坐骨神经分支选择性损伤模型大鼠右美托咪啶鞘内注射的镇痛作用

背景：右美托咪啶是一种高效、高选择性的α2肾上腺素受体激动剂,具有镇静、镇痛、抗焦虑等作用,对呼吸影响小。 目的：观察鞘内注射右美托咪啶对坐骨神经分支选择性损伤模型大鼠的镇痛作用。 方法：雄性SD大鼠36只按随机数字表法等分为正常对照组、生理盐水组和右美托咪啶组,后2组结断腓总神经和胫神经建立坐骨神经分支选择性损伤大鼠模型,右美托咪啶组在坐骨神经分支选择性损伤后14 d内每天鞘内注射右美托咪啶3μg/kg,生理盐水组大鼠注射生理盐水。 结果与结论：与生理盐水组相比,右美托咪啶组大鼠给药后的机械性缩足反射阈值与热缩足潜伏期显著性升高（P〈0.05）,脊髓背角中神经型一氧化氮合酶mRNA和蛋白的表达水平明显降低（P〈0.05）,脊髓背角神经元损伤程度明显减轻,且在给药14 d时脊髓背角神经型一氧化氮合酶mRNA和蛋白的表达水平及脊髓背角神经元损伤情况与正常对照组接近。提示鞘内注射右美托咪啶可抑制脊髓背角神经型一氧化氮合酶的表达,减轻大鼠坐骨神经损伤引起的疼痛。     

The antinociceptive activity of Muntingia calabura aqueous extract and the involvement of L-arginine/nitric oxide/cyclic guanosine monophosphate pathway in its observed activity in mice

The present study was carried out to investigate on the possible involvement of L-arginine/nitric oxide/cyclic guanosine monophosphate (L-arginine/NO/cGMP) pathway in the aqueous extract of Muntingia calabura (AEMC) leaves antinociception in mice assessed by abdominal constriction test. The AEMC, obtained by soaking the dried leaves in distilled water (DH(2)O) (1 : 2; w/v) for 24 h, was prepared in concentrations of 10%, 50% and 100% that were approximately equivalent to doses of 27, 135 and 270 mg/kg, and administered subcutaneously (s.c.) 5 min after pre-treatment (s.c.) of mice with DH(2)O, L-arginine (20 mg/kg), N(G)-monomethyl-L-arginine acetate (L-NMMA; 20 mg/kg), N(G)-nitro-L-arginine methyl esters (L-NAME; 20 mg/kg), methylene blue (MB) (20 mg/kg), respectively. The AEMC was found to exhibit a concentration-dependent antinociception after pre-challenge with DH(2)O. Interestingly, pre-treatment with L-arginine was found to block significantly (P < 0.05) the AEMC antinociception but only at the highest concentration (100%) of AEMC used. On the other hand, pre-treatment with L-NAME was found to significantly (P < 0.05) enhance the low concentration but inhibit the high concentration AEMC antinociception. MB was found to significantly (P < 0.05) enhance AEMC antinociception at all concentrations used. Except for the higher concentration of AEMC used, co-treatment with L-NAME was found to insignificantly and significantly (P < 0.05) reverse the L-arginine effect when given alone or with low concentration AEMC, respectively. In addition, co-treatment with MB significantly (P < 0.05) reversed the L-arginine effect when given alone or with 10% concentration AEMC but failed to affect the activity of the rest of concentrations used. As a conclusion, this study has demonstrated the involvement of L-arginine/NO/cGMP pathway in AEMC antinociception.     

