Immunohistochemical distribution of serum proteins in living mouse heart with In vivo cryotechnique

In vivo cryotechnique (IVCT), which immediately cryofixes target organs in situ, was used to clarify the morphological features of beating heart tissue of living mice. IVCT was performed for diastolic heart tissue under the condition of monitoring with electrocardiogram (ECG). Other mouse hearts were prepared with conventional perfusion-fixation (PF-DH) or immersion-fixation followed by dehydration (IM-DH), and quick-freezing of resected heart tissues (FQF). Immunolocalizations of albumin, immunoglobulin G1 (IgG1), intravenously injected bovine serum albumin (BSA), and connexin 43 were examined after different intervals of BSA injection. In the case of IVCT, the exact stop time of beating mouse hearts was recorded by ECG, and open blood vessels with flowing erythrocytes were observed with less artificial tissue shrinkage than with conventional preparation methods. Both albumin and BSA were well preserved in intercalated discs and t-tubules of cardiomyocytes in addition to blood vessels and interstitial matrices. IgG1 was immunolocalized in interstitial matrices of heart tissues in addition to their blood vessels. At 4 hr after BSA injection, it was immunolocalized in the intercalated discs of cardiomyocytes and lost later at 8 hr. IVCT should prove to be more useful for the morphofunctional examination of dynamically changing heart tissue than conventional preparation methods.     

Immunolocalization of phospho-Arg-directed protein kinase-substrate in hypoxic kidneys using in vivo cryotechnique

Protein kinases (PKs) phosphorylate proteins at active regions for signal transduction. In this study, normal and hypoxic mouse kidneys were prepared using an “in vivo cryotechnique” (IVCT) and examined immunohistochemically with specific antibodies against phospho-(Ser/Thr) PKA/C substrate (P-PK-S) and phospho-(Ser/Thr) Akt substrate (P-Akt-S) to capture their time-dependent regulation in vivo. Left kidneys were cryofixed with IVCT under normal blood circulation and after varying hypoxic intervals, followed by freeze-substitution with acetone containing paraformaldehyde. Deparaffinized sections were immunostained for P-PK-S, Na⁺/HCO₃ ⁻ cotransporter NBC1, and a membrane skeletal protein, 4.1B. The P-PK-S was diffusely immunolocalized in the cytoplasm of the proximal tubules in normal kidneys, whereas NBC1 and 4.1B were detected at the basal striations of S1 and S2 segments of the proximal tubule. After 10 or 30 s hypoxia, P-PK-S was still immunolocalized in the cytoplasm of kidneys, but it was detected at the basal striations after 1 or 2 min hypoxia. The immunolocalization of P-Akt-S was the same as P-PK-S in the normal and hypoxic kidneys. Immunoblotting analyses of the kidney tissues under normal or hypoxic condition clearly identified the same 40-kDa bands. The IVCT is useful for time-dependent analysis of the immunodistribution of P-PK-S and P-Akt-S.     

Fatigue and posttetanic potentiation in single muscle fibers of the frog.

At 15 degrees C, direct stimulation of frog single muscle fibers at a frequency of 20 Hz produced a tetanic tension that remained constant for 20 s and then declined. The decline was reversed during 1-s interruptions of the stimulus train in the first 50 s of stimulation, but not with longer stimulation. Posttetanic potentiation (PTP), characterized by prolonged twitch relaxation and contraction times and elevation of twitch height, remained for 10-40 min after a 10-s tetanus and for at least 90 min after a 50- to 150-s tetanus. Posttetanic fatigue appeared only after at least 50s of tetanic stimulation. Fatigue was manifested invariably by a reduction in the height of a 200-ms tetanic contraction and usually by a reduction in twitch height after PTP. Fatigued fibers recovered normal contractile responses in 40-160 min. Hypertonic solutions, which blocked contraction in response to tetanic stimulation, prevented posttetanic fatigue but not PTP. The observations suggest that fatigue is caused by a failure in excitation-contraction coupling, probably in relation to consumption of metabolic substrates. Even 10-s tetani which do not produce fatigue can affect muscle contractile function for up to 40 min.     

