心房钠尿多肽对麻醉大鼠血压和肾神经传出放电的影响

本实验观察了心房肽Ⅱ(Atriopeptin Ⅱ,APⅡ)对麻醉大鼠血压(AP)、心率(HR)和肾交感神经传出放电(RSNA)的影响,并与硝普钠对 AP 和 RSNA 的影响作比较。结果如下:(1)缓冲神经完整和迷走神经完整条件下(n=12)静脉注射 APⅡ(50μg/kg)后,动脉收缩压(SAP)降低23.0±1.66 mmHg(Μ±SE,p<0.001),HR 减慢9±3.5b/min(p<0.05),RSNA 降低4.89±2.95%(P>0.05)。迷走神经切断后,静脉注射 APⅡ引起的~⊿SAP 虽有所减小,但与切断迷走神经前的反应比较,无统计学意义,HR 减慢不再出现,而 RSNA 则有所增加;(2)缓冲神经切断和迷走神经完整条件下(n=7),静脉注射 APⅡ时 SAP 降低27.4±3.25mmHg(P<0.001),HR 减慢13±3.1b/min(P<0.01),RSNA 降低11.67±1.95%(P<0.001)。切断迷走神经后,静脉注射 APⅡ引起的 SAP 降低程度有明显減小(P<0.01),HR减慢不再出现,RSNA 则反而增加(3)无论在迷走神经完整还是切断条件下,静脉注射硝普钠(n=6) SAP 均明显降低,同时伴有 RSNA 的反射性增加。以上结果表明:APⅡ的降压效应,部分是通过迷走神经传入纤维;在切断缓冲神经条件下,APⅡ可经由迷走神经传入纤维的激活而反射地抑制 RSNA。     

电离辐射引起胃排空延迟机理的初步探讨

本文观察了800rad照射后胃肠肌电的变化及切斷内脏神经与电刺激迷走神经对官的影响,初步分析了电离辐射引起胃排空延迟的机理。结果是:800rad照后大鼠胃肠肌电的峰波平均振幅胃幽部窦部照后1小时至第4天明显降低(P<0.05);幽门括约肌政变不大;十二指肠球部照后第3～7天明显下降(P<0.01)。切断内脏神经后照射大鼠胃肠肌电的峰波平均振幅胃幽门窦部变化不大,幽门括约肌照后1小时至第5天明显升高(P<0.05),十二指肠球部照后第3～7天明显下降(P<0.05)。800rad照后第4天大鼠胃对电刺激迷走神经的反应性明显降低(P<0.01)。上述结果表明:照后胃排空延迟的原因不仅与神经-体液调节紊乱有关,而且与射线损伤了平滑肌,使其兴奋性暂时的功能性降低有关。此外照后由于十二指肠球部运动的变化而使内感受器对胃运动的调节发生紊乱也是值得重视的因素。     

牛蛙神经冲动产生和传导的低温效应

在5℃和15℃温度条件下,用牛蛙(Rana catesbeiana)离体坐骨神经标本测定0、24、48、96、120、144、168、192、216 h 9个时段的动作电位波幅和传导速度.结果表明:两个温度下离体坐骨神经的动作电位幅度在0 h和24 h差异均不显著,0 h时相对高温(15℃)下动作电位传导速度大于相对低温(5℃),24 h时两个温度下动作电位的传导速度差异不显著,相对高温下48 h时坐骨神经的兴奋性为零.相对低温条件下,坐骨神经兴奋性能维持7 d时间.     

