钩藤总碱对大鼠心电图和蟾蜍坐骨神经干动作电位的影响

本文研究了钩藤总碱对大鼠ECG和蟾蜍坐骨神经干APA的影响,并与抗心律失常药奎尼丁作了对比。实验结果表明钩藤总碱与奎尼丁对大鼠ECG改变相似——剂量依赖性地延长P-R、P-P、Q-T间期,增宽QRS波群;两药都随浓度增高而使蟾蜍坐骨神经干APA显著降低。提示钩藤总碱可能具有“奎尼丁样”作用。     

生物频谱对蟾蜍坐骨神经动作电位和传导速度的影响

本文采用电生理学方法通过坐骨神经损伤模型,测量蟾蜍离体坐骨神经干的动作电位和传导速度,观察生物频谱对外周神经功能的影响。结果显示频谱可部分恢复塘蜍损伤神经的动作电位和传导速度。频谱照射组与对照组比较有统计学差异(P<0.05)。     

葡萄糖溶液对坐骨神经动作电位的影响

目的研究5%、10%葡萄糖溶液对蟾蜍坐骨神经动作电位(AP)的影响。方法应用BL—420F生物机能实验系统进行研究。结果5%葡萄糖随着浸润蟾蜍坐骨神经时间的延长,蟾蜍坐骨神经复合AP传导幅度缓慢降低;传导速度逐渐抑制;对AP潜伏期产生延长作用明显。用任氏液分别再浸润可逐渐恢复。而10%葡萄糖对此作用更明显,且用任氏液再分别浸润无恢复。结论5%葡萄糖溶液浸润3min并未对坐骨神经产生不可逆的损害,而5%的葡萄糖溶液浸润10min,可能对神经有一定的损害,恢复得不好。而10%葡萄糖无论浸润多长时间,均可对坐骨神经产生不可逆的损害。     

注射用钩吻素子脂质体对离体蛙坐骨神经干动作电位的影响

目的应用电生理方法观察注射用钩吻素子脂质体对于蛙离体坐骨神经干动作电位的影响。方法采用薄膜分散法制备注射用钩吻素子脂质体,制备蛙离体坐骨神经干,将其分为任氏液组(C组)和注射用钩吻素子脂质体组(K组),分别用任氏液、注射用钩吻素子脂质体处理蛙离体坐骨神经干。使用BL-420F生物机能实验系统引导神经干复合动作电位,测定神经干复合动作电位的振幅、传导速度以及持续时间。结果任氏液组神经干复合动作电位的振幅、持续时间和传导速度各观察时点比较均无变化(P>0. 05);注射用钩吻素子脂质体可使蛙坐骨神经干复合动作电位的振幅变小、传导速度变慢(P <0. 05),进而使坐骨神经干动作电位消失。结论注射用钩吻素子脂质体能阻滞蛙离体坐骨神经干复合动作电位的传导,这可能是其发挥局部麻醉效应的电生理学基础。     

草乌甲素注射液对蛙离体坐骨神经干动作电位的影响

目的:探讨应用电生理方法比较草乌甲素注射液和普鲁卡因注射液对蛙离体坐骨神经干动作电位的影响及草乌甲素发挥局部麻醉作用的机制.方法:制备牛蛙离体的坐骨神经一腓神经标本,分为草乌甲素注射液组、普鲁卡因注射液组,以及草乌甲素注射液浓度组(10%,20%,50%,100%).用BL-420生物机能实验系统引导神经干动作电位,分别测定神经干动作电位的幅度、持续时间.结果:草乌甲素注射液和普鲁卡因注射液均可降低神经干动作电位的幅度,草乌甲素的作用大于普鲁卡因;但两者对神经干动作电位的持续时间无影响.结论:草乌甲素注射液对蛙离体坐骨神经干动作电位的产生有一定的抑制作用.     

