加巴喷丁联合经皮神经电刺激治疗带状疱疹后遗神经痛临床观察

目的 观察加巴喷丁联合经皮神经电刺激治疗带状疱疹后遗神经痛的疗效.方法 40例带状疱疹后遗神经痛患者,随机分成两组,A组(n=20)给予口服加巴喷丁治疗;B组(n=20)服用与A组相同剂量加巴喷丁,同时在其患处给予每日1次经皮神经电刺激治疗,分别观察两组患者治疗前以及治疗后3d,5d,7d,14d,28d的疼痛程度变化,以视觉模拟评分(VAS)评定治疗效果.结果 治疗后两组患者VAS评分均明显下降(P＜0.05),且B组VAS评分明显低于A组(P＜0.05).结论 加巴喷丁联合经皮神经电刺激是治疗带状疱疹后遗神经痛的一种有效方法.     

Vagus nerve stimulation in depression

Ever since the introduction of chemical and electrical convulsive treatment for psychiatric disorders in the 1930s and 1940s, biological techniques have been used extensively in the amelioration of a variety of psychiatric disorders. Techniques of recent vintage have included transcranial magnetic stimulation, deep brain stimulation and vagus nerve stimulation (VNS). Since VNS attenuates seizures in animal models, the treatment was initially developed and approved by the FDA for treatment of drug-resistant partial-onset epilepsy. Additional data, including the known neuroanatomy of the vagus nerve, effects of VNS on monoamines and mood improvement in patients with epilepsy who were treated with VNS, provided a rationale for further investigation in patients with primary mood disorders. VNS has been administered acutely for 10 weeks to 60 patients with treatment-resistant depression. Longer-term follow-up data has been analysed for the first 30 patients. Response rates have been at least 30% in the acute study. Similar to findings in epilepsy and in contrast to the usual results of long-term medication trials, longer term data regarding symptomatic and functional outcomes of depressed patients receiving VNS continue to look promising. As opposed to electroconvulsive therapy, VNS is not associated with cognitive impairment. These results have led to approval of VNS for the treatment of resistant depression (unipolar or bipolar) in both Europe and Canada. Currently, a pivotal double-blind acute study is underway in the US.     

A randomized trial of transcutaneous electric acupoint stimulation as adjunctive treatment for opioid detoxification

This pilot study tested the effectiveness of transcutaneous electric acupoint stimulation (TEAS) as an adjunctive treatment for inpatients receiving opioid detoxification with buprenorphine–naloxone at a private psychiatric hospital. Participants (N = 48) were randomly assigned to active or sham TEAS and received three 30-minute treatments daily for 3 to 4 days. In active TEAS, current was set to maximal tolerable intensity (8–15 mA); in sham TEAS, it was set to 1 mA. By 2 weeks postdischarge, participants in active TEAS were less likely to have used any drugs (35% vs. 77%, p < .05). They also reported greater improvements in pain interference (F = 4.52, p < .05) and physical health (F = 4.84, p < .01) over time. TEAS is an acceptable, inexpensive adjunctive treatment that is feasible to implement on an inpatient unit and may be a beneficial adjunct to pharmacological treatments for opioid detoxification.     

HPLC法测定复方卡托普利片中卡托普利和氢氯噻嗪的含量

目的:建立高效液相色谱法同时测定复方卡托普利片中卡托普利和氢氯噻嗪的含量。方法:色谱柱为 Venusil MP-C_(18)(250 mm×4.6 mm,5 μm);流动相为乙腈-水(磷酸调节 pH 至2.2)(25:75);检测波长212 nm;柱温:55℃;流速:1.0 mL·min~(-1)。结果:卡托普利和氢氯噻嗪的线性范围分别为0.01066～0.3198 mg·mL~(-1)(r=0.9999)和0.00631～0.1893 mg·mL~(-1)(r=0.9997);平均回收率分别为99.2%(RSD=1.4%)和99.6%(RSD=0.8%)。结论:2种成分分离效果好,卡托普利二硫化物与卡托普利和氢氯噻嗪均有良好的分离度,辅料无干扰,本法简便快速,结果准确可靠,可作为该复方制剂中2种成分的质量控制方法。     

The effects of vasodilating drugs and vasoconstrictor nerve stimulation on oxygen uptake in skeletal muscle

Oxygen uptake was studied in skeletal muscle of cat, dog, fox and hare during i.a. infusion of acetylcholine, isoproterenol, and histamine. All agents produced similar effects in the different species. After a brief initial increase, the calculated oxygen uptake returned to near resting levels and remained so throughout the infusion period.