刺激迷走神经引起的鲫鱼Mauthner细胞顺向激活

目的 :研究迷走神经感觉传入信息对Mauthner细胞 (M细胞 )兴奋性的影响。方法 :刺激鲫鱼迷走神经 ,并运用微电极穿刺技术记录鲫鱼M细胞胞内电位变化。结果 :在M细胞胞内记录到分级的、复合的兴奋性突触后电位(EPSP) ,分为第一成分和第二成分。随着刺激强度的增大 ,EPSP的幅度增大 ,反应持续时间延长。当刺激强度足够大时 ,在第一成分或第二成分的基础上可爆发动作电位。结论 :①刺激迷走神经可引起M细胞顺向激活 ,这与以往的观点不同 ;②从迷走神经到M细胞的感觉传入通路可能由含有兴奋性和抑制性成分的不同种类的神经链构成 ,M细胞的兴奋性取决于兴奋和抑制之间的相互关系     

迷走传入的投射区在电刺激颈迷走神经中枢端引起的降压反应中的作用

文献报道迷走传入直接或间接投射至多个脑区。本工作分别检验这些脑区在迷走传入引起的降压、降心率反应中的作用。在乌拉坦麻醉、双侧切断颈迷走神经的大鼠,将普鲁卡因微量注入孤束核或β-内啡肽抗血清注入延髓头端腹外侧区(RVL)均可明显减小电刺激预迷走神经中枢端引起的降压(DpV)和降心率反应,但分别将心得安、β-内啡肽抗血清注入室旁核或普鲁卡因注入最后区对DpV和心率减慢反应均无明显影响。保留右侧颈迷走神经的大鼠,在甲基阿托品(i.v.)阻断心迷走神经作用后DpV亦无明显变化,但心率减慢反应被衰减。鉴于我们以往的实验显示孤束核可通过其β-内啡肽能投射纤维作用于RVL而起降压作用,以上结果提示:迷走传入通过孤束核的β-内啡肽能神经元对RVL-交感兴奋神经元起抑制作用是引起降压反应的机制之一。     

二硫化碳染毒大白鼠运动神经传导速度的研究

用静式染毒室,以1 600-1 900mg/m~3浓度的CS_2将19只大白鼠染毒,每天6小时,每周六天,历时八周。用Fullerton法测定大白鼠坐骨神经MCV,染毒前为50.91+8.45m/s,染毒3周时,减慢到41.63+6.83m/s,相当于同期对照组的75.8％(P<0.001);停止染毒后,经过12周的恢复,达到51.60+9.92m/s,已恢复到染毒前水平。用Seppülüinen法测定大白鼠坐骨神经MCV,染毒前为25.51+3.72m/s,在染毒期间,仅有轻微减慢,停止染毒后的第7周,减慢到20.71+2.65m/s,相当于同期对照组的75.4％(P<0.001)。经过18周的恢复,达到24.43+3.54m/s,相当于同期对照组的88.1％(P<0.05)。 比较两种测定MCV的结果可看出,CS_2不仅能损伤脊髓前角细胞和轴突,还损伤运动终板和肌肉。 用标准MCV测定技术测定MCV对早期诊断CS_2神经病是个有用的指标。测定CS_2接触者的末端潜伏期,对了解治疗期间和恢复期间病人的情况也许是更有意义的。     

迷走神经刺激术在脑缺血中的应用及神经机制

长期以来,迷走神经刺激(vagus nerve stimulation,VNS)被广泛用于临床顽固性癫痫和药物抵抗性抑郁症的治疗,近年来又有文献报道迷走神经刺激术对脑缺血损伤也具有保护作用.VNS可以减少梗死灶面积和增加脑缺血后实验动物的功能评分,机制上它可以通过减少兴奋性谷氨酸的释放抑制神经元的兴奋性,通过抑制细胞因子的合成以减少炎症组织的损伤,并能够抑制神经元凋亡、提高神经营养因子表达水平、促进神经细胞新生以及促进去甲肾上腺素释放等.迷走神经刺激术作为未来治疗脑缺血损伤的一种新的方法,具有良好的应用前景,本文就其作用机制进行综述.     

