骨骼肌兴奋-收缩偶联超微结构瞬时变化研究

目的：从毫秒级功能变化水平实时观察骨骼肌在潜伏期内的细胞超微结构形态变化。方法：采用双向红外线探测器-计算机控制的电刺激与超低温快速冷冻固定同步技术，对电刺激后的蟾蜍腓肠肌组织作快速冷冻固定，采用透射电镜对该肌在电刺激后0.8,5.6,8.4ms及静息期的超微结构变化进行对比研究。结果：骨骼肌组织处于静息期时，其肌膜与肌纤维的间隙较宽，受电刺激后0.8ms开始至8.4ms，肌膜与肌细胞间的间隙大大变窄。并发现骨骼肌组织在电刺激后0.8，5.6及8.4ms时肌浆网前端的膜产生两个圆孔，而当骨骼肌处于静息期时肌浆网膜并无此形态结构。结论：当骨骼肌兴奋-收缩偶联发生时，肌膜在产生去极化的同时产生位移，并与肌纤维的间距发生改变；骨骼肌收缩时肌浆网膜出现小孔。     

模数转移技术在骨骼肌肌浆网形状功能研究中的应用

目的：利用模数转换技术进行骨骼肌肌浆网蚋功能形态变化的研究。方法 采用双向工外线探测器、模数转换卡、计算机和Ｒｅｉｃｈｅｒｔ Ｊｕｎｇ ＫＦ－８０快速冷冻仪组成计算机控制的电刺激超低温快速冷冻固定系统,在蟾蜍骨骼肌兴奋－收缩偶联变化的瞬间,实时测定功能变化经历的精确时间。结果：测量得到骨骼肌肌浆网功能的变化的０．８,５．６,８．４ｍｓ时间间隔,并同步获得骨骼肌肌浆网的超微结构形态图像。结论 计算机     

模数转换技术在骨骼肌肌浆网形态功能研究中的应用

目的：利用模数转换技术进行骨骼肌肌浆网确定时间内功能形态变化的研究。方法：采用双向红外线探测器、模数转换卡、计算机和Reichert Jung KF-80快速冷冻仪组成计算机控制的电刺激超低温快速冷冻固定系统,在蟾蜍骨骼肌兴奋-收缩偶联变化的瞬间,实时测定功能变化经历的精确时间。结果：测量得到骨骼肌肌浆网功能变化的0.8,5.6,8.4 ms时间间隔,并同步获得骨骼肌肌浆网的超微结构形态图像。结论：计算机模数转换技术控制电刺激超低温快速固定技术有效地实现了生物学中功能形态瞬时变化的同步研究。     

电刺激对失神经支配骨骼肌超微结构及酶活性的影响

目的：研究电刺激对失神经支配骨骼肌萎缩进程的影响。方法：选用SD大鼠，建立双下肢失神经支配腓肠肌的实验模型，电刺激右下肢腓肠肌，观察肌细胞直径、截面积、超微结构、Na，K-ATP酶和Ca-ATP酶活性变化。结果：电刺激能延缓肌细胞的线粒体、肌质网退变。肌细胞直径及截面积，电刺激侧较对照侧肢体下降速度明显减慢；Na，K-ATP酶活性下降速度，电刺激侧较对照侧慢15．59％和27．38％；Ca-ATP酶活性下降速度，电刺激侧较对照侧慢4．83％和21.64％。结论：电刺激对失神经支配骨骼肌具有保护作用，是延缓肌肉萎缩的有效方法。     

不同剂量复方氯胺酮口服液对鼠重要脏器超微结构的影响

目的：观察大鼠服用不同剂量复方氯胺酮口服液(KMA)后的行为变化和对大鼠脏器超微结构影响，探索应用KMA的安全性。方法：采用神经行为评分和透射电镜技术，检测30只SD大鼠服用不同剂量KMA后的神经行为变化，现察重要脏器超微结构。结果：未用KMA。接受电刺激的大鼠，其肝细胞内的结构发生功能改变。用1—2个剂量KMA的大鼠安静，超微结构元明显变化；服用4—6个剂量后，大鼠深睡，电镜可见肝细胞胞浆内糖原颗粒沉积，胞核出现切迹、线粒体肿胀，嵴紊乱甚至消失。结论：不用KMA，应激刺激导致鼠的机体损伤；预先应用KMA可减低对鼠应激反应；但过量使用KMA可引起肝脏毒性损害。     