During acetylcholine infusion and concomitant vasoconstrictor nerve stimulation, the oxygen uptake decreased compared to resting levels although blood flow was increased. During motor nerve stimulation, the oxygen uptake increased considerably and acetylcholine infusion did not change the magnitude of that increase.

It is concluded that acetylcholine, isoproterenol, and histamine do not influence the capillary surface area to such an extent as to cause major changes in the oxygen uptake of the resting skeletal muscle. On the other hand, sympathetic vasoconstrictor nerve stimulation decreased oxygen uptake, even during increased blood flow, indicating that under those circumstances the capillary surface area is considerably decreased.     

Antinociceptive and anti-inflammatory effects of isolated fractions from Apium graveolens seeds in mice

The antinociceptive and anti-inflammatory effects of the aqueous and hexane extracts obtained from Apium graveolens L. (Apiaceae) seeds were evaluated. Formalin and xylene-induced ear edema tests were used in mice. The fractions were administered intraperitoneally at doses of 100-500?mg/kg body weight (BW). Both extracts with the xylene-induced ear edema test showed significant anti-inflammatory activity at all doses as compared with control. Only the hexane fraction reduced the nociception produced by formalin solution in the first phase (0-5?min) at 300, 400, and 500?mg/kg BW, and in the second phase (20-30?min) at 500?mg/kg BW. It is concluded that the hexane fraction has major contribution to the overall antinociceptive activity. Both fractions showed remarkable anti-inflammatory effect which supported the traditional use of Apium graveolens in diseases associated with inflammation.     

Combination therapy of transcutaneous electric nerve stimulation and iontophoresis with benzydamine and diclofenac

Combined Therapy of Transcutaneous Electrical Nerve Stimulation and Iontophoresis with Benzydamine and Diclofenac. The combination of transcutaneous electrical nerve stimulation (TENS) and the iontophoresis of benzydamine and diclofenac in a counter-current field is a new method in the treatment of chronical pain of the head and neck region. Prior to a clinical study this method was tested in a preliminary examination in 15 healthy volunteers. Clinical and physical data were investigated from which a theoretical maximum value of the quantity of iontophorised non-steroidal antiphlogistics (NSAI) could be calculated. The actual achievable absorption is discussed. Based on these data it is concluded that a good effective tissue concentration of benzydamine and diclofenac can be achieved with iontophoresis by means of TENS.     

Comparison of corelease of noradrenaline and ATP evoked by hypogastric nerve stimulation and field stimulation in guinea-pig vas deferens

Contractions and overflow of tritium and ATP elicited by hypogastric nerve stimulation (HNS) and field stimulation (FS) were studied in the guinea-pig isolated vas deferens preincubated with [³H]-noradrenaline. ATP was measured by means of the luciferin-luciferase technique.HNS and FS elicited contraction, tritium overflow and ATP overflow. HNS at supramaximal current strength produced smaller responses than did FS at supramaximal current strength (210 pulses/7 Hz). Supramaximal HNS and submaximal FS were used in the remainder of the study. Prazosin (0.3 mol/l) reduced contractions and the overflow of ATP elicited by both HNS and FS; the evoked overflow of tritium was not changed (210 pulses/7 Hz). Combined administration of prazosin (0.3 mol/l) and suramin (300 mol/l) abolished contractions and reduced the overflow of ATP elicited by both HNS and FS slightly more than did prazosin alone; tritium overflow again was not changed (210 pulses/7 Hz). Contractions, tritium overflow and ATP overflow increased with the frequency of both HNS and FS (from 7 to 25 Hz; 210 pulses); the increase in ATP overflow with frequency was more marked than the increase in tritium overflow. The preferential increase of ATP overflow with the frequency of HNS and FS persisted in the combined presence of prazosin (0.3 mol/l) and suramin (300 mol/l).The study confirms for HNS, a more physiologic way of sympathetic nerve stimulation, several observations previously obtained with FS. First, HNS-evoked ATP release is detectable as an overflow of ATP into the superfusion fluid. Second, a large part of the HNS-evoked release of ATP is postjunctional in origin, due to activation of post-junctional ₁-adrenoceptors and presumably P₂-purinoceptors. Third, the average neural release of ATP per pulse facilitates with the frequency of stimulation to a greater extent than the average release of noradrenaline per pulse.     