Pharmacological approaches to improve endothelial repair mechanisms

Endothelial injury is thought to play a pivotal role in the development and progression of vascular diseases, such as atherosclerosis, hypertension or restenosis, as well as their complications, including myocardial infarction or stroke. Accumulating evidence suggests that bone marrow-derived endothelial progenitor cells (EPCs) promote endothelial repair and contribute to ischemia-induced neovascularization. Coronary artery disease and its risk factors, such as diabetes, hypercholesterolemia, hypertension and smoking, are associated with a reduced number and impaired functional activity of circulating EPCs. Moreover, initial data suggest that reduced EPC levels are associated with endothelial dysfunction and an increased risk of cardiovascular events, compatible with the concept that impaired EPC-mediated vascular repair promotes progression of vascular disease. In this review we summarize recent data on the effects of pharmacological agents on mobilization and functional activity of EPCs. In particular, several experimental and clinical studies have suggested that statins, angiotensin-converting enzyme inhibitors, angiotensin II type 1 receptor blockers, PPAR-γ agonists and erythropoietin increase the number and functional activity of EPCs. The underlying mechanisms remain largely to be defined; however, they likely include activation of the PI3-kinase/Akt pathway and endothelial nitric oxide synthase, as well as inhibition of NAD(P)H oxidase activity of progenitor cells.     

右美托咪定对心血管保护作用的研究进展

右美托咪定(dexmedetomidine,DEX)为α2肾上腺素能受体(α2-AR)激动剂,是目前临床常用的药物,其可能通过减轻血流动力学改变、减轻氧化应激反应、抑制心肌细胞凋亡、减轻心肌炎症反应、改善心肌缺血再灌注后微循环功能障碍、保护线粒体结构和功能、抗心律失常作用等机制对围手术期患者的心血管系统产生作用.本文就...     

Pharmacological characterization of alpha adrenoceptors involved in the antinociceptive and cardiovascular effects of intrathecally administered clonidine

The effects on nociception, blood pressure and heart rate of clonidine administered intrathecally to the lumbar level were determined in conscious rats and in rats anesthetized lightly with pentobarbital. In anesthetized rats, intrathecal (i.t.) clonidine (3.2-32.0 micrograms) inhibited the nociceptive tail-flick reflex and had biphasic effects on blood pressure; lesser doses (1.0-10.0 micrograms) produced depressor effects, whereas a greater dose (32.0 micrograms) produced a marked pressor response. Clonidine also produced biphasic effects on blood pressure in conscious rats, with the dose-response function shifted upward and to the left of that observed in anesthetized rats. The depressor and antinociceptive effects of 3.2 micrograms of clonidine were antagonized by pretreatment with yohimbine (30.0 micrograms i.t.) but not by prazosin (30.0 micrograms i.t.) or by yohimbine (0.1 mg/kg i.v.). Thus, these effects of clonidine are mediated by spinal alpha-2 adrenoceptors. The pressor response to 32.0 micrograms of clonidine (i.t., lumbar) was accompanied by marked bradycardia, and similar cardiovascular effects were observed when this dose of clonidine was administered either i.v. or to the cervical level of the spinal cord. The pressor response to 32.0 micrograms of clonidine (i.t., lumbar) was not reduced significantly by i.t. pretreatment with yohimbine (30.0 micrograms) or prazosin (30.0 micrograms), but was diminished significantly by i.v. pretreatment with yohimbine (1.0 mg/kg), prazosin (0.1 mg/kg) or phentolamine (2.0 mg/kg). Neither chlorisondamine (2.5 mg/kg i.v.) or the V1-vasopressin receptor antagonist [1-(beta-mercapto-beta,beta-cyclopentamethylene propionic acid), 2-(o-methyl)tyrosine]Arg8-vasopressin (10.0 micrograms/kg i.v.) reduced the clonidine-produced pressor response. After i.t. injection of 32.0 micrograms of [3H]clonidine, peak levels of radioactivity in the blood were observed at 2 min and corresponded to a blood concentration of 38.8 ng/ml. Injection of an i.v. bolus dose (2.5 micrograms/kg) sufficient to produce these blood levels resulted in a transient pressor response. These results suggest that after i.t. administration of greater doses of clonidine, sufficient amounts of the drug are rapidly redistributed systemically to produce pressor effects by stimulation of vascular alpha adrenoceptors.     