非洛地平缓释片对轻中度原发性高血压患者的降压疗效和对脉搏波 速度的影响

目的:探讨非洛地平缓释片对轻中度原发性高血压患者的降压疗效和对脉搏波速度的影响。方法:根据纳入标准选取我院260例原发性高血压患者,按计划方案给予非洛地平缓释片口服治疗。观察患者入院后、治疗2周末、14周末降压疗效及脉搏波传导速度的改变情况,并进行对比分析。结果:本组研究中接受治疗研究者共260例,其所有受检者在治疗2、6、10、14周后血压水平均有不同程度改善,与基线比较差异明显,有统计学意义(P<0.01)。脉搏波变化分析所有受试者脉搏波速度变化分析,基线脉搏波速度为(10.9±2.4)m/s,经过治疗后2周、14周基线脉搏波速度为(10.3±2.1)m/s,差异明显具有统计学意义(P<0.01);心率变化分析表明非洛地平缓释片在降压同时对心率影响不大,安全性评价表示,接受治疗期间曾有68例发生不良事件,占总数26.2%。笔者认为与药物无关,且均为轻度,经过适当处理后均缓解,对本研究无影响。结论:非洛地平缓释片降压效果良好,可同时降低颈动脉-股动脉脉搏波传导速度,改善大动脉僵硬度。     

家兔在个体发育中迷走神经机能发展的研究

(1947)和(1952)在报告中指出,狗在个体发育中迷走神经对心脏和小肠的机能效应,前者在生后第1小时出现,后者则在生后第1天发生。但是,(1964),(1964)和(1975)在狗的胎儿与小狗的实验中却提出不同的意见,他们认为胎儿在乏氧和小狗注射吗啡时,虽然能引起迷走神经中枢紧张,但此时缺乏支配心脏活动的迷走神经中枢紧张,出现支配心脏活动的迷走神经中枢紧张的时间,狗为生后10—12天和16—18天,猪为生后的5—10天,牛为生后10—12天。迷走神经对小肠运动的影响,发生在生后20天以后,20天以前小狗的迷走神经对     

正常小儿胫神经诱发脊髓电位特征和脑瘫小儿该电位的变化

采取刺激后胫神经(PTN)诱发叠加技术,利用体表无创伤性双极记录方法观察了16例正常小儿和43例脑瘫小儿的脊髓诱发电位(SCEP)。正常小儿的SCEP自下而上潜伏时逐渐延长、电压减小。从椎体C6到T10表现为Pa-Na-Pb三相波,T10～T12为Pa-Na1-Na2-Pb波,T12～L4为多相复合波。左右侧SCEP波形相似,潜伏时、电压相同,它们之间无统计学显著差别;但不同节段之间SCEP差异显著;脊髓传导速度为57.14m/s。脑瘫小儿SCEP正常者占14％;全髓反应低下者占20％;左右侧反应不对称者占46％;节段性反应低下者占15％;其它异常约占5％。不但节段间存在显著差异,而且全脊髓左右侧电压间以及颈、腰骶髓的潜伏时间出现显著差异。脊髓传导速度减低(患侧46.22m/s,对侧53.48m/s)。结果提示:(1)正常小儿脊髓活动左右对称,不同脊髓节段对PTN刺激反应不同。(2)脑瘫小儿脊髓活动左右不对称,一侧功能下降时对侧有一定代偿力,脊髓传导速度减慢。     

Reconstruction of the Abdominal Vagus Nerve Using Sural Nerve Grafts in Canine Models

Background

Recently, vagus nerve preservation or reconstruction of vagus has received increasing attention. The present study aimed to investigate the feasibility of reconstructing the severed vagal trunk using an autologous sural nerve graft.

Methods

Ten adult Beagle dogs were randomly assigned to two groups of five, the nerve grafting group (TG) and the vagal resection group (VG). The gastric secretion and emptying functions in both groups were assessed using Hollander insulin and acetaminophen tests before surgery and three months after surgery. All dogs underwent laparotomy under general anesthesia. In TG group, latency and conduction velocity of the action potential in a vagal trunk were measured, and then nerves of 4 cm long were cut from the abdominal anterior and posterior vagal trunks. Two segments of autologous sural nerve were collected for performing end-to-end anastomoses with the cut ends of vagal trunk (8–0 nylon suture, 3 sutures for each anastomosis). Dogs in VG group only underwent partial resections of the anterior and posterior vagal trunks. Laparotomy was performed in dogs of TG group, and latency and conduction velocity of the action potential in their vagal trunks were measured. The grafted nerve segment was removed, and stained with anti-neurofilament protein and toluidine blue.