大鼠岛叶电刺激点燃癫痫模型超微结构观察

目的:通过对电刺激岛叶点燃癫痫模型岛叶及同侧杏仁核神经元超微结构的观察,探讨在癫痫发作中发作起源的神经元变化特征及其与邻近结构的相互关系.方法:建立岛叶电刺激点燃癫痫发作模型,点燃成功后大鼠断头取脑,观察超微结构变化.结果:岛叶及同侧杏仁核神经元超微结构表现出凋亡特征,但杏仁核病理改变程度较轻.结论:癫痫的超微结构变化...     

源于肺静脉阵发性房颤动物模型研究

目的：本研究以肺静脉快速电刺激模拟肺静脉自发放电，起源于肺静脉的阵发性房颤犬模型。方法：采用S1S1刺激100ms和S1S2程控刺激起搏左右心房和四条肺静脉诱发房颤。结果：S1S1刺激时各部位的房颤总诱发率为29．58％，S1S1刺激时各部位房颤总诱发率为8．27％。结论：快速起搏肺静脉能够造成肺静脉的电重构,进而诱发房早、房速和房颠。     

心身5号对电击应激大鼠心肌超微结构的影响

[目的]探讨应激与冠心病发病的关系及心身5号中药的治疗效果。[方法]将72只大鼠随机分成6组,即正常对照组、单纯刺激组、高脂组、高脂加刺激组、中药高脂刺激组、西药高脂刺激组。分别给予电刺激、高脂饮食、电刺激与高脂饮食相结合、心身5号中药和消心痛,饲养3个月后处死大鼠,观察心肌超微结构变化。[结果]电击应激状态下心肌细胞的超微结构与冠心病的另一常见诱因高脂状态下心肌细胞的超微结构,其变化以高脂加刺激组最为明显,其次为刺激组,再次为高脂组,且刺激因素所引起的改变更明显。采用中药心身5号和消心痛治疗,大鼠心肌细胞超微结构与未治疗组心肌细胞超微结构相比,均有所改善,且中药高脂刺激组优于西药高脂刺激组。[结论]长期处于应激状态可导致冠心病的发生,中药心身5号具有防治冠心病的作用。     

吗啡对伤害性电刺激隐神经诱发大鼠脊髓Fos蛋白表达的影响

目的：观察躯体伤害性电刺激能否引起脊髓神经元Fos蛋白表达的改变,以及吗啡对该变化的影响.方法：采用免疫组化方法研究伤害性电刺激隐神经（saphenous nerve,SN）后脊髓神经元Fos蛋白表达的变化以及皮下注射吗啡对该变化的影响.结果：伤害性电刺激SN后30 min能够引起脊髓神经元Fos蛋白表达的显著增加;皮下注射吗啡可抑制伤害性电刺激SN引起的脊髓神经元Fos蛋白表达的增加.结论：伤害性电刺激SN模拟躯体痛后可致脊髓神经元Fos蛋白表达的显著增加,表明SN传入的伤害性信息能够到达脊髓腰骶段,吗啡抑制了伤害性电刺激SN引起的脊髓神经元Fos蛋白表达的增加,说明此反应具有伤害性感受性质.     

电针对脑缺血再灌注大鼠大脑颞顶叶皮层锥体细胞超微结构的影响

目的：观察大鼠脑缺血再灌注后,电针对其大脑顶叶皮层锥体细胞超微结构的影响。方法：参照Zea Longa MCAO模型制作法,用电镜观察脑缺血再灌注24h后锥体细胞超微结构的变化及电针对其病理改变的影响。结果：脑缺血再灌注24h后发现大脑颞顶叶皮层锥体细胞超微结构出现了凋亡样改变,电针治疗后,上述病理形态学改变明显减轻。结论：提示早期介入电针治疗可以抑制锥体细胞超微结构改变,为电针对脑缺血的防治作用提供了可靠的形态学依据。     