右美托咪定对带状疱疹患者免疫功能的影响

目的探讨右美托咪定对带状疱疹免疫功能的影响。方法将40例带状疱疹后遗神经痛患者随机分为2组,每组20例。观察组给予右美托咪定联合局麻药皮内注射,对照组给予单纯局麻药皮内注射。比较2组不同时段CD4、CD8、CD4/CD8,以及视觉模拟评分(VAS)的变化。结果观察组治疗24、48 h时CD8水平显著低于对照组,CD4/CD8水平显著高于对照组。治疗后5、10、30 d观察组VAS显著低于对照组。结论右美托咪定联合局麻药组治疗带状疱疹后神经疼痛,能增加患者的免疫力,并延长局麻药的镇痛时间,减少治疗次数,缩短疗程,且后期疗效明显,优于单纯局麻药治疗,值得临床推广。     

Pharmacological evidence of involvement of nitric oxide pathway in anti‐pruritic effects of sumatriptan in chloroquine‐induced scratching in mice

Chloroquine (CQ) induces histamine‐independent itch in human and mice. We recently reported the role of intradermal nitric oxide (NO)/cyclic guanosine monophosphate pathway in CQ‐evoked scratching in mice. Chloroquine stimulates neuronal nitric oxide synthase (nNOS) activity to over‐producing NO in the skin. Sumatriptan, a 5‐hydroxytryptamine 1b/1d receptors (5‐HTR1b/1d) agonist, is involved in pain and used to treat migraine and cluster headaches. According to previous studies, sumatriptan inhibits NOS activity. Thus, we aimed to investigate the effect of sumatriptan on CQ‐induced scratching. We used the rostral back model of itch. Chloroquine was injected intradermally into the rostral back of NMRI mice, and the scratching behavior was evaluated by measuring the number of bouts over 30 min. We evaluated the effect of sumatriptan and combination of sumatriptan and a non‐selective NO synthase inhibitor, L‐N‐nitro arginine methyl ester (L‐NAME), on the scratching behavior. Additionally, the changes of skin, hippocampus, and cortical nitrite level after different treatments were studied. Intraperitoneal and intradermal sumatriptan attenuates CQ‐induced itch which reversed by GR‐127935, the selective 5‐HTR1b and 5‐HTR1d antagonist. Co‐administration of subeffective doses of sumatriptan and L‐NAME significantly decreases the scratching behavior. Intradermal injection of CQ significantly increases the intradermal nitrite levels while it does not have any significant effects on hippocampal or cortical nitrite concentrations. Likewise, the effective doses of intraperitoneal and intradermal sumatriptan significantly reduce intradermal nitrite levels. We concluded that sumatriptan suppresses CQ‐induced itch most likely by activating 5‐HT1b/1d receptors. This effect probably mediates through NO pathway.     

Systemic physostigmine increases the antinociceptive effect of spinal morphine

In this study we evaluated the antinociceptive effect of concurrent intrathecal (i.t.) and subcutaneous (s.c.) administration of morphine and physostigmine, respectively. The experiments were performed on male Wistar rats. Intrathecal administration of morphine was performed through a catheter implanted in the subarachnoid space. The ‘tail-immersion' test was used to measure animals' responses to evoked nociceptive stimuli. Interaction of drugs was analyzed using a dose addition model. Both i.t. (1–5 μg) administration of morphine and s.c. (50–250 μg/kg) administration of physostigmine increased the latencies of nociceptive responses in a dose-dependent manner. Two micrograms of i.t. morphine and 100 μg/kg of s.c. physostigmine demonstrated 31.6±10.6 and 34.2±11.4 percentage of maximal possible effect (%MPE), respectively. Simultaneous administration of 1 μg of i.t. morphine and 50 μg/kg of s.c. physostigmine produced a %MPE equal to 84.8±16.9. Thus, combined administration of 1 μg i.t. morphine and 50 μg/kg s.c. physostigmine resulted in a strong, highly significant antinociceptive effect. This effect was much higher than the effect expected if both drugs acted in an additive manner. Supra-additive interaction observed in this study might be a result of simultaneous activation of different neurotransmitter systems involved in nociceptive processing at the spinal as well as at the supraspinal level of the CNS.     

