骨骼肌在重复电刺激下生理行为研究

为得到肌张力特性与其电生理特性间的实验关系,本文在0.1 ms的波宽下,用不同频率的三种强度的重复脉冲电流,对家兔的胫神经进行电刺激,用生物材料试验机和肌电仪记录其腓肠肌的肌张力和复合动作电位.结果表明,肌张力与脉冲电流频率呈较好的正相关关系,而肌张力随刺激电流强度的增加似乎并不明显.     

刺激脉宽对脉宽阈值积的影响

目的研究脉宽阈值积与刺激脉宽之间的关系,深化对电刺激听神经反应的认识。方法首先,根据已有的单根听神经刺激脉宽与阈值之间的表达式和电诱发复合动作电位(electrically evoked compound action potential,ECAP)刺激脉宽与阈值之间的表达式,推导出脉宽阈值积与刺激脉宽之间成线性关系。其次,利用Shepherd发布的实验数据与豚鼠实验数据进行研究,发现脉宽阈值积与脉宽的关系不能用简单的线性关系进行解释,其曲线中存在极值点。结果研究结果表明,由于实验结果中脉宽阈值积与刺激脉宽之间呈现较强的非线性特性,因此由刺激脉宽与阈值之间的关系式推导出的脉宽阈值积与脉宽之间的关系式与实验结果不符。结论需进一步研究刺激脉宽对听神经反应的影响,给出符合实验结果的表达式。     

大鼠下颌运动肌肉在电刺激下的响应

本实验对15只8周龄Wistar雄性大鼠深度麻醉后在自制的电刺激-力测试装置上测试并记录了大鼠嚼肌，二腹肌前腹，翼外肌在电刺激下的时间-收缩力关系曲线，得出了它们在电刺激下主动收缩的本构关系，在单一刺激下三种肌群的主动收缩可表达为F=A（e^-αt-e^-βt），拟和出了三种肌群常数A，α，β，当刺激频率大于等于3Hz时，肌群的主动收缩可表达为F=Ce^γ/t Dsinωt，拟和出了三种肌群的常数C，D，γ。电刺激频率大于30Hz。肌肉产生强直收缩。     

心室肌细胞电生理-力学复合模型在心力衰竭中的仿真研究

目的:研究心力衰竭情况下快速收缩心肌和慢速收缩心肌力学特性的变化及其对心脏电生理的影响。方法:基于心衰心肌生理实验数据建立心室肌细胞电生理-力学复合模型,仿真对比正常和心衰肌细胞内钙离子浓度的变化,进而研究其对细胞收缩力学特性的影响。结果:仿真显示与正常细胞相比,心衰肌细胞电生理特性的变化导致细胞内钙离子浓度降低。进而与肌钙蛋白的钙结合亚单位(TnC)结合的钙离子比正常时大大减小,直接导致细胞收缩力减小。结论:心衰时心室肌细胞的收缩力减小,肌细胞中正常的电力学反馈作用减弱,增大了心室壁细胞动作电位的透壁梯度,从而可能诱发心律失常。仿真结果与文献报道的实验发现一致,将来在组织和器官层次上的心脏建模工作可以整合单细胞的电力学模型,有助于深入研究心力衰竭的病理机制。     

刺激脉宽对电诱发复合动作电位阈值的影响

本文研究了电诱发复合动作电位(ECAP)的刺激脉宽与阈值之间的关系。首先通过对已有实验结果的拟合得到了单根听神经动作电位的刺激脉宽和阈值关系式中的基强度和时基;而后基于ECAP的机制提出了一个描述其刺激脉宽与阈值之间关系的数学表达式;进一步通过豚鼠实验得到了表达式的参数并验证了表达式的适用性。研究结果表明,ECAP与单根听神经动作电位对比,二者的刺激脉宽与阈值之间存在相似的函数关系,但前者的基强度比后者小一个数量级,而时基比较接近。这些结果对于临床的ECAP测量与深入研究人工耳蜗的语音处理策略具有一定的指导意义。     

