大鼠孤束核微量注射γ-氨基丁酸对电针抗应激性胃黏膜损伤的影响

[目的]探讨孤束核内γ-氨基丁酸(GABA)对电针(EA)抗应激性胃黏膜损伤的影响及机制。[方法]70只健康SD大鼠随机分为5组:单纯应激组、EA+应激组、0.85%氯化钠+EA+应激组、GABA+EA+应激组、荷苞牡丹碱+EA+应激组,每组14只。采用冷束缚法制备大鼠应激性胃溃疡模型,通过脑立体定位仪进行孤束核微量注射GABA和荷苞牡丹碱,测定各组大鼠胃黏膜溃疡指数(UI)、胃黏膜血流量(GMBF)、胃液酸度的变化。[结果]EA+应激组大鼠胃黏膜UI、胃液酸度降低,GMBF增加,与单纯应激组比较差异有统计学意义(P0.01)。预先孤束核给予GABA处理,可减弱EA抗胃黏膜损伤的作用,胃黏膜UI、胃液酸度增高,GMBF减少,与NS+EA+应激组比较差异有统计学意义(P0.01)。荷苞牡丹碱则明显加强EA对胃黏膜损伤的保护作用,胃黏膜UI、胃液酸度降低,GMBF增加,与NS+EA+应激组比较差异有统计学意义(P0.05)。[结论]GABA能削弱EA抗应激性胃黏膜损伤作用,其作用部分是通过孤束核内GABAA受体介导的。     

电针足三里穴抗大鼠应激性胃黏膜损伤作用与NTS内受体的关系

目的:探讨(EA)足三里穴抗大鼠应激性胃黏膜损伤作用与NTS(NTS)内受体关系．方法:健康♂SD大白鼠56只随机分为8组:应激模型组、EA-应激组、生理盐水(NS)-EA-应激组、哌唑嗪-EA-应激组、育亨宾-EA-应激组、心得安-EA-应激组、阿托品-EA-应激组、纳络酮-EA-应激组．采用束缚-冷方法制备大鼠应激性胃溃疡模型,观察NTS内微量注入不同受体阻断剂,胃溃疡指数(UI)的变化．结果:NS-EA-应激组、EA-应激组大鼠胃黏膜损伤明显减轻,UI分别为26．3±3．5,25．4±3．1,与应激模型组37．5±4．2比较有显著性差异(t= 5．42,t=6．13,P<0．01)．哌唑嗪-EA-应激组UI为34．6±3．4明显高于NS-EA-应激组(t=4．50, P<0．01)．育亨宾-EA-应激组和心得安-EA-应激组分别与NS-EA-应激组比较,UI无显著性差异．阿托品-EA-应激组大鼠UI为33．1±3．7明显高于NS-EA-应激组(t=3．53,P<0．01),纳络酮-EA-应激组与NS-EA-应激组比较,UI无显著性意义．结论:EA对大鼠应激性胃黏膜损伤的保护作用部分是通过NTS内α1,M受体介导的,而与α2,β和阿片肽受体无明显关系．     