The effects of dexmedetomidine on spontaneous contractions of isolated gravid rat myometrium

The direct effects of dexmedetomidine on isolated gravid rat myometrium were investigated in this in vitro study; such effects may have clinical repercussions in the administration of anesthesia to obstetric patients. Samples of myometrium were taken from 12 gravid rats. Myometrial strips were dissected microscopically and mounted on the myograph at a resting tension of 1 gin bath that contained Krebs solution. After spontaneous contractions of the myometrium had been steadily established, increasing concentrations of dexmedetomidine were added to baths via micropipette, and the effects of these additions were recorded via myograph. Dexmedetomidine in vitro caused a significant increase in the amplitude, frequency, and area under the curve of myometrial contractions in a dose-dependent manner. Results of this study demonstrate that dexmedetomidine increases spontaneous contractions in rat myometrium; however, further investigation is needed to clarify the usefulness of dexmedetomidine in the administration of obstetric anesthesia.     

Preconditionin effects of dexmedetomidine on myocardial ischemia/reperfusion injury in rats

Background: Preconditioning might protect the myocardium against ischemia/ reperfusion injury by reducing infarct size and preventing arrhythmias. Dexmedetomidine (DEX) is a highly selective α2-agonist used for sedoanalgesia in daily anesthetic practice. The cardioprotective effects of DEX on infarct size and on the incidence of arrhythmias observed after regional ischemia/reperfusion injury in vivo have not been reported.Objective: The aim of this study was to determine whether DEX exhibits a preconditioning effect and reduces infarct size and the incidence and duration of arrhythmias in a regional cardiac ischemia/reperfusion model in rats.Methods: Adult male Sprague-Dawley rats were anesthetized with sodium thiopental and mechanically ventilated (0.9 mL/100 g at 60 strokes/min) through a cannula inserted into the trachea after tracheotomy. Cardiac ischemia was then produced by ligating the left main coronary artery for 30 minutes, followed by a reperfusion period of 120 minutes. Blood pressure (BP) and heart rate (HR) were monitored and echocardiograms (ECGs) were performed. Arrhythmia was scored based on incidence and duration. The animals were randomly divided into 3 groups. The ischemic preconditioning (IPC) group underwent 5 minutes of ischemia followed by 5 minutes of reperfusion before the 30-minute ischemia/120-minute reperfusion period. In the DEX group, intraperitoneal (IP) DEX 1 mL (100 μg/kg) was administered 30 minutes before the ischemia/ reperfusion period. In the control group, IP saline 1 mL was administered 30 minutes before the ischemia/reperfusion period. After reperfusion, the heart was excised, demarcated with saline and ethanol to identify the occluded and nonoccluded myocardium, and cut into slices ~2 mm thick, that were then stained and placed between 2 glass plates. The risk zone and the infarct zone were compared between groups. The investigator assessing the infarcts was blinded to the study group.Results: Twenty-one adult (aged 4-6 months) male Sprague-Dawley rats weighing 280 to 360 g were included in the study; 7 rats were assigned to each group. BP, HR, and ECG readings were not significantly different between groups and did not change during the study. Arrythmias occurred during ischemia and reperfusion in all groups. The duration of the arrhythmias was significantly shorter and the arrhythmia score was significantly lower in the IPC group (all, P<0.05), compared with the control group; however, they were not significantly different in the DEX group. During the ischemic period, duration of ventricular tachycardia (VT) and ventricular premature contractions (VPC) in the DEX group was significantly longer than that observed in the IPC group (all, P<0.05). The duration of VPC was also significantly shorter than that observed in the control group (both, P<0.05). Duration of VT during the reperfusion period in the DEX group was significantly longer than that observed in both IPC and control groups (both, P<0.05). The mean (SD) percentage of damage was significantly lower in the IPC group (44.1% [2.0%]) and the DEX group (26.7% [2.0%]) compared with the control group (69.0% [3.0%]; both, P<0.05). The percentage of damage in the DEX group was also significantly lower compared with the IPC group (P<0.05).Conclusions: This small, experimental in vivo study found that DEX was associated with reduced infarct size in ischemia/reperfusion injury in regional ischemia in this rat model but had no effect on the incidence of arrhythmias. Future studies are needed to clarify these findings.     

