惊厥后的

Methods: Totally 16 healthy adult rabbits of both sexes were randomly divided into SP group and NS group. The rabbits in SP and NS group were given Thiopental (3 mg/kg) and normal saline (1 ml/kg) respectively by intravenous injection via ear vein after establishing convulsant models by injecting Strychnine into the other ear vein. QPEEG and power spectral analysis were used to analyze the changes of δ-band of QPEEG in convulsant rabbits before and after administering drugs.

成年家兔16只，雌雄不限，随机分为硫喷妥钠组和生理盐水组，每组8只，在建立惊厥兔模型后，分别耳缘静脉注射硫喷妥钠3 mg/kg、生理盐水1 ml/kg，应用QPEEG，采用功率谱分析法，分析惊厥家兔给药前后QPEEG δ频段的变化。

The EEG in 250 FC children at the age of 4 month to 6 years was recorded.

对250例6个月至6岁患儿的热性惊厥后的脑电图。

Methods: Experimental rats were injected with KA (10mg/kg, 5mg/ml) subcutaneously to make status epilepticus model. SE latter 10 day, Use subliminal dosages KA to check falling sickness paroxysm sensibility model; SE latter 10 day , Morris water maze was to evaluate cognitive function in the animals. Changing NPY adopt immunocyte chemistry method to check the rat brain inner is expressed.

本研究给Sprague-Dawley大鼠颈部皮下注射惊厥剂量的红藻氨酸(KA，10mg/kg，5mg/ml)，诱发癫痫持续状态(status epilepticus，SE)， 10天后，用阈下剂量的KA检测癫痫发作敏感性模型；10天后用Morris水迷宫实验检测动物学习记忆功能变化；用免疫组化技术检测动物海马CA1区CA3区NPY表达的变化。

Although the clinical experience and the results of animal experiments indicate that the adminis- tration of atracurium at recommended doese is unlikely to result in laudanosine concentrations capable of producing seizure activity, Hennis et al found that at a plasma concentration below that causing convulsions, laudanosine "awaken"dogs lightly anesthetized with halothane.

临床病人应用常用剂量阿屈宁后，血浆Laudanosine选低于使动物发生惊厥所需的浓度，数百万例应用阿屈宁的病人中也未见有因代谢生成之Laudanosine而发生惊厥体征或脑电征象者。可以认为，阿屈宁的临床应用是不会因Laudanosine的生成而引起惊厥的。

Result: 1、Ethology result:50 rats were injecting convulsive dose kainic acid, showing prodrome such as gaze, wet dog shake in the 0-30 minutes; 1-5 degree epileptic attack in the 30-60minutes; 4-5 degree repteately spontaneous epileptic attack in 60-90 minutes; then status epilepticus,SE-epileptic attack endurance became longer and interval became shorter with bulk salivas and various kinds psychomotor symptoms.

结果：1、行为学结果：SD大鼠(n=50)在注射惊厥剂量(10mg/kg)KA后，0-30min内动物出现凝视，湿狗样抖动(wet dog shake，WDS)等前驱症状；30-60min内动物出现1-5级癫痫发作；60-90min内动物反复自发出现4-5级癫痫发作；其后动物癫痫发作持续时间延长，间隔变短伴有大量唾液分泌，出现各种精神运动症状，呈现SE，SE后10天，用阈下剂量(5mg/kg)KA检测动物对癫痫刺激的敏感性。

IL-1βmRNA expression in the developmental brain in Wistar rat: IL-1β mRNA in hippocampus, cerebral cortex and subcortex was detected by postnatal day 1 and gradually increased with development, reached a peak at postnatal day 21, and then gradually decreased to lower level at adult; In P77PMC rat, IL-1β mRNA expression was similar to Wistar rat before postnatal day 14, then gradually increased and surpassed Wistar rat at postnatal day 28, reached a peak in adult.