Comparison of sarcomere alterations after muscle contraction and tension loading in the rat soleus muscle

Muscle contraction induced by 30 min of continuous nerve stimulation at 50 Hz resulted in sarcomere changes of the soleus muscle in the rat in our previous study. To further investigate the cause of sarcomere alterations, the sciatic nerve was electrically stimulated intermittently for 30 min. Nerve stimulation was also conducted after cutting the tendons of the soleus, gastrocnemius and plantaris muscles in order to prevent imposing tension on these muscles as a result to their own contractions. In addition, the muscles were pulled by weights via their tendons to load high tension for 30 min without nerve stimulation. Sarcomere alterations immediately after treatments were quantified by electron microscopy. The percentages of aberrant sarcomere areas of the soleus muscle were 25.7 ± 16.4% (mean ± SD) in the group of intermittent nerve stimulation with intact tendons and 21.1 ± 35.4% in the group of tenotomy and continuous nerve stimulation, which were roughly equal to or more severe than the group of continuous nerve stimulation with intact tendons (18.8 ± 15.8%) in our previous study. Sarcomere alterations consisted mainly of hypercontraction in these groups. Almost all sarcomere changes in the tension-loaded (pulled) soleus muscles were scarce myofilaments (1.7 ± 1.0% by 600 g; 4.5 ± 2.9% by 1200 g), and hypercontraction was not observed. These findings indicate that neither high tension nor a decrease of muscle blood flow during continuous contraction seems to be the primary cause of sarcomere alterations in the present study. There are probably other causes that produce aberrant sarcomeres.     

Fixation of spinal reflex alterations in spinal rats by sensory nerve stimulation

Two preparations in which sensory nerve stimulation was used to obtain peripherally induced spinal fixation in spinal rats are described. In the first preparation, proportionally greater amounts of persisting poststimulation flexor muscle contraction, as measured by a force displacement transducer, were produced as stimulation time was increased from 10 min to 40 min. In the second preparation, sensory nerve stimulation was delivered, and evoked whole-nerve responses were recorded from a flexor motor nerve. Results indicated that 30 min or more of sensory nerve stimulation produced increases in response amplitude and area that persisted for at least 30 min after stimulation.     

Localized muscle pain causes prolonged recovery after fatiguing isometric contractions

The purpose of this study was to investigate the force and electromyographic (EMG) signal recorded from the muscles immediately after a sustained fatiguing contraction with or without muscle pain. Ten subjects performed sustained dorsi- and plantarflexions at two contraction levels (50 and 80% of maximum voluntary contraction) until exhaustion with or without muscle pain induced by injection of 6% hypertonic saline in one of the torque producing muscles. The muscle pain intensity was scored on a visual analogue scale (VAS, 0–10 cm). The root mean square (RMS) of the surface EMG signal from plantarflexors and dorsiflexors were estimated during maximum voluntary contractions (MVC) and ramp contractions before and after the fatiguing task at 0, 5, 10 and 15 min during the recovery phase. VAS scores immediately after the contractions with hypertonic saline (on average 3.2 ± 1.1 cm) progressively decreased during recovery and no pain was experienced 15 min after the contraction. After the painful contraction the RMS-EMG during MVC was on average decreased (23.4 ± 7.4%) compared to the non-painful condition both in muscles where pain was previously induced and in non-painful synergists. During recovery, the slope of the torque–EMG curve during ramp contraction was significantly decreased (28.4 ± 8.1%) after the painful contraction compared to the control contraction both for the muscle previously exposed to pain and also the other active synergists. The decreased EMG during recovery after painful contractions compared with control was not accompanied by significant reductions in force during MVC indicating a change in the strategy for motor unit recruitment. This study shows that localized muscle pain inhibits muscle activation and increases the effects of fatigue on EMG recovery curves both for painful and non-painful synergists probably by a central effect. These effects can modify the normal patterns of synergistic activation and can also generate overload problems in muscle pain patients if compensatory motor control strategies are applied.     

Blockade of the pressor response to muscle ischemia by sensory nerve block in man.

Differential nerve block from peridural anesthesia was used to determine a) if the pressor response to muscle ischemia in man is caused by stimulation of small sensory nerve fibers and b) if these fibers contribute to cardiovascular-respiratory responses during dynamic exercise. Four men exercised at 50-100 W for 5 min. Muscle ischemia and a sustained pressor response were produced by total circulatory occlusion of both legs beginning 30 s before the end of exercise and continuing for 3 min postexercise. During regression of full motor and sensory block, motor strength recovered while sensory block continued; the pressor response was blocked as long as sensory anesthesia persisted (two subjects). During blockade of the pressor response, cardiovascular-respiratory responses to exercise gradually returned from augmented to normal (preblock) levels. Sensory blockade was incomplete in two subjects and the pressor response was not fully blocked. We conclude that stimulation of small sensory fibers during ischemia elicits the pressor response, but that these fibers appear not to contribute to cardiovascular-respiratory responses during mild dynamic exercise with adequate blood flow.     