不同速率输注右美托咪定预防腰麻后寒战的疗效观察

目的探讨不同速率输注右美托咪定预防腰麻后寒战的临床疗效。方法选择腰麻下手术患者100例,ASA分级Ⅰ、Ⅱ级,根据不同的右美托咪定输注速率将患者随机分为4组:D1组[0.2 g/(kg.h)]、D2组[0.4 g/(kg.h)]、D3组[0.6 g/(kg.h)]和对照组。记录4组患者术中生命体征变化、预防寒战的效果和不良反应发生情况。结果 D1、D2、D3组患者在T1、T2、T3时的HR较同组T0时显著下降(P<0.05),且D3组下降最为明显,部分患者需要阿托品干预;对照组患者T1、T2、T3的HR与D1、D2、D3组比较差异有统计学意义(P<0.05)。与对照组比较,D1、D2、D3组寒战发生率显著降低(P<0.05),且3组组内比较差异无统计学意义(P>0.05);D1、D2、D3组患者心动过缓的发生率明显高于对照组,且以D3组最为明显,阿托品的使用率最高,患者嗜睡情况也明显增多(P<0.05)。结论右美托咪定能有效预防腰麻后寒战的发生,以0.2~0.4μg/(kg.h)的静注速率维持较佳。     

右旋美托咪啶对慢性神经病理性疼痛大鼠的作用研究

目的探讨右旋美托咪啶(Dex)对慢性神经病理性疼痛模型大鼠的镇痛作用及对大鼠行为学的影响。方法成年雄性SD大鼠32只,随机分为假手术(Sham)组及坐骨神经慢性压迫模型(CCI)组。2组分别给予腹腔注射右旋美托咪啶50μg/kg或等量生理盐水。于给药前,给药后15、30、60、90、120、180、240 min及24 h以von Frey丝测定大鼠机械缩足反应阈值(MWT),以BME-410A型热痛刺激仪测定大鼠热痛缩腿反应潜伏期(PWLT)。腹腔注射右旋美托咪啶前后进行旷场实验、水迷宫等行为学实验。结果右旋美托咪啶可以增加CCI大鼠的机械缩足反应阈值,延长大鼠的热痛缩腿反应潜伏期,不影响大鼠旷场实验得分、粪便次数及修饰次数,不影响水迷宫实验的逃避潜伏期及穿环指数。结论右旋美托咪啶对慢性神经病理性疼痛大鼠有明显的镇痛作用,对大鼠运动能力、学习能力、空间认知能力无影响。     

右美托咪定在儿科中的应用

近年来,关于右美托咪定在儿科应用的报道逐渐增多。右美托咪定几乎不影响呼吸,具有镇静、镇痛、抗焦虑等作用。大量研究表明右美托咪定对缺血性和缺氧性损伤的组织有保护作用。右美托咪定不仅应用于小儿麻醉,而且用于小儿术后镇痛、辅助检查的镇静等,但其具有引起心动过缓及影响血液循环等副作用。本文对右美托咪定在儿科中的应用及其局限性进行综述。     