电学治疗在脊髓损伤领域从基础研究转化为临床技术的研究进展

目的 通过总结多种电学方法在脊髓损伤领域中的临床疗效,讨论电学技术从基础研究转化为临床技术的研究进展,为今后临床工作的开展提供转化医学的新思路。方法 分析电学治疗方法的起源及发展过程,讨论并分析4种电学技术转化为脊髓损伤领域治疗技术的临床疗效,这些技术包括:脊髓损伤部位的电刺激技术,瘫痪肢体的功能性电刺激技术,呼吸功能障碍的膈肌起搏技术和排尿功能障碍的神经电调节技术。结果 1)直流电场能够促进未完全断裂的脊髓轴突再生,振荡电场能够双向修复脊髓损伤近端和远端的神经轴突。2)功能性电刺激用于重建瘫痪肢体的运动功能,通过刺激肢体周围神经引起肌肉按照一定顺序收缩产生动作,可以预防多种合并症。3)膈肌起搏技术能够诱发膈肌收缩,保证脊髓损伤膈肌功能障碍患者呼吸时产生自然的负压状态,重建呼吸功能。4)频率为5~20 Hz,脉宽为1~5 ms的电流能够既抑制逼尿肌的过度活动,又改善诸多盆底功能。结论 电流作为一种治疗技术,既有作为生物电的共性,又在不同条件下具备不同的电学特性和临床疗效。今后的脊髓损伤研究中,应加强电学治疗技术与临床技术的结合,来解决更多的临床问题。     

应用BL-310生物机能实验系统测定骨骼肌的绝对不应期

目的建立测定骨骼肌的绝对不应期的实验方法。方法单刺激法确定其腓肠肌最适刺激强度,在最适刺激强度下以双刺激法逐渐缩小波间隔(400ms开始),并记录肌肉收缩的幅度,直到双刺激下肌肉收缩的幅度与单刺激法的相同。结果该方法测定的骨骼肌绝对不应期接近0·8ms。结论该方法简单、直观,可用于本科生及本硕生的机能实验课教学。     

Ultrastructural alterations of right and left ventricular myocytes in tetralogy of Fallot

We examined the ultrastructure of right and left ventricular myocardial biopsies obtained prior to cardiopulmonary bypass in fourteen patients undergoing total correction of tetralogy of Fallot (TOF). Twelve patients were undergoing primary one-stage repair and two patients had had a previous Blalock-Taussig shunt operation. The ages of the patients ranged from 3 to 35 years. In left ventricular (LV) myocytes, the sarcolemma often formed pouches filled with mitochondria and the muscle fibers showed a disoriented arrangement. In addition, the myofibrils showed hypercontraction and the Z-bands were thickened; the degree of the myofibril contraction was more severe than that in right ventricular (RV) myocytes. These ultrastructural findings are similar to those observed in myocytes under hypoxic conditions. The number of lysosomes in LV myocytes, but not in RV myocyte increased in the older patients. While we have not established a causal relationship between the ultrastructural findings and clinical features in our cases, our observations are consistent with the possibility that early total correction of TOF may be required to prevent the development of hypoxic changes and degeneration of heart muscle.     

Myocardial contraction maps using tissue Doppler acceleration imaging

Objective To evaluate the tissue Doppler acceleration imaging (TDAI) data which can be used to determine the intramural site of origin of myocardial contraction in response to electrical stimulation. Methods Six open-chest pigs with left ventricle (LV) pacing were evaluated with TDAI. An epicardial surface scanning method was used to collect short-axis views of the left ventricle. The electrode was implanted from the epicardium through the anterior free wall to an intramural position. Results During pacing, the intramural onset of myocardial acceleration occurred within 33 ms after electrical stimulation and always surrounded the embedded subendocardial end of the pacing needle. The observed short-axis diameter of the area of initial myocardial acceleration ranged from 2.9 mm to 5.0 mm (4.2±0.9 mm, n=6). The onset of myocardial acceleration allowed appreciation of the initial intramural myocardial contraction. The spatial size and acceleration magnitude of the initial myocardial acceleration distribution were irregular. Conclusion Two-dimensional myocardial acceleration mapping can show the intramural site of origin of myocardial contraction in response to paced electrical stimulation. The location of myocardial acceleration conformed to the site of initial electrical stimulation. The delay to the earliest regional myocardial contraction, 33 ms after paced electrical stimulation, was related to the frame rate of image acquisition.     