电针神经刺激治疗前列腺癌术后尿失禁疗效分析

目的：评价电针神经刺激疗法治疗前列腺癌根治术后尿失禁的临床疗效。方法：选择2010年9月—2015年8月前列腺癌根治术后尿失禁患者32例,予电针神经刺激疗法治疗,取穴“骶四穴”,治疗时间60 min/次,每周3次,疗程1个月。记录治疗前和治疗结束时的症状积分、盆底肌能力评分并评定疗效。结果：患者症状评分从治疗前的（17.36±3.53）分降至治疗后的（8.79±2.65）分,差异有统计学意义（P＜0.01）;盆底肌肉功能评分从治疗前的（47.21±10.38）分上升至（77.72±9.21）分,差异有统计学意义（P＜0.01）。治疗结束时临床有效率为81.25%（26/32）。结论：电针神经刺激疗法治疗前列腺癌根治术后尿失禁效果良好,且无明显不良反应,可作为前列腺癌根治术后尿失禁的首选物理治疗方法。     

Antinociceptive action of tizanidine in mice and rats

Summary The antinociceptive action of tizanidine [5-chloro-(2-imidazolin-2-yl-amino)-2,1,3-benzothiadiazole], a centrally acting muscle relaxant, was evaluated after subcutaneous or peroral administration in mice and rats. Tizanidine strongly inhibited the writhing response induced by acetic acid, phenyl-p-benzoquinone and acetylcholine in mice, and its potency was found to be greater than that of morphine. Tizanidine showed antinociceptive action like morphine not only in tail pressure and electrical stimulation tests in mice but also in tail-flick tests in mice and rats. The antinociceptive action of tizanidine was unaffected by pretreatment with naloxone. These findings suggest that tizanidine develops relatively strong antinociceptive action by a nonopioid mechanism.     

Brain-derived neurotrophic factor serum concentrations in depressive patients during vagus nerve stimulation and repetitive transcranial magnetic stimulation

Background Vagus nerve stimulation (VNS) and repetitive transcranial magnetic stimulation (rTMS) of the dorsolateral prefrontal cortex are brain stimulation techniques used as therapeutic interventions in major depression.Methods In this study, we report the impact of these stimulation techniques on serum concentrations of brain-derived neurotrophic factor (BDNF) in treatment-resistant patients with a diagnosis of major depression.Results We found no changes of BDNF serum concentrations and no association of neurotrophin concentrations in serum with clinical parameters in our sample.Conclusion Our preliminary results suggest that brain stimulation techniques—in contrast to several antidepressant medications—do not change BDNF serum concentrations.     

神经电刺激仪电流强度对糖尿病兔坐骨神经阻滞的影响

目的观察神经电刺激仪电流大小对糖尿病兔坐骨神经定位的影响。方法静脉注射链脲菌素复制糖尿病兔模型,神经电刺激仪起始电流分别为1mA(高电流组)或0.5mA(低电流组)定位糖尿病兔坐骨神经,记录最低刺激电流,固定阻滞针注射0.5mL墨水后,将相应组织冰冻切片,观察墨水渗入神经的程度。结果低电流组,阻滞针与坐骨神经距离平均为―(1.3±0.4)mm;高电流组,阻滞针与坐骨神经距离平均为(1.4±0.2)mm。低电流和高电流组分别有16只和2只实验兔墨水直接注入坐骨神经(P<0.05)。结论在链脲菌素建立的糖尿病兔模型中,神经电刺激电流大小与阻滞针-坐骨神经距离成正相关。     

Antinociceptive and anti-hyperalgesic effects of bis(4-methylbenzoyl) diselenide in mice: Evidence for the mechanism of action

Abstract

Context: The organoselenium compounds have been described to demonstrate several biological activities, including pain management.

Objective: This study investigated the antinociceptive, hyperalgesic, and toxic effects of oral administration of bis(4-methylbenzoyl) diselenide (BMD) in mice.

