神经源性声带运动障碍与喉神经电生理

声带运动障碍的病因和临床表现复杂多变，涉及多学科，从病因上分为神经源性和非神经源性。对于神经源性声带运动障碍的诊治，首先通过喉镜等检查明确有无声带运动障碍及严重程度，值得注意的是声带纵向张力变化障碍也属于运动障碍的范畴；然后采用喉肌电图（LEMG）检查进行定性分析，在确诊神经源性损伤后，进一步对神经损伤部位进行定位诊断并查找导致神经损伤的病因；同时根据喉部神经电生理评估结果，判断预后。最后综合上述的评估结果制定相应的治疗策略。     

Postsynaptic and spiking activity of pyramidal cells,the principal neurons in the rat hippocampal CA1 region,does not control the resultant BOLD response: a combined electrophysiologic and fMRI approach

The specific role of postsynaptic activity for the generation of a functional magnetic resonance imaging (fMRI) response was determined by a simultaneous measurement of generated field excitatory postsynaptic potentials (fEPSPs) and blood oxygen level-dependent (BOLD) response in the rat hippocampal CA1 region during electrical stimulation of the contralateral CA3 region. The stimulation electrode was placed either in the left CA3a/b or CA3c, causing the preferentially basal or apical dendrites of the pyramidal cells in the right CA1 to be activated. Consecutive stimulations with low-intensity stimulation trains (i.e., 16 pulses for 8 seconds) resulted in clear postsynaptic responses of CA1 pyramidal cells, but in no significant BOLD responses. In contrast, consecutive high-intensity stimulation trains resulted in stronger postsynaptic responses that came along with minor (during stimulation of the left CA3a/b) or substantial (during stimulation of the left CA3c) spiking activity of the CA1 pyramidal cells, and resulted in the generation of significant BOLD responses in the left and right hippocampus. Correlating the electrophysiologic parameters of CA1 pyramidal cell activity (fEPSP and spiking activity) with the resultant BOLD response revealed no positive correlation. Consequently, postsynaptic activity of pyramidal cells, the most abundant neurons in the CA1, is not directly linked to the measured BOLD response.     

Electrophysiological evaluation in 4 patients with diabetic pseudotabes

BACKGROUND: Researches on diabetic nervous system lesion are mainly focus on peripheral nerve and vegetative nerve, so there are few investigations on diabetic pseudotabes. OBJECTIVE: To investigate the electrophysiological examinations on the diagnosis of diabetic pseudotabes. DESIGN: Case study. SETTING: Department of Electrophysiology and Department of Neurology, Zhongshan Hospital Affiliated to Xiamen University. PARTICIPANTS: A total of 4 patients with type 2 diabetes mellitus, including 3 males and 1 female aged from 50 to 72 years, were selected from Department of Neurology, Zhongshan Hospital Affiliated to Xiamen University from March 2002 to February 2005. All accepted subjects met the modified diagnostic criteria of diabetes mellitus, which was set by American Diabetes Mellitus Association (ADA) in 1997. Otherwise, the subjects had typical symptoms and physical signs of spinal posterior funiculus damage. However, patients with spinal cord lesion which was caused by other factors were excluded. All accepted subjects provided the confirmed consent. METHODS: Nicolet NT electromyography (EMG)/evoked potential meter (made in the USA) was used to detect spinal cord conduction velocity (SCCV), somatosensory evoked potential (SEP) of lower limbs, motor nerve conduction velocity (MNCV) and sensory nerve conduction velocity (SNCV) of extremities. Determining criteria: Measurements were performed based on the laboratory standards. SCCV, which was less than lower limit of normal value (T2–12: 40–55 m/s, T12–L4: 20–41 m/s, T2–L4: 36–45 m/s), was regarded as abnormal. SEP value of lower limbs: P40, P60 and PF, which were more than standard deviation of normal value (x(—)+2.5), were regarded as the abnormality. Normal value of P40, P60 and PF latencies (x(—)±s) in this study: P40, P60 and PF in males were (37.6±1.9) ms, (59.8±3.9) ms and (7.6±0.9) ms, respectively; meanwhile, those in females were (35.5±1.7) ms, (55.2±2.7) ms and (6.3±0.7) ms, respectively. MNCV and SNCV, which were less than 50 m/s in upper limbs and 40 m/s in lower limbs, were regarded as the abnormality. MAIN OUTCOME MEASURES: Electrophysiological examinations. RESULTS: All 4 patients with type 2 diabetes mellitus were involved in the final analysis. ① SCCV: Among 4 patients, SCCV of three patients was decreased in T2–12, T12–L4 and T2–L4, and that of the other one was decreased in T2–12 and T2–L4; however, SCCV in T12–L4 was normal. There was significant difference as compared with normal value (P < 0.01). ② SEP of lower limbs: SEP values of lower limbs were abnormal in all 4 patients. Among them, P40, P60 and PF latencies of two patients were delayed; P40 of one patient was delayed and PF was not drained out; P40 and P60 of the last one were delayed and PF was normal. ③ MNCV and SNCV: The MNCV and SNCV were normal in one patient and abnormal in three patients. The results demonstrated that MNCV and SNCV of extremities decreased; especially, sensory nerve action potential (SNAP) of both lower extremities of one patient were not drained out. CONCLUSION: Detections of SCCV, SEP of lower limbs, MNCV and SNCV of extremities are helpful to investigate whether peripheral nerve and deep sensory passage are damaged or not and determine whether deep sensory damage is caused by peripheral nerve and spinal posterior funiculus.     