精氨酸加压素参与电针对大鼠应激性胃黏膜损伤的保护作用

目的：探讨精氨酸加压素(AVP)参与电针(EA)对应激性大鼠胃黏膜损伤保护作用及机制.方法：健康SD大鼠98只,随机分为模型组、电针组、生理盐水对照组、AVP 100ng组、AVP 200ng组、AVP 300ng组和AVP-V_1受体阻断剂组.采用束缚冷应激胃黏膜损伤大鼠模型,观察孤束核微量注射AVP,AVP-V_1受体阻断剂,大鼠胃黏膜血流量(GMBF)、溃疡指数(UI)、胃液酸度的变化.结果：与模型组比较,电针组大鼠UI减少(t= 7.5201,P＜0.01),GMBF(mv)增加(t=2.9606,P＜0.05),胃液酸度降低(t=4.2090,P＜0.01). AVP 100,200,300ng组分别与生理盐水对照组比较,UI明显减少(t=2.2718,t=4.9082,t =6.0413：P＜0.05-0.01),GMBF明显增加(t= 2.6845,t=3.8269,t=4.8795；P＜0.05-P＜0.01),胃液酸度明显降低(t=3.0526,t=3.8565,t= 5.6251；P＜0.05-P＜0.01),并且表现明显的剂量-效应依赖关系(r=0.9978,r=0.9980,r= 0.9829；P＜0.05).AVP-V_1受体阻断剂组与生理盐水对照组比较UI增大(t=5.6815,P＜0.01),GMBF减少(t=2.3750,P＜0.05),胃液酸度增高(t=2.2046,P＜0.05).结论：孤束核内AVP参与了电针对大鼠应激性胃黏膜损伤保护作用过程.     

左金丸及拆方对胃溃疡大鼠胃黏膜愈合和表皮生长因子受体表达的影响

[目的]探讨左金丸及其拆方对胃溃疡（GU）愈合的影响、机制及配伍依据。[方法]建立乙酸性GU大鼠模型，54只动物随机均分成模型组、黄连组、吴茱萸组、左金丸组，并设立空白组和假手术组，每组9只，观测各组大鼠溃疡指数（UI）和表皮生长因子受体（EGFR）的表达。[结果]①黄连组、吴茱萸组、左金丸组UI显著低于模型组（P〈0．01），且依次降低（P〈0．01，〈0．05）；②溃疡形成后模型组GU边缘EGFR表达显著高于空白组（P〈0．01），左金丸组显著高于模型组（P〈0．01），各治疗组间比较差异无统计学意义。[结论]左金丸及其拆方均有促进溃疡愈合的作用。显著性上调EGFR的表达可能是左金丸促进溃疡愈合的重要机制之一。     

下丘脑外侧区注射五肽胃泌素对大鼠胃黏膜细胞应激性损伤的影响

目的研究下丘脑外侧区（LHA）注射五肽胃泌素（G5）对应激性胃黏膜细胞损伤的作用及机制。方法将24只SD大鼠随机分为对照组、水浸—束缚应激（WRS组）、G5＋WRS组、溶剂对照＋WRS组各6只。LHA注射G5，制备大鼠WRS模型；用western-blot法检测胃黏膜细胞凋亡及凋亡相关基因c-Jun氨基末端激酶（JNK）磷酸化水平。结果与WRS组及溶剂对照＋WRS组比较，G5＋WRS组应激后胃黏膜细胞损伤明显增加（P〈0．05或〈0．01），caspase-3蛋白表达及JNK磷酸化水平升高（P均〈0．01）。结论LHA内注射G5可加重大鼠应激性胃黏膜细胞损伤，其机制与增加胃黏膜细胞凋亡有关。     

巯基物质对小剂量阿司匹林所致大鼠胃黏膜损伤的保护作用

背景：很多胃黏膜损伤模型中发现巯基物质含量下降，巯基物质对胃黏膜细胞具有保护作用。目的：探讨巯基物质对小剂量阿司匹林所致胃黏膜损伤的保护作用。方法：80只雄性Sprague-Dawley（SD）大鼠随机分为正常对照组、纯巯基对照组、阿司匹林模型组、巯基预防组、硫糖铝预防组、NaCl治疗对照组、巯基治疗组和硫糖铝治疗组8组。测定黏膜溃疡指数（UI），行大体、组织学和透射电子显微镜观察，测定胃黏膜组织中还原型谷胱甘肽（GSH）、超氧化物歧化酶（SOD）、丙二醛（MDA）、6-酮．前列腺素F1α（6-keto-PGF1α）水平。结果：阿司匹林模型组胃黏膜发生病变，UI与其余各组相比显著升高（P〈0．01），GSH、6-keto-PGF1α含量较正常对照组显著降低（P〈0．05），MDA含量显著增高（P〈0.001）。巯基预防或治疗后，胃黏膜损伤明显减轻，UI显著下降（P〈0．001），GSH、6．keto．PGF1α含量显著增高（P〈0．05），MDA含量显著降低（P〈0．05）。各组SOD含量无显著差异。结论：小剂量阿司匹林可致大鼠胃黏膜损伤，胃黏膜GSH下降可能是其机制之一。外源性GSH具有增强胃黏膜抗氧化作用和细胞保护作用。     

