对比观察钼和硒对培养心肌细胞电生理特性的影响

钼(Mo)和硒(Se)都是人体必需微量元素,与某些心脏病、克山病病因及发病机制有关。但是,哪一个与上述疾病关系更密切说法不一。我们曾证明 Mo 和 Se 对培养心肌细胞生长发育和自发性收缩都有良好的促进作用,Se 比 Mo 更明显。为进一步验证这一结果,本实验利用细胞内微电极技术,对比观察二者对培养心肌细胞电生理特性的影响。其结果表明:Mo 和 Se对心肌细胞跨膜电位各项指标均有一定影响,其中具有统计学意义的是,动作电位时程延长;静息电位绝对值减小。这提示了,Mo 和 Se 可能与 Ca~(2+)、K~+通道的活性有关,对比之下,Se 比 Mo更明显。     

伊布利特对犬心脏电生理特性的影响

观察伊布利特对犬心脏电生理特性的作用特点,初步探讨其终止心房扑动(简称房扑)的机制。15只成年健康雄性杂种犬,麻醉后气管插管,开胸并缝合电极,伊布利特按0.10mg/kg静脉推注给药(10min缓推,给药30min后按照0.01mg/min静脉滴注维持),观察给药前后心率、房内房间传导时间、峡部缓慢传导区传导速度、各部位不应期的变化。结果:伊布利特对心率有明显的抑制作用,作用的高峰时间在给药后20~30min,2h后心率基本恢复到用药前的水平;伊布利特能显著延长心房肌、心室肌以及肺静脉的不应期(P<0.05~0.001),但对房内、房间以及峡部的传导作用影响不明显(P>0.05)。结论:伊布利特终止房扑的机制可能是由于该药造成不应期延长,使折返环可激动间隙兴奋性降低,进而使波锋不能向前推进,终止房扑。其房扑折返环传导的减慢可能不是房扑终止的主要作用。     

房室折返性心动过速合并房室结双径现象

目的 分析射频消融术证实的房室帝道（ＡＰ）合并房室结双径（ＤＡＶＮＰ）,以了解其电生理特点。方法 以食管心房调博及心内电生理检查,确诊室上速合并房室结双径１２例,并行射频消融枚。结果 ＡＰ合并ＤＡＶＮＰ占ＡＰ的１６．４％（１２／７３）,多为陷匿性ＡＰ（１０／１２）,其折返途径多为ＡＰ逆传（１０／１２）,房室结单一径路前传,房室结快径道不应期及心动过速时ＲＰ’（ＶＡ）与ＲＰ意期,在食道电生理与心内电     

犬房室结电图记录报告

为证实房室结电图的真实性,采用体外转流方法,直视记录房室结区电位。结果表明N波代表房室结的电活动。直视记录结果与导管记录结果相一致。     

A novel pacing maneuver to verify the postpacing interval minus the tachycardia cycle length while adjusting for decremental conduction: Using “dual-chamber entrainment” for improved supraventricular tachycardia discrimination

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电生理监测技术联合解剖定位在脑运动区手术中的应用

目的探讨电生理监测技术联合解剖定位在脑运动区手术中的应用。方法在Pubmed和中国知网数据库,以电生理监测技术、解剖定位和脑运动区手术为关键词,查阅1997年5月—2013年12月关于电生理监测技术与脑运动区解剖定位在脑运动区手术中应用的相关文献,进行分析总结。结果解剖定位包括功能MR和影像导航。电生理监测脑功能定位技术包括体感诱发电位位相倒置技术、经颅电刺激运动诱发电位、皮层电刺激运动区定位、皮层电刺激语言区定位、皮质下电刺激定位运动通路。解剖定位和电生理监测技术在脑运动区手术中各有利弊,目前趋势是联合应用。结论在脑运动区手术中,应用电生理监测联合解剖定位可提高脑运动区解剖定位的精确度,达到最大限度切除肿瘤、保留神经功能的作用。     

Intraoperative Electrophysiological Studies to Predict the Efficacy of Neurolysis After Nerve Injury—Experiment in Rats