局部肌疲劳过程与表面肌电信号分维值变化关系的研究

利用肱二头肌在不同收缩力水平上持续恒力收缩时采集的表面肌电信号，研究局部肌疲劳过程中肌电信号的分形维变化规律。结果表明，随着疲劳程度的加深，表面肌电信号的分维值在不同收缩力水平上均呈下降趋势，与中值频率的下降趋势相一致。     

基于运动神经元激励的表面肌电信号仿真研究

以单纤维动作电位的仿真为基础,结合运动单位的生理结构特点,利用神经肌肉系统激励与运动单位募集、发放间的近似关系,建立一个比较符合生理学特性的表面肌电(sEMG)信号模型,以仿真不同激励情况的sEMG信号.仿真实验发现,肌纤维与电极间距离的增加将使皮肤表面检测到的动作电位峰值下降;随着激励水平的提高,与仿真sEMG信号相关的收缩力逐渐增大,且仿真sEMG信号的时域波形以及频谱也与真实sEMG信号相似.实验结果表明仿真sEMG信号能够较有效地逼近真实sEMG信号,可用于运动单位发放检测等相关研究领域.     

心衰情况下心室肌细胞透壁电生理特异性的仿真研究

仿真研究心衰情况下心室肌细胞离子通道的变异对细胞电生理和透壁特异性的影响机制,以及心力衰竭下心室透壁复极化的改变与心律失常之间的关系.基于反映正常和衰竭人体心肌细胞离子通道透壁特异性的实验数据,建立离子通道水平的心肌细胞电生理数学模型,模拟仿真研究心衰情况下心室肌心外膜、中层、心内膜细胞电生理透壁特异性的变化.结果:仿真研究发现心衰导致透壁心室肌细胞电生理重建,透壁细胞的动作电位持续时间都有明显的延长,改变了动作电位的透壁特异性,进而减小了动作电位的透壁梯度,同时衰竭心脏中快步率时动作电位的比率依赖性会增加.模型研究认为这可能与心衰细胞中离子电流ICaL和Iks的透壁特异性的电生理重构有关.所发展的细胞模型不仅可以辅助细胞电生理实验分析研究,同时也是今后仿真研究心衰情况下心肌细胞兴奋-收缩耦联力学特性的重要基础.     

不同刺激参数对SD大鼠肌肉收缩的影响

目的研究不同电刺激参数对SD大鼠肌肉收缩的影响,为临床应用电刺激治疗周围神经损伤提供参考。方法采用低频脉冲发射器对SD大鼠的颈项部肌群进行局部电刺激。刺激时改变频率、脉宽、电压及占空比等参数,观察参数变化对肌肉收缩及动物行为的影响。同时记录受刺激肌肉的肌电图。结果 8只SD大鼠在10~60Hz的频率范围内,随频率增加肌肉收缩率逐步增强。肌电图结果显示在刺激频率不变的前提下,随脉宽的增加（50~200μs）,肌电幅值显著上升,且肌电幅值的变化与大鼠行为改变成正相关。结论不同的刺激参数可影响肌肉的收缩状态与强度,选择合适的参数可使失神经支配肌肉发生有节律地收缩,防止肌萎缩,并有助于建立局部肌痉挛动物模型。     

腹直肌与腹白线关系的形态学及生理学研究

本文在70例童尸上观察腹直肌附着于白线的情况;并通过2只猕猴的生理实验,探讨腹直肌和锥状肌对白线张力和腹腔内压的影响。实验结果如下:(1)94.3%腹直肌以肌纤维及腱纤维附着于白线下段。(2)腹直肌收缩,白线张力降低;而锥状肌收缩则白线张力升高(P<0.001);两者同步收缩则白线张力不呈任何改变(P<0.05)。(3)腹直肌和锥状肌收缩对腹腔内压无明显影响。但是,用强的电刺激使锥状肌强烈短缩时,腹腔内压略有升高;而腹直肌强烈收缩时,腹腔内压反而呈下降趋势。以,上结果表明该两块肌肉对白线张力和腹腔内压似有拮抗作用。最后,作者认为白线张力与白线疝之间的关系留待进一步探讨。     