激光对血小板膜粘附分子表达的影响及其一氧化氮机制

目的 探讨低能量激光血管内照射（ILIB）对血小板膜粘附分子表达的影响及其一氧化氮（NO）机制。方法 对球囊损伤动脉内膜犬行ILIB,观察ILIB对血小板CD41、CD62p表达和血浆NO含量的影响。结果 ILIB可显著抑制血小板CD41、CD62P的表达（P＜0．01）,提升血浆NO含量（P＜0．01）。结论 ILIB可提升血浆NO含量,并通过NO抑制血小板CD41、CD62P的表达。     

右美托咪定在慢性阻塞性肺疾病急性发作患者机械通气镇静中的疗效分析

目的：评估右美托味定在慢性阻塞性肺疾病急性发作（AECOPD）患者机械通气镇静中的疗效及安全性。方法：选择60例AECOPD并发呼吸衰竭在ICU接受有创机械通气的患者,按随机数字表法分成右美托咪定组30例和咪达唑仑组30例,观察两组患者镇静的成功率、机械通气时间、ICU住院时间、谵妄发生率、呼吸机相关性肺炎（VAP）的发生率以及心血管不良事件的发生率。结果：两组患者均能达到良好的镇静效果（93．33％：96．67％,P〉0．05）,但右美托咪定组所需吗啡用量明显少于咪达唑仑组[（1．2±0．3）mg／h：（2．5±0．4）mg／h,P〈0．05];右美托咪定组机械通气时间、谵妄发生率、呼吸机相关性肺炎（VAP）的发生率、ICU住院时间均少于咪达唑仑组[（5．22±2．36）d、10％、16．67％、（4．25±1．25）d：（5．63±2．86）d、（2．58±1．36）h、42％、34％、（6．33±2．74）d,P〈0．osJ;右美托咪定组心动过缓发生率较咪达唑仑组高（12％：4%,P〈0．05）,低血压发生率两者相似（22％：20％,P〉0．05）。结论：右美托咪定在起到较好理想镇静效果的同时,所需吗啡应用剂量小,并可以减少机械通气时间、ICU住院时间,减少谵妄发生率,减少呼吸机相关性肺炎发生。其临床不良反应发生率低,安全性较高,可作为AECOPD行机械通气患者镇静的一线用药。     

COX-dependent mechanisms involved in the antinociceptive action of NSAIDs at central and peripheral sites

Despite the diverse chemical structure of aspirin-like drugs, the antinociceptive effect of NSAIDs is mainly due to their common property of inhibiting cyclooxygenases involved in the formation of prostaglandins. Prostaglandins are potent hyperalgesic mediators which modulate multiple sites along the nociceptive pathway and enhance both transduction (peripheral sensitizing effect) and transmission (central sensitizing effect) of nociceptive information. Inhibition of the formation of prostaglandins at peripheral and central sites by NSAIDs thus leads to the normalisation of the increased pain threshold associated with inflammation. The contribution of peripheral and central mechanisms to the overall antinociceptive action of NSAIDs depends on several factors including the location of the targets of drug action, the site of drug delivery and the uptake and distribution to the site of action. The present work reviews the data on the regulation and location of cyclooxygenases at central and peripheral sites of the nociceptive pathway and focuses on the role of COX in the generation and maintenance of pain hypersensitivity. Experimental and clinical evidences are used to evaluate the significance of the peripheral and central antihyperalgesic effects of NSAIDs.     