低血容量性休克大鼠心肌细胞Ca2+浓度及膜电位的变化

目的 旨在探讨低血容量性休克大鼠心肌细胞Ca2 浓度及其膜电位的变化.方法 选用Wistar大鼠84只,随机分成休克高渗复苏组(HES组)、生理盐水复苏组(NS组).建立休克模型,按7个时相(休克前、休克、复苏后5、15、30、60、90min)处死大鼠.取心室肌细胞培养传代,用Fluo-4/AM为游离钙荧光探针、JC-1荧光染色,流式细胞仪分别检测不同时相心肌细胞Ca2 浓度及线粒体膜电位.结果 HES组在休克、复苏后5、15、30min各时间点心肌细胞Ca2 浓度较休克前明显升高,其膜电位较休克前显著降低(P＜0.01);在复苏后60、90min心肌细胞Ca2 浓度及线粒体膜电位与休克时比较差异有显著性意义(P＜0.01);NS组在休克、复苏后各个时相与休克前比较心肌细胞Ca2 浓度均明显升高,其膜电位明显下降(P＜0.01);复苏后各时间点与休克时比较差异无显著性意义(P＞0.05);HSE组和NS组在休克后60、90min心肌细胞Ca2 浓度及其膜电位差异有显著性意义(P＜0.01).结论 低血容量性休克可诱发大鼠心肌细胞Ca2 浓度升高,线粒体膜电位下降,导致心肌细胞电生理活动障碍;高渗盐溶液不但可改善低血容量休克时心肌细胞Ca2 浓度,而且能有效地稳定其线粒体膜电位;而生理盐水对心肌细胞Ca2 浓度及其膜电位的作用不显著.     

关附甲素对豚鼠乳头肌动作电位最大除极速度的频率依赖性抑制作用

应用标准微电极技术，研究了关附甲素对豚鼠右心室乳头肌动作电位最大除极速率(V_max)的频率依赖性抑制作用(RDB)，并与美西律，奎尼丁，劳卡尼进行了比较. 在相同刺激间隔(300 ms)，产生50%左右RDB的药物浓度下，美西律的RDB开始最快，其第2个V_max所产生的抑制已占RDB的64%，奎尼丁，劳卡尼和关附甲素的RDB开始速率常数分别为每个动作电位0.165, 0.076和0.136. 美西律，奎尼丁，劳卡尼和关附甲素产生RDB的恢复时间常数分别为1.4, 9.0, 18.2和44.0 s，而且它们的恢复时间常数是不依赖于药物浓度而变化的，结果提示，关附甲素是一个慢动力学钠通道阻滞剂.     