Materials and methods: The antinociceptive and anti-hyperalgesic effects of BMD (1, 5, 10, 25, and 50?mg/kg, p.o.) were evaluated using models of nociception: formalin, capsaicin, bradykinin (BK), cinnamaldehyde, phorbol myristate acetate (PMA), 8-bromo-cAM, and glutamate-induced nociception; and mechanical hyperalgesia induced by carrageenan (Cg) or complete Freund's adjuvant (CFA). The acute toxicity was evaluated by biochemical markers for hepatic and renal damages.

Results: BMD significantly inhibited the licking time of the injected paw in the early and late phases of a formalin test with ED₅₀ values of 14.2 and 10.8?mg/kg, respectively. This compound reduced nociception produced by capsaicin (ED₅₀ of 32.5?mg/kg), BK (ED₅₀ of 24.6?mg/kg), glutamate (ED₅₀ of 28.7?mg/kg), cinnamaldehyde (ED₅₀ of 18.9?mg/kg), PMA (ED₅₀ of 9.6?mg/kg), and 8-bromo-cAMP (ED₅₀ of 24.8?mg/kg). In the glutamate test, the pretreatment with nitric oxide (NO) precursor, l-arginine, reversed antinociception caused by BMD or N^ω-nitro-l-arginine (_L-NOARG), but the effect of BMD was not abolished by naloxone. Mechanical hyperalgesia induced by Cg and CFA was attenuated by BMD, 70?±?4% and 65?±?4%, respectively. Furthermore, a single oral dose of BMD did not change plasma aspartate (AST) and alanine aminotransferase (ALT) activities or urea and creatinine levels.

Conclusion: BMD demonstrated as a promising compound because of the antinociceptive and anti-hyperalgesic properties in mice.     

急慢性迷走神经刺激对大鼠海洛因复吸行为的影响及作用机制

目的:探讨急慢性迷走神经刺激(VNS)对大鼠海洛因复吸行为可能的干预作用及机制。方法:SD大鼠每天进行4h的海洛因自身给药训练,持续14d,建立具有强迫性觅药和给药特征的自身给药模型。随后所有大鼠植入VNS电极,恢复后进行10d的海洛因觅药行为消退训练,期间分组给予急性VNS、慢性VNS或假刺激。消退结束后测定各组大鼠条件性线索诱导下的海洛因觅药行为的恢复(即海洛因复吸行为)。免疫荧光法检测中枢核团c-Fos的表达水平。结果:海洛因复吸行为测定结果显示,与假刺激对照组比较,急性VNS组和慢性VNS组的有效鼻触数均明显降低(P<0.01)。免疫荧光的结果显示,与对照组比较,急性VNS组(P<0.05)和慢性VNS组(P<0.01)中央杏仁核(Ce)的c-Fos表达水平均明显降低,而边缘下区(IL)的c-Fos表达水平均明显升高(P<0.05)。结论:急慢性VNS均能够显著抑制大鼠的海洛因复吸行为,其机制可能与Ce和IL脑区神经元激活的改变有关。     

电刺激迷走神经对血管壁c-kit+细胞迁移和分化的影响

目的　观察电刺激迷走神经对颈动脉损伤大鼠血管壁c-kit+细胞迁移和分化的影响。方法　将24只SD大鼠随机分为假手术组、模型组、迷走神经刺激组,每组8只。制备SD大鼠左颈总动脉球囊损伤模型后,迷走神经刺激组电刺激左侧迷走神经。通过HE染色及免疫组织化学染色分别观察血管内膜厚度和c-kit+细胞在血管壁中的分布;酶联免疫吸附试验（ELISA）检测大鼠血清中肿瘤坏死因子（TNF）-α和白细胞介素（IL）-6水平。原代培养血管壁c-kit+细胞,分为对照组（不加入乙酰胆碱）、1×10-5 mol/L乙酰胆碱组、1×10-8 mol/L乙酰胆碱组及1×10-5 mol/L乙酰胆碱+α7烟碱样乙酰胆碱受体（α7nAChR）拮抗剂组。Transwell检测细胞迁移能力变化,Western blot检测平滑肌22α（SM22α）蛋白表达。结果　（1）与模型组比较,迷走神经刺激组新生内膜厚度变薄,新生内膜中c-kit+细胞数量减少（P＜0.05）,血清TNF-α和IL-6水平也下降（P＜0.01）。（2）乙酰胆碱抑制c-kit+细胞迁移,上调SM22α的表达,α7nAChR拮抗剂可逆转上述效应。结论　迷走神经通过抑制c-kit+细胞迁移并促进其向平滑肌细胞分化而抑制新生内膜形成,其作用机制可能与神经末梢释放的递质乙酰胆碱结合α7nAChR,进而激活抗炎系统有关。     