损毁孤束核对电针足三里穴抗大鼠应激性胃溃疡作用的影响

目的:探讨孤束核(NTS)在电针(EA)足三里穴抗大鼠应激性胃溃疡中的作用.方法:健康♂SD大白鼠56只随机分为应激组、EA 应激组、NTS电损毁组、NTS假损毁组.通过脑立体定向仪电损毁大鼠孤束核,采用束缚-浸水制备大鼠应激性胃溃疡模型,分别测定各组胃黏膜损伤指数(UI)、超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量.结果:与应激组比较,EA 应激组UI明显减少(t=9.5071,P<0.01),SOD活性升高(t=3.8729,P<0.01),MDA降低(t=2.3578,P<0.05).NTS电损毁组分别与假损毁组和EA 应激组比较UI提高(t=4.4223,7.2579,均P<0.01),SOD活性降低(t=3.5625,3.7242,均P<0.01),MDA含量升高(t=2.9045,2.4960,均P<0.05).结论:电损毁孤束核后,电针足三里穴对应激性胃黏膜损伤的保护作用减弱.     

电针猫足三里穴对下食管括约肌压力调节功能的影响

[目的]研究电针（EA）猫足三里穴对下食管括约肌压力（LESP）的影响,探讨足三里穴与食管动力调节之间的关系。[方法]将28只健康家猫行内镜检查,确定无镜下食管病（炎）。随机分为足三里穴组、非经非络穴组。应用加拿大E-7-1-1-1-2-5-5-5型8通道细微注水测压管和荷兰UPS-2020型食管测压系统测定猫LESP。[结果]EA猫足三里穴和非经非络穴期间和停止后,LESP较EA前均有显著性升高,足三里穴组EA期间LESP由（16．21±5．49）mmHg（1mmHg=0．133kPa）升高至（23．14±8．81）mmHg（P〈0．01）,EA停止后LESP升至（25．50±6．73）mmHg（P〈0．01）;非经非络穴组EA期间LESP由（15．64±3．61）mmHg升至（18．93土5．57）mmHg（P〈0．01）,EA停止后LESP升至（20．43±5．24）mmHg（P〈0．01）。EA足三里穴对LESP的升高程度在EA期间和停止后均明显高于非经非络穴（P〈0．05）。[结论]EA健康猫足三里穴可以升高LESP,对下食管括约肌具有良性调理功能,其机制尚未完全阐明。     

神经生长因子对大鼠心肌损伤后交感神经去支配及巢蛋白表达的影响

目的研究神经生长因子（NGF）预处理对异丙肾上腺素（Iso）致大鼠心肌急性损伤后交感神经去支配及巢蛋白（Nestin）表达的影响。方法雄性Wistar大鼠60只，随机分成3组：对照组、Iso损伤组和NGF预处理组．每组20只。观察心肌损伤的病理变化和血清肌酸激酶（CK）改变；免疫组化和RT～PCR方法检测心肌酪氨酸羟化酶（TH）和Nestin的表达。结果NGF预处理组较Iso损伤组心肌坏死面积明显减小（P〈0．05）。CK值在Iso损伤组最高，NGF预处理组次之，均高于对照组（P〈0．01）。TH染色阳性的交感神经纤维密度在Iso损伤组[（20．63±6．04）个／mm^2]明显下降，与对照组[（31．40±8．96）个／mm^2]比较，差异有统计学意义（P〈0．05），而NGF预处理组[（29．22±9．11）个／mm^2]TH阳性表达与对照组水平接近，并未发生显著减少。各组THmRNA表达水平与免疫组化结果平行。对照组NestinmRNA表达水平最低，Iso损伤组和NGF预处理组较高，以NGF预处理组为著。结论NGF预处理可拮抗Iso致大鼠心肌损伤的，心脏交感神经去支配，减轻Iso的心肌损伤作用，提示NGF可通过神经营养作用在心肌损伤修复过程中起重要作用。     

