镇痛效应。本工作的结果提示,脑内AVP参与针刺镇痛,这种作用与脑内内源性β-内啡肽和强啡肽的关系不甚密切。     

生长抑素通过中缝大核发挥镇痛和增强电针镇痛的作用

本工作以钾离子透入引起大鼠甩尾为痛指标,观察了中缝大核微量注射生长抑素、生长抑素的耗竭剂半胱胺和抗生长抑素血清对大鼠痛阈和电针镇痛效应的影响。中缝大核微量注射生长抑素可提高大鼠的痛阈,并使电针镇痛的效应加强。用半胱胺耗竭或用抗生长抑素血清中和中缝大核中的生长抑素,均可使大鼠的痛阈降低,并减弱电针镇痛的效应。这表明生长抑素可能通过中缝大核发挥镇痛和增强电针镇痛的作用。     

家兔隔核中去甲肾上腺素对皮肤与内脏痛阈的影响

本工作以电刺激内脏大神经或耳尖部皮肤测定清醒家兔内脏痛阈或皮肤痛阈,以探讨隔核去甲肾上腺素在内脏镇痛和皮肤镇痛中的作用以及与中脑导水管周围灰质(PAG)中内阿片肽系统的关系。实验观察到,双侧隔核内微量注射α受体激动剂可乐宁(10μg/2μl)或α受体阻断剂酚妥拉明(10μg/2μl)对内脏痛阈无明显影响。注入β受体激动剂异丙肾上腺素(1μg/2μl)使内脏痛阐明显升高;而注入β受体阻断剂心得安(1Cμg/2μl)则内脏痛阈明显降低。隔核内注入酚妥拉明(10μg/2μl)或心得安(10μg/2μl)均可使皮肤痛阈明显提高。提示,隔核内NA通过β受体调制内脏痛;通过α受体和β受体调制皮肤痛。隔核内注入异丙肾上腺素(1μg/2μl)明显地镇内脏痛,此作用可被PAG内注射纳洛酮(1μg/2μl)或注射抗亮啡肽抗血清(1:20,000)所减弱;但可使PAG内亮啡肽样物质释放量增加。这提示,隔核内NA的镇内脏痛作用与PAG的内阿片肽系统有关;其中亮非肽在这一过程中具有重要作用。     

大鼠中脑导水管周围灰质微量注射孤啡肽对痛和针刺镇痛的影响

孤啡肽是新近发现的神经肽,结构与内阿片肽相似,但作用明显不同。本文采用脑核团内微量注射方法,在大鼠电刺激甩尾测痛模型上,观察ＯＦＱ在中脑导水管周围灰质内对痛和针刺镇痛的影响。结果表明：ＰＡＧ内微量注射ＯＦＱ可使大鼠痛阈降低,并明显对抗针刺镇痛;另外还发现,ＯＦＱ在ＰＡＧ内还可以对抗μ受体激动剂羟甲芬太尼加强针刺镇痛的效应。     

Synergetic Analgesia of Propentofylline and Electroacupuncture by Interrupting Spinal Glial Function in Rats

Previous studies indicated that disruption of glial function in the spinal cord enhanced electroacupuncture (EA) analgesia in arthritic rats, suggesting glia is involved in processing EA analgesia. To probe into the potential value for clinical practice, the present study was to investigate the effect of propentofylline, a glia inhibitor, on EA analgesia in rats. Mechanical allodynia induced by tetanic stimulation of sciatic nerve (TSS) was used as a pain model. On day 7 after TSS, EA treatment induced a significant increase in paw withdrawal threshold to mechanical stimulation. Intrathecal or intraperitoneal injection of propentofylline relieved TSS-induced mechanical allodynia. The combination of low dosage of propentofylline and EA produced more potent anti-allodynia than propentofylline or EA alone. Immunohistochemistry exhibited that TSS-induced activation of microglia and astrocytes was inhibited significantly by propentofylline. These results indicate that propentofylline and EA induce synergetic analgesia by interrupting spinal glial function.     

Further investigations on neurotensin as central modulator of intestinal motility in rats

Previous studies have shown that neurotensin (NT) administered intracerebroventricularly (i.c.v.) to rats provokes an inhibition of intestinal propulsion linearly related to the log of administered doses. In the present study it is demonstrated that, in contrast to morphine, repeated i.c.v. administrations of NT (2.5 nmol/rat/day) did not result in tolerance to the intestinal effect. Naloxone (Nx) administered i.c.v. fully antagonized the intestinal inhibition of i.c.v. morphine, but did not significantly alter the NT effect. However, centrally administered thyrotropin-releasing hormone (TRH) inhibited NT-induced (but not morphine-induced) intestinal inhibition. Direct microinjections of NT into the periaqueductal gray matter (PAG) produced complete inhibition of intestinal propulsion when the microinjections were localized in the dorsal portion. Finally, subdiaphragmatic vagotomy totally abolished the inhibition induced by NT into the PAG, while morphine was not affected. Some considerations are put forward concerning the existence in the central nervous system of a peptidergic pathway modulating intestinal function.     

家兔中脑导水管周围灰质中注射八肽胆囊收缩素（CCK—8）拮抗吗啡镇痛和...

We have reported that intracerebroventricular (i. c. v.) injection of 1-4 ng of CCK-8 to the rat produced a remarkable antagonistic effect on morphine analgesia. In order to study the species specificity and the site of action, CCK-8 was microinjected into the PAG of the rabbit, and its influence on morphine analgesia and electroacupuncture analgesia was observed. The latency of the escape response (ERL) to radiant heat focused on the snout was measured as an index of the pain threshold. Microinjections were made via cannulae chronically implanted into the PAG. The drug solutions were delivered in a volume of 1 microliter, at a speed of 0.125 microliter/min. The ERL was measured for a period of 60 or 70 minutes at 10 min intervals. 1. CCK-8 administered unilaterally to the PAG of the rabbit at a dose of 3 ng antagonized the analgesia induced by morphine (4 mg/kg, i. v.) by 73% (P less than 0.001), and reduced the analgesic effect of electroacupuncture by 67% (P less than 0.001). These effects were dose-dependent within the range from 1.5 ng to 6.0 ng. The effect of CCK-8 was reversed by CCK receptor blocker proglumide (4 microliters, intra-PAG injection). Unsulfated CCK-8 (CCK-us) had no effect in this regard. These results indicate that in the PAG of the rabbit, exogenously administered CCK-8 was capable of antagonizing opioid analgesia by the activation of CCK receptors. 2. Two groups of rabbits were given with morphine (2 mg/kg, i. v.) and simultaneous injection of CCK-8 antiserum (CCK-AS, 1 microliter) or normal rabbit serum (NRS) into the PAG.(ABSTRACT TRUNCATED AT 250 WORDS)