Phosphorylase activity in needle biopsy samples--factors influencing transformation

Phosphorylase was determined in biopsy samples frozen immediately or after a delay of 10 s to 6 min. Muscle biopsies were performed at rest without and with propranolol, or adrenalin infusion and after electrical stimulation. The phosphorylase a fraction was 36% (28-44) in resting samples frozen immediately and 12% (12-13) after 10 s delay and remained at the same level when the freezing was further delayed (up to 6 min). It is suggested that an increase in [Ca2+] in the cytoplasm due to the insertion of the needle in muscle or cutting of tissue membranes may cause transformation of phosphorylase from b to a form, a transformation which is restored when Ca2+ is pumped back during the delay. Also the increased phosphorylase a fraction observed in biopsy samples obtained during adrenalin infusion reverted partially back when freezing was delayed for 10 s and 30 s, respectively. In muscle samples taken during contraction the mole fraction of phosphorylase a decreased from 53 to 12% when freezing was delayed for 10 s. The lowest value of the phosphorylase a mole fraction was observed in resting muscle after beta-blockade when the tissue samples were frozen 10 s after sampling and corresponded to 10% of the total phosphorylase. It is concluded that both muscle sampling and circulating adrenalin will increase phosphorylase a fraction in resting muscle and probably also augment the effect of adrenalin infusion.     

Sustained muscle contractions maintained by autonomous neuronal activity within the human spinal cord

It is well known that muscle contraction can be easily evoked in the human soleus muscle by applying single-pulse electrical stimulation to the tibial nerve at the popliteal fossa. We herein reveal the unexpected phenomenon of muscle contractions that can be observed when train stimulation is used instead. We found, in 11 human subjects, that transient electrical train stimulation (1-ms pulses, 50 Hz, 2 s) was able to induce sustained muscle contractions in the soleus muscle that outlasted the stimulation period for greater than 1 min. Subjects were unaware of their own muscle activity, suggesting that this is an involuntary muscle contraction. In fact, the excitability of the primary motor cortex (M1) with the sustained muscle contractions evaluated by transcranial magnetic stimulation was lower than the excitability with voluntary muscle contractions even when both muscle contraction levels were matched. This finding indicates that M1 was less involved in maintaining the muscle contractions. Furthermore, the muscle contractions did not come from spontaneous activity of muscle fibers or from reverberating activity within closed neuronal circuits involving motoneurons. These conclusions were made based on the respective evidence: 1) the electromyographic activity was inhibited by stimulation of the common peroneal nerve that has inhibitory connections to the soleus motoneuron pool and 2) it was not abolished after stopping the reverberation (if any) for approximately 100 ms by inducing the silent period that followed an H-reflex. These findings indicate that the sustained muscle contractions induced in this study are most likely to be maintained by autonomous activity of motoneurons and/or interneurons within the human spinal cord.     

Submaximal-exercise-induced impairment of human muscle to develop and maintain force at low frequencies of electrical stimulation

The aim of this study was to test the hypothesis that low intensity exercise-induced low frequency fatigue is caused by failure of excitation-contraction coupling. Changes in knee extension torque at 5, 10, 15, 20 and 50 Hz electrical stimulation of quadriceps muscle in ten healthy, young, male subjects were recorded during 20-min voluntary exercise followed by 60-min recovery. In seven of the ten subjects, changes in torque during 3 min of 10-Hz stimulation were recorded 2 min and 20 min after 20 min voluntary exercise. Exercise was performed at 30% of maximal voluntary contraction with a contraction plus relaxation period of 6 plus 4 s. Torque at 5, 10, 15, 20 and 50-Hz stimulation at the end of exercise was reduced to mean 91.0 (SEM 5.4)%, 68.7 (SEM 5.4)%, 67.2 (SEM 3.9)%, 66.5 (SEM 4.5)% and 74.7 (SEM 4.3)% of control values, respectively. During the first 30 s of the 3 min 10-Hz stimulation, torque was reduced in exercised muscle and increased in nonfatigued muscle. The reduction in torque was more marked 20 min after exercise than after 2 min. In conclusion, the pattern of depression and recovery of muscle force observed was in agreement with the hypothesis that the main cause of low intensity exercise-induced low frequency fatigue is an impairment of excitation-contraction coupling.     