Measurement of contractile and electrical properties of single human thenar motor units in response to intraneural motor-axon stimulation

1. A method is described for measuring contractile properties of single human motor units. Conventional human microneurographic techniques were adapted to stimulate individual motor axons in the median nerve, with the use of negative current pulses and a tungsten microelectrode, while recording motor-unit electromyographic activity (EMG) and isometric force responses from the thenar muscles. 2. EMG signals were recorded from both proximal and distal thenar muscle surfaces. Force was recorded in two directions (thumb flexion and abduction). This allowed calculation of the direction and magnitude of resultant force exerted by each unit. 3. Data accepted as originating from a single unit satisfied all the traditional "all-or-none" criteria. Additional criteria also required the following: 1) a wide safety margin between the threshold for unit activation and the current intensity needed to elicit responses from other units; 2) that the characteristic direction in which each unit generated force did not change during the recording period; and 3) whenever F-responses were encountered, the second EMG waveform was identical to the first--a highly improbable event if more than one unit had been excited. 4. Respiration and blood pressure waves introduced baseline fluctuations that distorted the force measurements. These fluctuations were minimized by synchronizing stimuli to the pulse pressure cycle and resetting the baseline electronically just before stimulus onset. 5. Combining motor-axon stimulation at a site remote from the muscle with electronic resetting of the force baseline and delivery of stimuli at fixed intervals after the pulse pressure waves allowed the full time course of human motor-unit twitch and tetanic force and EMG signals to be recorded accurately without signal averaging.     

Neural compensation for fatigue-induced changes in muscle stiffness during perturbations of elbow angle in human.

1. The contribution to muscle force regulation provided by reflex pathways was studied in the elbow flexor muscles of seven normal human subjects, with the use of voluntary fatigue to induce a deficit in the force-generating capability of these muscles. To estimate the changes in the mechanical state of the muscle and the compensatory actions taken by reflex pathways to minimize the impact of fatigue, stochastic and "step" angular perturbations were applied to the joint, and the resulting joint stiffness and electromyographic (EMG) responses were compared before and after fatigue. 2. The magnitude of contractile fatigue, induced by repeatedly lifting a weight via a pulley system, was quantified by comparing the slope of the isometric torque-EMG relationship before and after fatigue. The exercise routine was quite effective in producing severe and long-lasting fatigue, with average percentage changes in the isometric torque-EMG slope of 210-306% for biceps and 129-205% for brachioradialis, depending on the point in time examined. 3. The torque response to a rapid step stretch of the elbow joint was quite similar before and after fatigue for the time interval before reflex action (less than 20 ms after stretch onset), suggesting that intrinsic muscle stiffness for a given mean torque level was not changed by fatigue. The steady-state torque level attained after completion of the stretch was always decreased after fatigue, indicating a decrease in the reflex component of joint stiffness, but this decrease was small compared with the change in the isometric torque-EMG relationship and was accompanied by a significantly larger incremental EMG response after fatigue. This increase in incremental EMG after fatigue was found to be of reflex origin, with activation-related reflex gain changes apparently playing a significant role only at low contraction levels. 4. Torque and angle responses recorded during stochastic perturbations were used to identify elbow joint compliance impulse responses. A second-order mechanical model was fit to each impulse response, and the parameters representing joint inertia, elastic stiffness, and viscous stiffness were used to summarize changes in joint mechanical properties as the mean contraction level was varied. For a perturbation with a relatively wide bandwidth (0-25 Hz), fatigue had little or no effect on the form of the compliance impulse response, apparently because the stimulus disabled reflex force generation in elbow flexor muscles, whereas a perturbation with a more restricted bandwidth (0-10 Hz) demonstrated consistent decreases in joint stiffness after fatigue.(ABSTRACT TRUNCATED AT 400 WORDS)     