Results

Latency of the action potential in the vagal trunk was longer after surgery than before surgery in TG group, while the conduction velocity was lower after surgery. The gastric secretion and emptying functions were weaker after surgery in dogs of both groups, but in TG group they were significantly better than in VG group. Anti-neurofilament protein staining and toluidine blue staining showed there were nerve fibers crossing the anastomosis of the vagus and sural nerves in dogs of TG group.

Conclusion

Reconstruction of the vagus nerve using the sural nerve is technically feasible.     

Conduction along myelinated and demyelinated nerve fibres with a reorganized axonal membrane during the recovery cycle: model investigations

The changes in the excitability of the reorganized axonal membrane in myelinated and demyelinated nerve fibres as well as the causes conditioning such changes have been investigated by paired stimulation during the first 30 ms of the recovery cycle. The variations of the action potential parameters (amplitude and velocity) are traced also. The simulation of the conduction along the normal fiber is based on the Frankenhaeuser and Huxley (1964) and Goldman and Albus (1968) equations, while the demyelination is considered to be an elongation of the nodes of Ranvier. The axonal membrane reorganization is achieved by means of potassium channel blocking and increase of the sodium-channel permeability. It is shown that potassium channels block decreases membrane excitability for the myelinated and demyelinated fibres in the cases of initial and paired stimulation. With increasing sodium-channel permeability on the background of the blocked potassium channels, the membrane excitability is increased. For the fibres with a reorganized membrane, a supernormality of the membrane excitability is obtained, the latter remaining unrecovered during the 30 ms cycle under investigation. The supernormality of the excitability grows from the demyelinated fibre without reorganized membrane to the demyelinated fibre with reorganized one. For short interstimulus intervals, the second action potential propagates along the fibres with a reduced velocity and a decreased amplitude. No supernormality of the potential parameters (amplitude, velocity) is observed during the cycle up to 30 ms. The membrane properties of the myelinated and demyelinated fibres with blocked potassium channels recover in the interval from 15 to 20 ms depending on whether the sodium channels' increase of the permeability is added on the background of the blocked potassium channel or not. In the recovery cycle, the axonal membrane reorganization leads to an improvement of the conduction along most severely demyelinated fibres.     

Modeling the interactions between stimulation and physiologically induced APs in a mammalian nerve fiber: dependence on frequency and fiber diameter

Electrical stimulation of nerve fibers is used as a therapeutic tool to treat neurophysiological disorders. Despite efforts to model the effects of stimulation, its underlying mechanisms remain unclear. Current mechanistic models quantify the effects that the electrical field produces near the fiber but do not capture interactions between action potentials (APs) initiated by stimulus and APs initiated by underlying physiological activity. In this study, we aim to quantify the effects of stimulation frequency and fiber diameter on AP interactions involving collisions and loss of excitability. We constructed a mechanistic model of a myelinated nerve fiber receiving two inputs: the underlying physiological activity at the terminal end of the fiber, and an external stimulus applied to the middle of the fiber. We define conduction reliability as the percentage of physiological APs that make it to the somatic end of the nerve fiber. At low input frequencies, conduction reliability is greater than 95% and decreases with increasing frequency due to an increase in AP interactions. Conduction reliability is less sensitive to fiber diameter and only decreases slightly with increasing fiber diameter. Finally, both the number and type of AP interactions significantly vary with both input frequencies and fiber diameter. Modeling the interactions between APs initiated by stimulus and APs initiated by underlying physiological activity in a nerve fiber opens opportunities towards understanding mechanisms of electrical stimulation therapies.     