Compound muscle action potentials (CMAPs) can be used to analyze injury and recovery of nerve. This standardized study evaluates the value of CMAP analysis in predicting the long-term efficacy of neurolysis. CMAP amplitude is also used to determine the optimal extent of neurolysis. The left peroneal nerves of 30 rats were crushed. CMAPs were recorded for both crushed (left) and control (right) nerves. Fifteen rats underwent neurolysis 3 months post crush injury; the remaining 15 were sham controls and did not undergo neurolysis. CMAP measurements were taken after: (1) release of the nerve from the fascia, (2) opening the epineurium, and (3) opening the perineurium. At 3 months post crush injury, opening the epineurium resulted in a statistically significant increase in CMAP. CMAP increase with perineurial neurolysis was greater than with fascial release of the nerve but was not statistically different from that of epineurial release. At 5 months post crush injury, recovery of crushed nerves that underwent neurolysis was 90% and significantly less at 70.5% in rats not treated with neurolysis, according to CMAP analysis. Two conclusions can be made from this study. First, intraoperative neurophysiologic studies can monitor the immediate results of neurolysis and predict long-term results in the injured nerve. Second, epineurotomy is important in neurolysis, improves the function of the nerve, less invasive, and a slightly more effective technique than perineurotomy.     

Potassium channel dysfunction and depolarized resting membrane potential in a cell model of SCA3

Spinocerebellar ataxia type 3 (SCA3) is an autosomal dominant inherited neurodegenerative disease caused by the expansion of a polyglutamine repeat within the disease protein, ataxin-3. There is growing evidence that neuronal electrophysiological properties are altered in a variety of polyglutamine diseases such as Huntington's disease and SCA1 and that these alterations may contribute to disturbances of neuronal function prior to neurodegeneration. To elucidate possible electrophysiological changes in SCA3, we generated a stable PC12 cell model with inducible expression of normal and mutant human full-length ataxin-3 and analyzed the electrophysiological properties after induction of the recombinant ataxin-3 expression. Neuronally differentiated PC12 cells expressing the expanded form of ataxin-3 showed significantly decreased viabilities and developed ultrastructural changes resembling human SCA3. Prior to neuronal cell death, we found a significant reduction of the resting membrane potential and a hyperpolarizing shift of the activation curve of the delayed rectifier potassium current. These findings indicate that electrophysiological properties are altered in mutant ataxin-3 expressing neuronal cells and may contribute to neuronal dysfunction in SCA3.     

Peripheral and central changes combine to induce motor behavioral deficits in a moderate repetition task

Repetitive motion disorders, such as carpal tunnel syndrome and focal hand dystonia, can be associated with tasks that require prolonged, repetitive behaviors. Previous studies using animal models of repetitive motion have correlated cortical neuroplastic changes or peripheral tissue inflammation with fine motor performance. However, the possibility that both peripheral and central mechanisms coexist with altered motor performance has not been studied. In this study, we investigated the relationship between motor behavior changes associated with repetitive behaviors and both peripheral tissue inflammation and cortical neuroplasticity. A rat model of reaching and grasping involving moderate repetitive reaching with negligible force (MRNF) was used. Rats performed the MRNF task for 2 h/day, 3 days/week for 8 weeks. Reach performance was monitored by measuring reach rate/success, daily exposure, reach movement reversals/patterns, reach/grasp phase times, grip strength and grooming function. With cumulative task exposure, reach performance, grip strength and agility declined while an inefficient food retrieval pattern increased. In S1 of MRNF rats, a dramatic disorganization of the topographic forepaw representation was observed, including the emergence of large receptive fields located on both the wrist/forearm and forepaw with alterations of neuronal properties. In M1, there was a drastic enlargement of the overall forepaw map area, and of the cortex devoted to digit, arm–digits and elbow–wrist responses. In addition, unusually low current amplitude evoked digit movements. IL-1β and TNF-α increased in forearm flexor muscles and tendons of MRNF animals. The increases in IL-1β and TNF-α negatively correlated with grip strength and amount of current needed to evoke forelimb movements. This study provides strong evidence that both peripheral inflammation and cortical neuroplasticity jointly contribute to the development of chronic repetitive motion disorders.