双蒲散对大鼠慢性胃溃疡愈合质量及抗复发的影响

[目的]研究双蒲散对实验性大鼠慢性胃溃疡（GU）愈合质量及抗复发的影响，并探讨其可能机制。[方法]采用乙酸注射至大鼠浆膜下形成慢性GU模型，随机分为模型组、雷尼替丁组、双蒲散组，分别灌服0．85％氯化钠、雷尼替丁及双蒲散。[结果]双蒲散组溃疡指数（UI）、扩张腺体数和炎细胞数目明显低于模型组和雷尼替丁组，再生黏膜厚度、胃黏膜超氧化物歧化酶（SOD）及前列腺素E2（PGE2）水平显著高于模型组和雷尼替丁组，丙二醛（MDA）水平明显低于模型组和雷尼替丁组（均P〈0．01，〈0．05）。[结论]双蒲散可提高GU愈合质量，减少溃疡复发。其机制可能是通过增加胃黏膜组织PGE2和SOD水平，降低MDA水平，促进黏膜修复而实现的。     

躯体传入神经刺激与室性心律失常

室性心律失常是临床上发病率和致死率均较高的疾病,其治疗方式主要涉及药物治疗、植入型心律转复除颤器及射频消融治疗,这些治疗方式的联合应用已极大地改善了患者的生活质量及预后,但仍不能完全治愈其发生。研究指出室性心律失常与自主神经系统存在密切的关系,交感神经-副交感神经活性的失衡可诱发或抑制室性心律失常的发作,躯体传入神经刺激可能调节自主神经系统进而干预心律失常事件的发生。现综述自主神经系统、躯体传入神经刺激与室性心律失常之间的关系。     

小儿膀胱的神经分布

目的研究小儿膀胱的神经节和神经纤维分布情况。方法采用免疫组化及电镜技术对小儿膀胱壁全层标本进行观察和研究。结果小儿膀胱存在胆碱能神经节和胆碱能神经纤维，且各组织层次的分布差别较大，未观察到逼尿肌、颈部和三角区存在肾上腺素能神经和肽能神经纤维。结论副交感神经纤维(胆碱能神经纤维)在排尿生理中有重要作用。是否存在其它抑制性神经纤维，有待于进一步探讨。     

Utilization of Nerve Conduction Studies for the Diagnosis of Polyneuropathy in Patients with Diabetes: A Retrospective Analysis of a Large Patient Series

Background

Diabetic polyneuropathy (DPN) is a disabling complication of diabetes mellitus. A population-based analysis of physician utilization of nerve conduction studies (NCS) for the assessment of DPN was conducted.

Methods

All electrodiagnostic encounters over a 30-month period using a computer-based neurodiagnostic instrument linked to a data registry were analyzed retrospectively. The DPN case definition was abnormal sural and peroneal nerve conduction.

Results

The study cohort consisted of a total of 63,779 electrodiagnostic encounters performed by 3468 physician practices. Primary care and internal medicine physicians represented 80.1% of the practices and accounted for 65.7% of the encounters. Endocrinologists represented 4.6% of the practices and 20.1% of the encounters. The demographics of patients were 52.7% female; 63.4±11.8 (mean±standard deviation) years (age); 168.1±10.9cm (height); 92.2±22.6 kg (weight); and 32.6±7.2 kg/m² (body mass index). The most common peroneal abnormality was F-wave latency (33.6%). The sural nerve response latency and amplitude parameters had similar abnormality rates (58.3 and 62.7%). DPN was identified in 52.6% of the encounters; in another 19.3% no neuropathy was found.