The velocity of conduction in nerve fiber and its electric characteristics

The theory developed in this paper shows that the propagation of spike potential along a nerve fiber and the conduction of an electric wave along an inert inorganic conductor follow a common quantitative relationship. This result gives further support to the belief that propagation of excitation is an electrical process. The basic idea of the theory is derived from the consideration that velocity has, by its mathematical definition, a local meaning; conduction in a nerve is completely determined by the local characteristics of the latter, as well as those of the wave. The final formula derived does not make use of any other field of science beyond the fundamental principles of electricity. It gives the conduction velocity in terms of the electric characteristics of the fiber and of the duration of the spike potential. The formula is in agreement with the known dependence of the conduction velocity on various parameters characterizing the axon. The computed velocity agrees with the measured ones on the squid giant axon, crab nerve axon, frog muscle fiber and Nitella cell. The membrane inductance appears as a velocity controling agent which prevents also a possible distortion of the spike potential during conduction. The structural meaning of the electric characteristics of the axon membrane is discussed from the viewpoint of the diffusion theory. A formula for the velocity of spread of the electrotonus is also derived.     

On the cable theory of nerve conduction

Conduction of an impulse in the nonmyelinated nerve fiber is treated quantitatively by considering it as a direct consequence of the coexistence of two structurally distinct regions, resting and active, in the fiber. The profile of the electrical potential change induced in the vicinity of the boundary between the two regions is analyzed by using the cable equations. Simple mathematical formulae relating the conduction velocity to the electrical parameters of the fiber are derived from the symmetry of the potential profile at the boundary. The factors that determine the conduction velocity in the myelinated nerve fiber are reexamined.     

Theoretical consideration of a possible mechanism in the conduction process of thin-sheathed nerve fibers

The propagation of a transverse disturbance along a tubular membrane enclosing a fluid medium and embedded in another is considered. It is shown that the velocity of propagation of such a disturbance can be identified with the velocity of the conduction process of thin-sheathed nerve fibers. The required values of the associated parameters, tension and pressure, appear not unreasonable. The results obtained indicate that experimental observations on the relation between the conduction velocity and the fiber diameter, as well as the effects of longitudinal stretching and transverse squeezing on the velocity of the conduction process in nerve, may be correlated on such a basis.     

A study of conduction velocity in nonmyelinated nerve fibers.

By treating a nonmyelinated nerve fiber as a continuous cable consisting of three distinct zones (Resting, transitional, and excited), the following mathematical expression was derived: (formula: see text) where v is the conduction velocity, d the diameter of the fiber, R the resistance of the membrane of unit area at the peak of excitation, rho the resistivity of the medium inside the fiber, and C the capacity of membrane per unit area. The validity of this expression was demonstrated by using squid giant nerve fibers intracellularly perfused with dilute salt solutions. The relationship between these results and previous theories and experiments on conduction velocity is discussed.     

Peripheral nerve at extreme low temperatures 2: Pharmacologic modulation of temperature effects

Changes in temperature have profound and clinically important effects on the peripheral nerve. In a previous paper, the effects of temperature on many properties of the peripheral nerve action potential (NAP) were explored including the NAP amplitude, conduction velocity and response to paired pulse stimulation. In this paper, the effects of pharmacologic manipulations on these parameters were explored in order to further understand the mechanisms of these effects.The reduction in conduction velocity with temperature was shown to be independent of the ionic composition of the perfusate and was unaffected by potassium or sodium channel blockade. This implies that the phenomenon of reduced conduction velocities at low temperature may be related to changes in the passive properties of the axon with temperature. Blockade of sodium channels and chronic membrane depolarization produced by high perfusate potassium concentrations or high dose 4-aminopyridine impair the resistance of the nerve to hypothermia and enhance the injury to the nerve produced by cycles of cooling and rewarming. This suggests the possibility that changes in the sodium inactivation channel may be responsible for the changes in the NAP amplitude with temperature and that prolonged sodium inactivation may lead more permanent changes in excitability.     