河豚毒素对电刺激诱发的兔隐动脉双相血管收缩反应的作用

目的采用兔离体隐动脉环标本,建立了双相血管收缩反应模型,并分析TTX(1~100 nmol.L-1)对两种收缩成分的影响。方法兔离体隐动脉血管环张力记录法及电场刺激诱发血管收缩法。结果本实验条件下的电场刺激(电压15 V、波宽1 m s、刺激频率2~16 Hz,连续刺激时程32 s)可诱发兔离体隐动脉产生双相收缩反应,且具有频率(2~16Hz)依赖性。钠通道选择性阻滞剂TTX 3 nmol.L-1对第一相收缩反应无影响,但是明显抑制第二相收缩反应,抑制率达44%~67%;TTX的浓度增加至10 nmol.L-1时,其对4~16 Hz电刺激诱发的第一相反应的抑制率为40%~57%,而对第二相反应的抑制率达90%以上。TTX(0.1μmol.L-1)对NA(0.01~30μmol.L-1)的累积量效曲线无任何影响,但是完全抑制了电刺激诱发的动脉环双相收缩反应。胍乙啶(10μmol.L-1)完全抑制电刺激诱发的双相收缩反应,但是不抑制外源性NA的收缩反应。结论建立了电场刺激诱发兔离体隐动脉环双相收缩反应模型,该双相收缩与交感神经兴奋及其递质的释放有关。     

Co-transmitter mediated facilitation by sympathetic nerve stimulation of evoked acetylcholine release from the rabbit perfused atria preparation

Rabbit atria were isolated with the extrinsic right sympathetic and vagus nerves attached and perfused with Tyrode solution. Acetylcholine overflow was determined after labelling of the transmitter stores with [¹⁴C]choline and fractionation of the radioactivity on cation exchange columns. Sympathetic nerve stimulation (SNS, 2 Hz, 3 min) carried out together with vagus nerve stimulation (VNS, 2 Hz, 3 min), but each SNS pulse preceding a vagal one by 19 ms, caused a facilitation of acetylcholine overflow of about 60% versus independent controls in the absence of SNS. Antagonists of putative neurotransmitters were tested to find out the prejunctional mediator involved in the facilitation.The facilitation was not significantly reduced by prazosin, rauwolscine, idazoxan, or propranolol, excluding mediation by - or \-adrenoceptors. However, guanethidine abolished evoked noradrenaline release and facilitation, suggesting that it is due to a compound co-released with noradrenaline from postganglionic noradrenergic nerves. Pretreatment of rabbits with reserpine which reduced noradrenaline content of atria and SNS evoked overflow by 94% did not affect the facilitation of acetylcholine release which, due to the cardiostimulatory action of SNS being absent, resulted in enhanced depression of atrial force. We conclude that the facilitation is due to release of a reserpine-resistant co-transmitter from sympathetic nerves.Possible mediation of the facilitation by ATP through P_2X- or P_2Y-purinoceptors was excluded by ineffectiveness of , \-methylene ATP-preperfusion, of suramin and cibacron blue, respectively. However, the selective A₂ adenosine receptor antagonist CP 66,713 reduced the facilitation by 25% whereas DPCPX (A₁-selective) had no effect. Of the non-subtype-selective antagonists only 8-phenyltheophylline but not XAC decreased the facilitation by 40%. Mediation of the facilitation by tachykinin-, angiotensin-, opioid, AMPA/kainate-, M₁ muscarinic, 5-hydroxytryptamine 5-HT_1–4-receptors, or by nitric oxide, was excluded by administration of respective antagonists or inhibitors. Thus, whilst adenosine seems to be responsible for about one-fourth of the effect of sympathetic nerve stimulation, the major part of the facilitation of acetylcholine release remains unexplained.Under conditions of a low rate of evoked acetylcholine overflow prazosin enhanced the facilitatory action of SNS, suggesting an ₁-adrenoceptor mediated prejunctional inhibition of acetylcholine release.     