Conclusions

For over 70% of the patients, the specific diagnostic question of the presence of DPN was addressed by NCS with evidence-based criteria. The demographic features were strongly associated with risk of diabetes and DPN, suggesting that NCS were applied to appropriate demographic subgroups. The rate of DPN was also comparable to levels seen by academic electromyography laboratories. In 32.6% of the encounters the NCS suggested a posttest diagnosis other than DPN. This rate was similar to the results of referral to traditional electromyography laboratories. This study demonstrated that NCS using computer-based electrodiagnostic equipment was a suitable tool for the diagnosis of DPN. Furthermore, this technology permits examination of DPN in large populations.     

Persistent Postoperative Complaints After Whole Sural Nerve Biopsies in Diabetic and Non-diabetic Subjects

The postoperative effects of a whole sural nerve biopsy in diabetic (11) and non-diabetic (10 healthy controls, 10 patients with impaired glucose tolerance and 2 patients with polyneuropathy) subjects were investigated by a mailed questionnaire 20–44 months after the surgical procedure (10/11 vs 21/22 answers received). Pain in the biopsy area at follow-up was reported in 4/10 of the diabetic patients (p = 0.01) but in none of the non-diabetic subjects (0/21). An increased number (p = 0.01) of diabetic patients (5/10 vs 1/21) had cold intolerance in their foot or leg whereas 11/31 of all patients had dysaesthesia in the affected skin. Overall 6/31 patients described serious problems at the time of the questionnaire, and 4 of this 6 having diabetes. Loss of sensation was reported in almost all subjects irrespective of diabetes or not; however, a decrease in the area of loss of sensation was reported most often in diabetic patients (8/10 vs 8/21, p = 0.02). It is concluded that whole surval nerve biopsies give rise to persistent problems both in diabetic and non-diabetic subjects. The reason for a sural nerve biopsy has always to be carefully considered before being conducted. © 1997 by John Wiley & Sons, Ltd.     

Biopsy of the posterior interosseous nerve: a low morbidity method for assessment of peripheral nerve disorders

Aims The sural nerve is the commonest peripheral nerve biopsied to help in the diagnosis of peripheral neuropathy of unknown cause. However, associated complications limit its use. The aim was, as an alternative, to asses biopsy of the terminal branch of the posterior interosseous nerve (PIN) in the forearm. Methods PIN pathology was morphometrically quantified in 10 male patients with Type 2 diabetes and compared with six PIN biopsy specimens taken post mortem from male cadavers with no history of neuropathy or trauma. Results The PIN biopsy procedure provides a long (approximately 3 cm) mono‐ or bifascicular nerve biopsy with generous epineurial tissue and adjacent vessels. Our results show a significantly lower myelinated fibre density in subjects with diabetes [5782 (3332–9060)/mm²] compared with autopsy control material [9256 (6593–12 935)/mm², P < 0.007]. No postoperative discomfort or complications were encountered. Conclusions A reduction in myelinated fibre density has previously been shown to be a clinically meaningful measure of neuropathy in diabetic patients. We demonstrate similar findings using the PIN biopsy. The PIN biopsy procedure fulfils the criteria for nerve biopsy and was well tolerated by the patients. It may be a possible alternative to sural nerve biopsy to allow for diagnosis of neuropathy.     