外周诱发电位的模型研究

本文根据容积导体中有关动作电位的电生理理论,用三点源模型模拟单根纤维动作电位(SFAP),并假设神经束的复合动作电位(CAP)是由SFAP线性叠加而成,给出了神经束CAP的模型.通过运用上述模型,计算了正常人正中神经纤维传导速度分布,分析了刺激腕部正中神经引导的传感诱发电位(SEP)的N~-_9成分;另外,还得出一些描述此外周传导通路性质的其它参数,如平均传导速度、神经纤维活动最可几传速度分布范围等.此方法可用来研究其它各种外围诱发电位.     

Nerve Excitability Assessment in Chemotherapy-induced Neurotoxicity

Chemotherapy-induced neurotoxicity is a serious consequence of cancer treatment, which occurs with some of the most commonly used chemotherapies^1,2. Chemotherapy-induced peripheral neuropathy produces symptoms of numbness and paraesthesia in the limbs and may progress to difficulties with fine motor skills and walking, leading to functional impairment. In addition to producing troubling symptoms, chemotherapy-induced neuropathy may limit treatment success leading to dose reduction or early cessation of treatment. Neuropathic symptoms may persist long-term, leaving permanent nerve damage in patients with an otherwise good prognosis³. As chemotherapy is utilised more often as a preventative measure, and survival rates increase, the importance of long-lasting and significant neurotoxicity will increase.There are no established neuroprotective or treatment options and a lack of sensitive assessment methods. Appropriate assessment of neurotoxicity will be critical as a prognostic factor and as suitable endpoints for future trials of neuroprotective agents. Current methods to assess the severity of chemotherapy-induced neuropathy utilise clinician-based grading scales which have been demonstrated to lack sensitivity to change and inter-observer objectivity⁴. Conventional nerve conduction studies provide information about compound action potential amplitude and conduction velocity, which are relatively non-specific measures and do not provide insight into ion channel function or resting membrane potential. Accordingly, prior studies have demonstrated that conventional nerve conduction studies are not sensitive to early change in chemotherapy-induced neurotoxicity^4-6. In comparison, nerve excitability studies utilize threshold tracking techniques which have been developed to enable assessment of ion channels, pumps and exchangers in vivo in large myelinated human axons^7-9.Nerve excitability techniques have been established as a tool to examine the development and severity of chemotherapy-induced neurotoxicity^10-13. Comprising a number of excitability parameters, nerve excitability studies can be used to assess acute neurotoxicity arising immediately following infusion and the development of chronic, cumulative neurotoxicity. Nerve excitability techniques are feasible in the clinical setting, with each test requiring only 5 -10 minutes to complete. Nerve excitability equipment is readily commercially available, and a portable system has been devised so that patients can be tested in situ in the infusion centre setting. In addition, these techniques can be adapted for use in multiple chemotherapies.In patients treated with the chemotherapy oxaliplatin, primarily utilised for colorectal cancer, nerve excitability techniques provide a method to identify patients at-risk for neurotoxicity prior to the onset of chronic neuropathy. Nerve excitability studies have revealed the development of an acute Na⁺ channelopathy in motor and sensory axons^10-13. Importantly, patients who demonstrated changes in excitability in early treatment were subsequently more likely to develop moderate to severe neurotoxicity¹¹. However, across treatment, striking longitudinal changes were identified only in sensory axons which were able to predict clinical neurological outcome in 80% of patients¹⁰. These changes demonstrated a different pattern to those seen acutely following oxaliplatin infusion, and most likely reflect the development of significant axonal damage and membrane potential change in sensory nerves which develops longitudinally during oxaliplatin treatment¹⁰. Significant abnormalities developed during early treatment, prior to any reduction in conventional measures of nerve function, suggesting that excitability parameters may provide a sensitive biomarker.