手法按摩联合低频脉冲电刺激对产后乳汁淤积的干预效果

目的 探讨手法按摩联合低频电脉冲对产妇乳汁淤积的治疗效果.方法 将我院收治的128例产后乳汁淤积产妇随机分为两组,每组64例.对照组给予热敷、吸奶等常规性治疗,治疗组给予手法按摩联合低频电脉冲治疗.比较两组产妇临床疗效、母乳喂养率和乳腺炎发生率.结果 治疗组产妇治疗总有效率为96.875％,明显高于对照组的78.125％,差异有统计学意义(P＜0.05).治疗组母乳喂养率和乳腺炎发生率分别为93.750％、6.250％,对照组母乳喂养率和乳腺炎发生率分别为75.000％、15.625％,差异有统计学意义(P＜0.05).结论 手法按摩联合低频电脉冲治疗产后乳汁淤积临床疗效显著,可有效预防乳房肿胀和乳腺炎,提高母乳喂养率,值得推广应用.     

Sleep and serotonin in two strains of Mus musculus

Two strains of Mus musculus, C57BL/10J and BALB/CJ, were studied in an attempt to check for any naturally occurring correlation between sleep and brain serotonin. The C57BL/10J compared with the BALB/CJ had more slow wave sleep throughout the day and particularly during hours of darkness. During peak sleep periods, C57BL/10J also had more REM sleep. At three different times of the day (1200, 1600, and 0400 hr) neurochemical assays were done on brain stem and cerebral cortex for tryptophan and serotonin levels and for tryptophan hydroxylase activity. An inspection of the ordering of means for strains suggested that the greater amount of slow wave sleep for C57BL/10J was paralleled by higher brain stem and cortex tryptophan levels, higher cortex tryptophan hydroxylase activity, and higher cortex serotonin levels. An inspection of temporal trends across strain and time of day suggested that slow wave sleep may vary negatively with brain stem tryptophan hydroxylase activity, brain stem serotonin level, and cortex tryptophan level. While no simple sleep-serotonin relationship obtained, because of such trends the data were interpreted as being generally consistent with the hypothesis of an active serotonergic sleep inducing mechanism in brain.     

Impulse interval-dependent effect of sympathetic nerve stimulation on evoked acetylcholine release from the rabbit perfused atria preparation

The aim of the present study was to explore possible prejunctional effects mediated by impulse activity of sympathetic terminals on evoked acetylcholine release in an organ innervated by the autonomic ground plexus. Rabbit atria were isolated with the extrinsic right vagus and sympathetic nerves intact and perfused with Tyrode solution. Acetylcholine overflow was determined after labelling of the transmitter stores with [¹⁴C]choline and fractionation of the radioactivity on cation exchange columns. The overflow of endogenous noradrenaline was measured by HPLC and electrochemical detection.The vagus nerve was stimulated at 2 Hz for 3 min four times at intervals of 10 min. During the second stimulation the postganglionic sympathetic nerves were stimulated (2 Hz, 3 min) in such a way that the impulses preceded the vagus stimuli by a fixed time interval which was varied in different experiments (0, 7, 19, 50, 132, and 350 ms). Evoked acetylcholine release was significantly enhanced when the vagus was excited 7, 19 and 50 ms after the sympathetic nerves but it was unaltered at the 132 or 350 ms intervals, and when both nerves were stimulated simultaneously. Noradrenaline release was similar (about 6 ng per stimulation period) in all experimental groups. When sympathetic nerve stimulation had little effect in releasing noradrenaline (<2.0 ng per stimulation period), facilitation of acetylcholine release at the 19 ms pulse interval was absent. The resting outflow of acetylcholine was unaffected by sympathetic nerve stimulation.The experiments show a facilitation of evoked acetylcholine release by sympathetic activity. As revealed by the pulse-to-pulse method this effect is confined to a relatively brief interval immediately following the excitation of the noradrenergic terminal, and is unlikely to be mimicked by exogenous drug application.