胆囊收缩素在胃电节律失常中的作用及其神经病理学机制

目的：探讨胆囊收缩素（CCK）在胃电节律失常中的作用及其神经学机制。方法：在建立胃窦肌间神经丛铺片方法的基础上,用酶组织化学与免疫细胞化学方法,观察胃电节律失常大鼠胃窦肌间神经丛内胆碱能（Ach）神经、一氧化氮合酶（NOS）神经及CCK神经的变化。结果：模型组和CCK组大鼠均出现胃电节律失常,异常节律指数及慢波频率变异系数均显著高于正常组（P＜0．01）;模型组和CCK组NOS神经显著增加,Ach神经含量显著减少（P＜0．01）。结论：外源性及内源性CCK增加,能诱发胃电节律失常。CCK通过激活NOS,产生胃电节律失常。胃窦肌间神经丛神经中CCK及NOS神经含量异常增加,Ach神经减少是发生胃电节律失常的神经病理学机制之一。     

Peripheral neuropathies of the forearm and hand in rheumatoid arthritis: diagnosis and options for treatment

Although the clinical hallmark of rheumatoid arthritis (RA) involves inflammatory joint disease, extra-articular manifestations may be evident in 20% of patients. Among them neurologic features involving both the peripheral and central nervous system are one of the more common, but little has been noticed about it in clinic. The same mechanisms participating in joint destruction, synovial inflammation, and vasculitis contribute to the various RA neurological complications. In this article, we reviewed clinical outcomes of peripheral neuropathies of the upper extremity associated with RA and discussed the proper diagnosis and operative indication. Magnetic resonance imaging and electrophysiological examination are the best tools to lead the final diagnosis of nerve palsy secondary to RA synovial cyst. Such neuropathies require consideration in the differential diagnosis of wrist and hand disability. Surgical decompression is recommended at prompt timing if neurophysiologic studies demonstrate denervation or significant motor abnormalities, or sensory symptoms progress despite adequate medication.     

自主神经与心房颤动关系研究进展

心房颤动是临床最常见的快速性心律失常。心房颤动的发生机制非常复杂,近年来的研究表明,心脏局部的自主神经即交感和副交感神经在心房颤动的发生及维持中均起着重要作用。消融自主神经可以提高心房颤动导管消融的成功率并降低术后复发率。     

吻合口位置对周围神经端侧吻合术后神经再生的影响

目的观察吻合口位置对神经端侧吻合术后再生神经的影响。方法取新西兰大白兔58只,随机选10只为定位组,行胫神经干功能束鉴定,确定运动神经纤维集中、混合神经集中位置;余48只随机分为A、B组,各24只,切断腓总神经远端,并与外膜开窗的胫神经端侧缝合。A组为实验组,吻合口位于运动神经纤维集中处;B组为对照组,吻合口位于混合神经纤维集中处。于术后1、2、3个月,A、B组每次各取8只,于吻合口近端行电生理检测,取吻合口远端0.5 cm处的腓总神经进行组织学及抗神经丝蛋白免疫组化检测。结果光镜下可区分有髓神经纤维及无髓神经纤维团块并定位。随着术后时间延长,A、B组再生神经诱发电位的潜伏期逐渐缩短,波幅逐渐增大、肌湿重和肌纤维截面积逐渐增大、腓总神经有髓神经纤维数和神经束截面积显著增大,抗神经丝免疫组化阳性表达逐渐增强,且A组均优于B组。结论周围神经端侧吻合时,吻合口位于运动神经束集中处,其再生的运动神经纤维数目多,质量高,所支配肌肉的功能恢复较好。     

电激心脏植物神经对心率变异性的影响

大量文献表明，心率变异性（HRV）功率谱的高频成份（HF）是迷走神经活动对窦房结影响程度大小的标志；HRV功率谱的低频成份（LF）表示了心交感神经或心交感与迷走神经共同对窦房结的紧张作用；在很多生理和病理情况下，RF（LF／HF的比值）代表了心交感迷走神经对窦房结调制的均衡状态。本文直接使用方波电刺激狗的心交感神经或迷走神经128S，观察到刺激心交感神经时的平均心率（HR）、LF和HF较刺激前无显著性变化，但平均心率的标准差（SD）和RF却显著增大；刺激心迷走神经时RF明显降低，其余指标与刺激前相比，无明显变化。说明直接使用电刺激心交感或迷走神经，可造成对窦房结调制作用的均衡状态改变。