糖尿病对大鼠坐骨神经动作电位潜伏期影响的观察

目的：观察糖尿病对大鼠坐骨神经动作电位潜伏期的影响。方法：剥离大鼠坐骨神经,利用BL-310生物信号处理系统测量其动作电住的潜伏期。结果：糖尿病大鼠坐骨神经动作电位潜伏期约为0．92ms，比正常大鼠动作电位潜伏期延长。     

甲基莲心碱对大鼠心电图和蟾蜍坐骨神经动作电位的影响

在麻醉大鼠观察了恒速iv甲基莲心碱对ECG的影响,并与奎尼丁和粉防己碱进行了对比性研究。甲基莲心碱对大鼠ECG的影响与奎尼丁相似,剂量(2～40mg/kg)依赖性地延长P-R和Q-T,使QRS增宽;粉防己碱不增宽QRS。结果显示甲基莲心碱作用机理与奎尼丁相似,不同于粉防己碱。甲基莲心碱与奎尼丁都可依浓度抑制蟾蜍坐骨神经APA,二者作用强度相近。     

大鼠和狗坐骨神经干复合动作电位的引导

本实验以大鼠、狗作为实验对象，采用细胞外引导法，分别观察了大鼠和狗坐骨神经干复合动作电位的形态、潜伏期、幅度及传导速度．结果显示，大鼠及狗坐骨神经干复合动作电位在形态上与蟾蜍坐骨神经干复合动作电位类似，但其动作电位的潜伏期明显短于蟾蜍，动作电位的幅度均高于蟾蜍，传导速度也明显比蟾蜍快．实验结果提示，大鼠和狗坐骨神经干复合动作电位的引导，可作为教学、科研及药效学研究模型．     

蝙蝠葛碱对蟾蜍坐骨神经动作电位的影响

<正> 蝙蝠葛碱(dauricine,Dau)具有降血压、抗实验性心律失常和阻Na~+内流作用。到目前为止,Dau对心肌以外的组织,如神经等动作电位的影响,尚未见报道。     

花椒浸液影响蟾蜍神经干动作电位的实验研究

本文应用电生学方法观察了不同浓度的花椒浸液对蟾蜍离体神经干 A、C 两类纤维动作电位幅度和传导速度的影响。结果表明:花椒浸液对 A、C 两类纤维动作电位幅度和传导速度均有明显的抑制效应。而且随着花椒浸液浓度的增高,两类纤维动作电位幅度明显下降(P<0.01),动作电位消失时间明显缩短(P<0.01)。动作电位幅度和传导速度与花椒浸液作用时间呈显著负相关(r=-0.901～-0.977,P<0.01)。在同一时间内给予花椒浸液,C 类纤维动作电位先被阻断,然后 A 类纤维动作电位被阻断。两类纤维动作电位均消失后,用标准Ringer 液(任氏液)浸泡均可再现。     

三邻甲苯基磷酸酯诱导母鸡坐骨神经动作电位特性的时效性变化

目的研究三邻甲苯基磷酸酯(TOCP)诱发母鸡迟发性神经毒性(OPIDN)发生过程中坐骨神经动作电位特性的时间效应关系及其与症状分级间的关系,寻找敏感指标,为探讨TOCP引起OPIDN的发病机制及早期诊断提供依据。方法成年罗曼母鸡,一次po750mg·kg-1TOCP,在d0,5,10,15和21测定母鸡坐骨神经动作电位。结果TOCP处理母鸡逐渐出现下肢行走不协调、站立行走困难等症状,至d15完全瘫痪。坐骨神经动作电位特性随各时间点及症状分级变化。在d5,10,15和21与d0对照组相比,坐骨神经传导速度减慢,分别降低16%(P<0.05),33%,47%和47%(P<0.01);复合动作电位(CAP)潜伏期渐延长,分别增加27%(P<0.05),39%,45%和73%(P<0.01);波幅分别减小6%(P>0.05),22%,37%和40%(P<0.01);最大刺激强度分别增加10%和10%(P>0.05),31%和34%(P<0.01);阈值强度在各时间点变化不明显;痛觉阈值分别升高30%,56%,79%和80%(P<0.01)。在OPIDN症状分级为1～2,3～4,5～6和7～8级时与0级时相比,坐骨神经传导速度分别降低16%(P<0.05),33%,43%和50%(P<0.01);潜伏期分别升高27%(P<0.05),33%,40%和73%(P<0.01);波幅分别降低6%和9%(P>0.05),36%和39%(P<0.01);最大刺激强度分别升高10%和10%(P>0.05),21%和35%(P<0.01);阈强度变化不明显。结论TOCP诱导母鸡坐骨神经动作电位特性随时间延长及症状加重进行性变化,以神经传导速度及复合动作电位潜伏期变化最早、最为敏感。     