右美托咪定经鼻使用在麻醉中的研究进展

右美托咪定为美托咪定的活性右旋异构体,是一种高效、高选择性的α2肾上腺素能受体激动剂,具有良好的镇静、镇痛和抗交感作用。同时对呼吸无抑制,可作为围手术期麻醉合并用药。右美托咪定经鼻给药是临床常用的方式之一,鼻腔黏膜毛细血管丰富,吸收药物迅速。与静脉给药相比,经鼻给药无创简便、刺激性小,起效缓慢平稳、易于被患者接受,因而在临床上广泛用于围手术期或手术室外有创检查等操作的镇静、镇痛。     

Further analysis of acute antinociceptive and anti‐inflammatory actions of 4‐phenylselenyl‐7‐chloroquinoline in mice

A new quinoline containing selenium, 4‐phenylselenyl‐7‐chloroquinoline (4‐PSQ), was described and synthetized by our research group. Recently, we demonstrated the potential antinociceptive and anti‐inflammatory of 4‐PSQ. For this reason, the first objective of this study was to expand our previous findings by investigating the contribution of glutamatergic, serotonergic, and nitrergic systems to the acute antinociceptive action of this compound. Pretreatment with 4‐PSQ (0.01–25 mg/kg, p.o.) reduced the nociception induced by glutamate. MK‐801 (an uncompetitive antagonist of the N‐Methyl‐d ‐aspartate (NMDA) receptor) blocked the antinociceptive effect exerted by 4‐PSQ (25 mg/kg, p.o.) in the acetic acid‐induced abdominal writhing test. The pretreatment with WAY100635 (a selective antagonist of 5‐HT_1A receptor), ketanserin (a selective antagonist of 5‐HT_2A/2C receptor), and pindolol (a nonselective antagonist of 5‐HT_1A/1B receptors) partially blocked the antinociceptive effect caused by 4‐PSQ (25 mg/kg, per oral, p.o.) in the acetic acid‐induced abdominal writhing test. Nitric oxide precursor, l ‐arginine hydrochloride, partially reversed antinociception caused by 4‐PSQ or ω‐nitro‐l ‐arginine (l ‐NOARG). Treatments did not modify the locomotor and exploratory activities of mice. Additionally, the acute anti‐inflammatory effect of 4‐PSQ in a model of pleurisy induced by carrageenan in mice was investigated. 4‐PSQ reduced the cellular migration, pleural exudate accumulation, and myeloperoxidase activity induced by carrageenan exposure. 4‐PSQ protected against the increase in reactive species levels and reduction of nonprotein thiol levels induced by carrageenan. Data presented here showed that the modulation of serotonergic, nitrergic, and glutamatergic systems contributed to the antinociceptive effect of 4‐PSQ and it reinforced the therapeutic potential of this quinolinic compound for acute inflammation.     

电针刺激大肠俞对炎症性肠病小鼠内脏痛的影响及机制研究

目的:观察电针刺激炎症性肠病(IBD)模型小鼠双侧大肠俞治疗内脏痛的效果并初步探讨其机制。方法:利用直肠注射2,4,6三硝基苯磺酸(TNBS)诱导炎症性肠病模型。32只8周龄C57BL/6J小鼠随机分为对照组、造模组、电针组和假针刺组,根据分组给予各组小鼠相应治疗,一共治疗7d。造模24h后每天采用腹泻指数评分评估小鼠肠道炎症的严重程度,共7d。治疗第7天,行结直肠扩张实验记录腹壁撤退反射评分;行旷场实验分别评估小鼠内脏痛觉过敏程度和焦虑情绪严重程度。完成行为学试验后,利用免疫印迹法(WB)检测小鼠结肠组织和背根神经节(DRGs)中诱导性一氧化氮合酶(iNOS)的表达;利用免疫荧光双标法检测小鼠胸11～腰1节段DRGs内脏痛敏感神经细胞中iNOS表达。结果:治疗第7天,电针组小鼠腹泻指数评分较造模组降低(P<0.01),电针组小鼠的腹壁撤退反射评分较造模组和假针刺组显著降低(均P<0.01);电针组小鼠的中心区域停留时间较造模组和假针刺组小鼠显著增加(均P<0.05)。WB结果显示,与造模组和假针刺组相比,电针组小鼠的结肠组织和DRGs中iNOS蛋白含量显著减少(均P...