Cardiac cell membrane repolarization is required for onset of mechanical restitution in papillary muscle

In 10 voltage clamped ferret papillary muscles at 37 degrees C (single sucrose gap), the duration of resting (diastolic, holding) potential was varied in order to define the mechanical restitution process. Following a period of steady state voltage clamp depolarizations to +20 mV, a single test depolarization clamp of 200 or 500 ms duration was introduced. Then, the following period at resting (holding) potential was varied. All the mechanical restitution curves for the 500 ms clamps were delayed by 300 ms compared with the 200 ms clamps. When mechanical restitution was plotted as the relationship between contractile force and test electrical diastolic interval, all processes started from zero interval (i.e. the time of repolarization). Variation of diastolic holding potential between -70 mV and -40 mV did not affect the starting time, but the final force values at full restitution were approached faster and were higher for -70 mV than for -40 mV. There was an inverse relationship between force and second inward current during mechanical restitution after an initial phase of restitution of current. Mechanical restitution is postulated to be due to passage of contractile calcium with time from an uptake to a release compartment within the sarcoplasmic reticulum. Thus the rise of contractile force with increasing test cycle duration should have been independent of whether a 200 or 500 ms depolarization was used. In order to accommodate the discrepancy, we postulate either that (1) sarcoplasmic reticulum calcium release channels require sarcolemmal repolarization to begin to be reactivated or (2) that trigger calcium (calcium induced calcium release from the sarcoplasmic reticulum) is derived from the sarcolemma.     

Relation between the motor units recruitment threshold and their potentials propagation velocity at isometric activity.

The relationship between the propagation velocity of the excitation along the muscle fibers of the motor units (MUs) and their threshold of recruitment at different level of isometric voluntary contraction was investigated. The threshold of recruitment was measured by the value of the muscle force, expressed in percents from the maximal voluntary contraction (MVC) at which the first impulse of the MU appeared. A wire subcutaneous branched electrode was used to select the potentials from a single MU. The selected in this way MU impulses were used as a trigger to average two electromyographic (EMG) signals picked up by means of two monopolar surface electrodes with small leading-off areas mounted on a common plate at a distance of 10 mm from one another. The propagation velocity of the extraterritorial potentials of the MUs increased non-linearly with the increase of the recruitment threshold. The relationship was fitted as V = square root of a+b.theta, where v is the propagation velocity, theta is the threshold of recruitment and a and b are constants. The consideration of the velocity of propagation as a "size principle parameter" was discussed and the limitations of the latter are pointed out.     

Potentiation of the contraction following a prolonged depolarization in isolated ferret myocardium

The contractile force was studied in ferret papillary muscles during voltage clamp depolarizations, using the single sucrose gap method. Prolongation of a test depolarization within a train produced potentiation of the following contraction. The effects of varied duration and membrane potential of the test depolarization upon the potentiated force of the following beat were studied. We assumed that force of a beat was an index of calcium entry on the previous depolarization. The relationship between the peak contractile force of the following potentiated beat and the systolic membrane potential of the test depolarization revealed an equilibrium around ?18 mV. This was manifest after l00 ms of no effect. Positive potentials caused potentiation of force of the following beat; negative potentials caused suppression of force of the following beat. Calcium entry, if carried by an electrogenic exchange mechanism, would be revealed as a membrane current developing after l00 ms. Membrane current at these times was always outward. When the duration of the test depolarization was prolonged, outward current prior to repolarisation progressively increased. When the duration of the test depolarization was held constant, outward current was varied by variation in membrane potential. Force of the following beat was proportional to the test clamp membrane potential. The potentiation of the contraction following a prolonged depolarization was abolished by substituting 75% of the sodium in the perfusion medium with lithium. These results are compatible with the hypothesis that potentiation of force following a prolonged depolarization is derived from calcium entry into myocardial cells by reversed sodium-calcium exchange.     