用静息张力表征离体蟾蜍腓肠肌等长收缩能力

目的 考察用静息张力表征离体蟾蜍腓肠肌等长收缩能力的有效性.方法 SOD抑制剂和维生素C联合作用蟾蜍腓肠肌,记录电刺激(12V DC,2 ms波宽,2 s间隔)下等长收缩张力变化,单指数函数加权拟合90%峰张力后的松弛过程测定松弛速度和静息张力表征收缩能力.结果 收缩1.0min后对照静息张力在7.0min内单调下降而药物处理后静息张力先降后升,7.0min后处理组静息张力相对初始值的增加值显著高于对照组.同时,对照松弛速度大多单调下降.药物处理后松弛速度多数先升后降,且10.0min内其松弛速度总低于相同时刻的对照组.结论 静息张力可反映肌肉收缩能力.     

^3H-TdR标记人骨髓间充质干细胞移植治疗mdx鼠的实验研究

OBJECTIVE: To investigate the feasibility of using human bone marrow-derived mesenchymal stem cells (hBM- MSCs) for repairing the skeletal muscle sarcolemma lesions in mdx mice and characterize the distribution of the transplanted hBM-MSCs. METHODS: Eighteen 8- to 10-week-old immunosuppressed mdx mice received transplantation with 1x10(7) of hBM-MSCs (the fifth passage) with 3H-thymidine (3H-TdR) labeling by injection of the cells into the tail vein. The mice were killed at 24 h, 48 h, 2 weeks, and 1, 2 and 4 months after the transplantation, respectively, to measure the radioactivity in the tissues and organs. Dystrophin expression on the sarcolemma was detected by immunofluorescence analysis. RESULTS: One month after transplantation, the mice with cell transplantation showed greater radioactivity in most of the tissues and organs than the control mice, especially in the bone marrow, liver and spleen. The radioactivity was then gradually lowered but in the skeletal muscle, the radioactivity increased progressively since 2 weeks after transplantation, reaching the peak of 27.65+/-3.53 Bq/mg at 1 month. Compared with that in the control mice, the radioactivity in the bone marrow and skeletal muscle was persistently higher in mice with cell transplantation 1 month after transplantation. No dystrophin-positive cells were found in the mdx mice at 2 weeks but detected at 1 month. The percentage of dystrophin-positive fibers in each section ranged from a 6.6% (1 month) to 8.9% (4 months). CONCLUSIONS: hBM-MSCs engrafted in immunosuppressed mdx mice may differentiate into skeletal muscle cells to repair the pathological lesion of the skeletal muscle sarcolemma. The hBM-MSCs reside mainly in the bone marrow, liver and spleen in the early stage following transplantation, homing into the bone marrow and skeletal muscle later.     

高频电刺激对神经动作电位阻断作用的研究

目的:研究了高频交流电信号对神经动作电位的阻断作用?方法:采用离体的蟾蜍坐骨神经进行实验,对神经施加高频的正弦信号,观察动作电位的幅度和肌肉的状态来确定阻断的效果?结果:在一定频率下,高频正弦信号能完全阻断神经传导,阻断的阈值随阻断信号频率的增加而增加?给肌肉一小段时间高于阻断信号频率的刺激,肌肉对高频信号的强直效应会消失,之后肌肉的收缩也能被高频信号阻断?结论:高频电刺激对神经动作电位阻断作用为临床局麻?镇痛和解痉探索提供了新的依据?     

电刺激诱导前庭电位

OBJECTIVE: To identify the evoked potentials (VsEPs) by electrical stimulation were from vestibule. METHODS: The stimulating electrode was set on the round window of guinea pig. Constant current shocks of 0.05 ms (0.25-1.2 mA) were used to evoke VsEPs by means of vertex-pinna skin electrodes. RESULTS: These potentials were short latencies of (0.973 +/- 0.086) ms, (1.618 +/- 0.176) ms and (2.416 +/- 0.274) ms respectively, which reflected true potentials and were not from electrical stimulus artefacts. It was pure vestibular origin. As being masked with a continuous white noise (120 dB SPL) or removed ipsilateral auditory nerve, and even after facial neurectomy, waves were still existing, but disapeared after selective vestibular neurectomy. The twitching responses in the facial region had never been detected during the whole test. These potentials were bioelectric responses in the vestibular sensory pathway, characterized by threshold saturation, adaptability of excitation, dependent on intact vestibular nerve. CONCLUSIONS: We have set up animal model of recording VsEPs evoked by electrical stimulation on the round window of guinea pigs.