Essential oil of croton nepetaefolius and its main constituent, 1,8-cineole, block excitability of rat sciatic nerve in vitro

1. The effects of the essential oil of Croton nepetaefolius (EOCN) and its major constituent, 1,8-cineole, on the compound action potential (CAP) of nerve were investigated. 2. Experiments were performed in sciatic nerves dissected from Wistar rats, mounted in a moist chamber and stimulated at a frequency of 0.2 Hz, with electric pulses of 100 micros duration at 20-40 V. Evoked CAP were displayed on an oscilloscope and recorded on a computer. The CAP control parameters were as follows: peak-to-peak amplitude 8.1 +/- 0.6 mV (n = 15); conduction velocity 83.3 +/- 4.2 m/s (n = 15); chronaxie 58.0 +/- 6.8 msec (n = 6); and rheobase 2.8 +/- 0.1 V (n = 6). 3. Lower concentrations of EOCN (100 and 300 microg/mL) and 1,8-cineole (153 and 307 microg/mL; i.e. 1 and 2 mmol/L, respectively) had no significant effects on CAP control parameters throughout the entire recording period. However, at the end of 180 min exposure of the nerve to the drug, peak-to-peak amplitude was significantly (P < 0.05) reduced to 27.4 +/- 6.7 and 1.7 +/- 0.8% of control values by 500 and 1000 microg/mL EOCN, respectively (n = 6), and to 76.5 +/- 4.4, 70.0 +/- 3.9 and 14.8 +/- 4.1% of control values by 614, 920 and 1227 microg/mL (i.e. 4, 6 and 8 mmol/L) 1,8-cineole, respectively (n = 6). Regarding conduction velocity, at the end of the 180 min exposure period, this parameter was significantly reduced to 85.8 +/- 7.3 and 48.7 +/- 12.3% (n = 6) of control values by 500 and 1000 microg/mL EOCN, respectively, and to 86.4 +/- 4.5 and 76.1 +/- 5.2% (n = 6) by 920 and 1227 microg/mL 1,8-cineole, respectively. Chronaxie and rheobase were significantly increased by the higher concentrations of both EOCN and 1,8-cineole. 4. It is concluded that EOCN and its main constituent 1,8-cineole block nerve excitability in a concentration-dependent manner, an effect that was totally reversible with 1,8-cineole but not with EOCN. This suggests that other constituents of EOCN, in addition to 1,8-cineole, may contribute to the mediation of this effect of EOCN.     

Toxic effect of acetamiprid on Rana ridibunda sciatic nerve (electrophysiological and histopathological potential)

In this study, the effects of a neonicotinoid insecticide acetamiprid on the sciatic nerve of Rana ridibunda were investigated by using electrophysiological and histological methods. A total of 35 preparations of sciatic nerve isolated from 35 frogs (Nervus ischiadicus) were used in the experiments. Experiments were designed as four different dose groups (n?=?8 per group). Acetamiprid solutions of 1 (group 1), 10 (group 2), 100 (group 3), and 1000?µM (group 4) were applied to the nerves in dose groups. In each group, action potentials were recorded before application of acetamiprid which served as control data. The extracellular action potentials were recorded for each group of 30th, 60th, 90th and 120th min of application time. Action potential amplitude and area were measured from recordings. Histological evaluation was performed by transmission electron microscopy.

In electrophysiological examination, all doses in which acetamiprid applied have shown the effect from the 30th min and suppressed the sciatic nerve action potential. Acetamiprid significantly reduced the amplitude at the rate of 78–96% and the area at the rate of 79–98% (p?<?0.05). In electron microscopic examination, the control nerves were in normal appearance. Disorganization, irregularity, dense ovoid body formation, fragmentation of the myelin sheath, and loss on some axoplasm of the nerves in the dose group have been observed. Our findings showed that acetamiprid can cause neuropathic changes in sciatic nerve at all applied doses. These results indicate that acetamiprid as other insecticides can have harmful effects on non-target organisms.