Newer aspects of antiarrhythmic drug development: Introduction

Although cardiac arrhythmias remain a serious clinical problem in many patients with heart disease, the exact role of antiarrhythmic drug therapy is currently under intense evaluation. Within the last several years it has become clear that there are significant risks as well as potential benefits associated with existing agents. Ongoing studies in large patient populations should help determine the benefit/risk ratio of traditional therapy. Regardless of the outcome of these trials, current electrophysiological dogma will have to be re-evaluated and newer concepts evolve for drug development to make further progress. The goal of this symposium is to exchange information among basic and clinical investigators so as to facilitate the emergence of novel electrophysiological concepts that will form the basis for future generations of antiarrhythmic drugs.     

ELECTRICAL REMODELLING OF CHRONIC ATRIAL FIBRILLATION

1. It is now recognized that atrial fibrillation (AF) is not a benign condition, as it is associated with a 40% increase in mortality and a doubling of the risk of stroke. 2. The development of AF leads to mechanical, electrophysiological and cellular changes in the atria that tend to sustain AF. This process is known as atrial remodelling. 3. The three electrophysiological elements in the atria that initiate and sustain AF are: (i) shortening of the refractory period and an increase in dispersion; (ii) slowing of conduction velocity; and (iii) the presence of triggerin. foci. 4. As AF is a heterogeneous disorder, therapeutic strategies include the use of devices (pacemakers and atrial defibrillators), radiofrequency ablation (focal ablation or the creation of linear lines) and drug therapy that may reverse a remodelle. atrium.     

Age-related Changes in Excitability and Recurrent Inhibition in the Rat CA1 Hippocampal Region

In hippocampal slices from male Wistar rats aged 1–34 months, we recorded the synaptic field potential responses of the CA1 neurons to stimulation of Schaffer collaterals. Eight electrophysiological indexes were extracted from input/output curves and compared in 11 age groups from 1 to 30 months. Neuronal excitability presented a U-shaped curve of development with a minimum at ˜7–8 months of age. There was a significant continuous increase in neuronal excitability, i.e. a decrease in excitatory postsynaptic potential (EPSP) producing both the threshold and half-maximal population spike from middle age (8–10 months) to senescence (30 months). Synaptic efficiency also increased in old rats to reach a maximum during senescence, i.e. both the current for threshold EPSP and that for half-maximal EPSP reached a minimum in senescence, although the earlier developmental patterns of these two indexes were non-linear. The duration of the field EPSP elicited with maximal stimulation presented an abrupt decay after the first month. Aged animals presented a relatively small maximal population spike. Recurrent inhibition was most prominent on neuronal excitability rather than synaptic strength. Measured as the percentage change in the half-maximal EPSP and half-maximal population spike, recurrent inhibition was found to decrease during the first 7–10 months of life and remained small in later development.     

Relation Between Cycle Length, Volume, and Pressure in Type I Atrial Flutter

Assuming that type I atrial flutter is a macroreentrant circuit, its cycle length should vary with the atrial dimensions. In order to test this hypothesis, flutter cycle length was measured while inducing atrial volume and pressure changes by postural and pharmacological means in seven patients undergoing a therapeutic programmed stimulation for type 1 atrial flutter conversion. Right atrial volume was estimated from B-mode echocardiography data. Basal values were compared with those obtained during inspiration, expiration, Valsalva maneuver, negative tilt (head down), and positive tilt (head up) with 0.8–1.6 mg p.o. nitroglycerin. The right atrial size increased slightly from 17.8 to 18.3 cm² (P = 0.04) during the pressure load induced by negative tilt (+ 3 mmHg), with a corresponding lengthening of the flutter cycle length from 228 to 233 msec (P = 0.02). Similarly, pressure unloading of -2 mmHg by positive tilting and nitrates was accompanied by a decrease in right atrial size to 16.6 cm² (P = 0.04), with a corresponding decrease in cycle length from 228 to 219 msec (P = 0.03). Respiratory maneuver yielded similar results with an inspiratory cycle lengthening, expiratory shortening, and further shortening during Valsalva maneuver. These experiments demonstrate a direct relation between cycle length and atrial volume in human type I atrial flutter. They underline the importance of the right heart preload and atrial size for the electrophysiological characteristics of type I atrial flutter. Beside its fundamental interest, this finding is important for the understanding of the mechanism of maintenance and therapeutic responses of this common arrhythmia.