原位杂交显示谷氨酸诱导Wistar大鼠惊厥和P77PMC大鼠听源性惊厥后脑内IL-1βmRNA表达情况。结果发现，两种不同惊厥模型大鼠惊厥后脑内IL-1βmRNA表达存在明显的差异。谷氨酸引起惊厥诱导脑内皮层、海马和丘脑IL-1βmRNA表达增高的程度远较P77PMC大鼠听源性惊厥为低，而且惊厥后IL-1βmRNA表达增加较慢，于4-8h达高峰，而听源性惊厥可于惊厥后2h迅速达高峰。但两种形式惊厥诱导脑内IL-1βmRNA表达最高的部位均是海马。

For lidocaine, 100 mice were divided into 10 groups,with10rates in each group who received dose of 183.11, 163.77, 146.48,131.02, 117.19, 93.75, 75.00, 60.00, 48.00, 38.40 mg/kg respectively. For each local anes thetic, the rates of convulsion or death were tried to distribute on both sides of 50％ symmetrically.

不同剂量的局麻药腹腔注射时，尽量使每种麻醉药致各组小鼠的惊厥率和致死率对称分布在50％左右，给药5 min后记录各组的致惊厥率和死亡率。

Meanwhile, in the CA3 area of hippocampus in NS group, a small amount of N-Cadherin positive cells were visible and were slightly stained. Compared with NS group, in PTZ seizure group, N-Cadherin positive cells had a marked increase in area CA3 and dentate hilus (P.01), but they were strongly inhibited in PDTC group (P.05). There was no correlation between the expressions of N-cadherin, Timm-stained granules and between the age of rats with seizure.

同时，NS组14天和28天大鼠海马CA3区可见少量的N-Cadherin阳性细胞，着色不深；PTZ致惊组海马CA3和齿状回门区的N-Cadherin阳性细胞与NS组相比明显增多（P＜0.01），PDTC预处理后相同区域内N-Cadherin阳性细胞较PTZ致惊组明显减少（P＜0.05）。N-Cadherin与Timm染色颗粒的表达结果与惊厥鼠的日龄并无关联性。

Take the blood specimen to measure the hepatic and renal function and the tissue biopsy after the active and motive abnormities called toxical manifestation such as posture changes, abnormal sound, uneasiness, quiet, thrill, ataxia, convulsion and so on with toxic dose. Measure the tissue biopsy after death with lethiferous dose. If no toxicity or death occur after the experiment of 12 weeks, measure the hepatic and renal function and the tissue biopsy. There was no rat which had the toxical manifestation such as active or motive abnormities and 3 rats died because of environment or others after the experiment of 12 weeks.

实验中分别测定治疗剂量组小鼠在用药4周，8周，12周后的肝肾功能，并进行组织病理检查；中毒剂量组小鼠在出现行为、动作异常，如改变姿势、叫声异常、不安、安静、震颤、运动失调、惊厥等中毒表现时，取血液标本测定肝肾功能，并进行组织病理检查；致死剂量组小鼠发生死亡后进行组织病理检查；若12周实验结束时无小鼠出现中毒表现或死亡，则取血液标本测定肝肾功能，并进行组织病理检查。12周实验结束时，无小鼠出现动作、行为异常等中毒表现，有3只小鼠因为环境或其它原因发生死亡，病理检查结果正常。

Objective: To detect changes in levels of glutamate and asparate in rat discrete brain regions which may be involved in the mechanism of seizure initiation and maintenance in soman induced seizures.

目的 ：对脑内兴奋性氨基酸的变化进行定位研究。方法：应用Beckman 6300氨基酸分析仪和601黄金系统色谱工作站，对梭曼惊厥后不同时相大鼠的新鲜脑组织进行定位检测。

The split between the two groups can hardly be papered over.

这两个团体间的分歧难以掩饰。

This approach not only encourages a greater number of responses, but minimizes the likelihood of stale groupthink.

这种做法不仅鼓励了更多的反应，而且减少跟风的可能性。