Myocardial contractile force as a function of coronary blood flow.

The contractile force of the deep and superficial myocardial fibers was examined in the open-chest anesthetized dog as a function of coronary blood flow (CBF). When 1) dogs that failed to demonstrate coronary autoregulation were eliminated from the data base and 2) CBF and contractile force data were both normalized as a percent of their vaues when perfusion was from aortic pressure (autoperfusion), the relationship between them became very reproducible. Contractile force was highly dependent on the flow rate when the CBF was below that chosen by autoregulation (the rate during autoperfusion). Conversely contractile force was relatively independent of flow at higher CBF. The contractile force-CBF curve thus was found to break precisely at the autoperfused CBF. When myocardial metabolism was elevated by paired electrical stimulation this relationship was unchanged. It was concluded that coronary blood flow is tightly regulated to match metabolic needs over a range of metabolic rates.     

基于小波包变换的肌电信号去噪研究

肌电信号的检测与分析对临床诊断以及康复医学具有重要意义.肌电信号的特点是强噪声背景下的生物信号,对肌电信号的检测和提取具有一定的难度.我们针对肌电信号的特点以及与噪声的关系,采用小波包变换的方法进行去噪研究.通过仿真以及在自主开发的便携肌电诱发电位测量系统中的应用,说明该方法对肌电信号的去噪是有效的.     

Motor unit properties after operant conditioning of rat H-reflex

Operant conditioning of the H-reflex produces plasticity at several sites in the spinal cord, including the motoneuron. This study assessed whether this spinal cord plasticity is accompanied by changes in motor unit contractile properties. Thirty-one adult male Sprague-Dawley rats implanted for chronic recording of triceps surae electromyographic activity and H-reflex elicitation were exposed for at least 40 days to HRup or HRdown training, in which reward occurred when the H-reflex was greater than (12 HRup rats) or less than (12 HRdown rats) a criterion value, or continued under the control mode in which the H-reflex was simply measured (7 HRcon rats). At the end of H-reflex data collection, rats were anesthetized and the contractile properties of 797 single triceps surae motor units activated by intraaxonal (or intramyelin) current injection were determined. Motor units were classified as S, FR, Fint, or FF on the basis of sag and fatigue properties. Maximum tetanic force and twitch contraction time were also measured. HRdown rats exhibited a significant increase in the fatigue index of fast-twitch motor units. This resulted in a significant decrease in the percentage of Fint motor units and a significant increase in that of FR motor units. HRup conditioning had no effect on fatigue index. Neither HRup nor HRdown conditioning affected maximum tetanic force or twitch contraction time. These data are consistent with the hypothesis that conditioning mode-specific change in motoneuron firing patterns causes activity-dependent change in muscle properties.     

The Effects of Fatigue and Task Repetition on the Surface Electromyographic Signal

The effects of fatigue and repetition of the task on the surface electromyographic signal were examined during 4 sessions using an isometric motor control task. The muscle chosen for this study was one of the main ankle dorsiflexors (m. tibialis anterior). The electromyographic output and a functional (force) output of this muscle were recorded during two conditions: a SHORT-F condition in which the effect of task repetition on the relationship between force and IEMG was studied, and a LONG-F condition in which the effect of fatigue was studied. The results indicated that repetition of the task resulted in a significant increase in the ratio between the electromyographic and functional output of the m. tibialis anterior, indicating an increase in efficiency across the 4 sessions. Fatigue on the other hand resulted in a significant decrease in the ratio between the electromyographic and functional output of the m. tibialis anterior, indicating a decrease in efficiency. Fatigue also resulted in a significant and rapid increase in the electromyographic activity. The implications of these results for the therapeutic use of the electromyographic signal were discussed.