The pudendal nerve-evoked response in axial muscle

Summary In 39 Urethane-anesthetized rats we have recorded the afferent volley in the dorsal roots and the electrical activity of the lateral longissimus muscle and its motor nerves during electrical stimulation of a cutaneous branch of the pudendal nerve. Male and female rats were used; the females were ovariectomized and either pretreated with estradiol or left without hormonal treatment. Conduction velocities in the pudendal nerve were 54 m/s for the largest Abeta fibers and averaged 10 m/s for A-delta fibers. Excitation of pudendal nerve afferents strongly potentiated the firing of axial motoneurons, at stimulus currents below threshold for A-delta fibers. Trains of three shocks to the pudendal nerve were considerably more effective than double or single shock trains. Repetition rates as low as 1/s had a long lasting excitatory effect on the lateral longissimus muscle and the magnitude of the responses increased gradually for several seconds with continued stimulation. Recordings from the axons of the epaxial motoneurons of female rats showed a strong activation of neuronal firing with an onset latency of 5.8 ms from the last shock of a three ms, three shock train; the onset in male rats, 8.4 ms, differed significantly. Peak spike activity occurred at mean latencies of 11, 22 and 102 ms in both sexes. A period of depressed firing was usually present from 34 to 50 ms. Males differed in having a larger peak in activity at 102 ms, but the overall profile of the responses was similar in males and females. No differences were seen in the overall response patterns of the estrogen-treated and untreated females. Responses of comparable magnitude were seen with ipsilateral or contralateral pudendal nerve stimulation; these were facilitated by bilateral stimulation. In electromyographic recordings, the onset of unit firings was seen at 6.4 ms latency in response to pudendal nerve stimulation. This unit activity was consistent with the firing pattern seen in the muscle nerves.Supported by US PHS grant HD13795     

Reduction of Ib autogenetic inhibition in motoneurons during contractions of an ankle extensor muscle in the cat

1. Triceps surae and plantaris (Pl) motoneurons were recorded intracellularly in chloralose or pentobarbital sodium (Nembutal)-anesthetized cats during unfused tetanic contractions of gastrocnemius medialis muscle (GM) produced by stimulating either a cut branch of the GM nerve or the muscle directly. 2. In alpha-motoneurons, during a series of GM twitches at 10/s, contraction-induced inhibitory potentials, probably the result of input from Golgi tendon organs (autogenetic inhibition), rapidly subsided before the end of the series. In contrast, excitatory potentials, probably the result of the activation of spindle primary endings during relaxation from contraction, persisted. 3. In gastrocnemius lateralis-soleus (GL-S) and Pl motoneurons lacking an excitatory connection with Ia afferents from GM, the sustained contraction of this muscle also elicited a declining inhibition. Rapid reduction of contraction-induced autogenetic inhibition was also observed in homonymous gamma-motoneurons. During unfused tetanic contractions lasting 0.5-4s, inhibitory potentials quickly subsided, but an abrupt increase in contractile force elicited a new series of decreasing inhibitory potentials. 4. The assumption that the inhibition induced by GM unfused tetanic contractions was due to activation of homonymous Ib afferents was supported by observations of the effects of electrical stimulation of the GM nerve. In Pl motoneurons lacking an excitatory connection with Ia afferents from GM, repetitive trains applied to the GM nerve, at a strength just above threshold for group I fibers, elicited rapidly declining inhibitory potentials similar to those produced by GM contraction. It was verified that during such stimulation, the amplitude of the group I afferent volleys did not decrease. 5. Reduction of contraction-induced Ib inhibition during sustained GM contraction was still present after a low spinalization of the preparation. As GM tendon organ discharges were verified to persist throughout prolonged contractions, the observed decline of autogenetic inhibition is likely to depend on a spinal mechanism, possibly involving presynaptic inhibition of Ib afferents and/or mutual inhibition of Ib-inhibitory interneurons.     

The muscle spindles in slow and twitch skeletal muscle of the lizard

1. Responses from stretch receptors, identified as muscle spindles, were recorded in filaments of the nerve supplying a twitch muscle, semimembranosus, and a slow muscle, semitendinosus in the lizard Tiliqua.2. While recording afferent discharges in one filament of the motor nerve, several adjacent filaments were each in turn stimulated repetitively until one was encountered which on stimulation produced a powerful increase in spindle firing. Such an effect of the motor stimulus was interpreted as resulting from intrafusal contraction. Any interference with spindle firing patterns from extrafusal contraction produced by the motor stimulation was removed by differentially blocking the contraction with the drug curare.3. Discharge patterns of spindles in response to a slow stretch of the muscle were compared with the response to the same stretch, but during repetitive stimulation of the motor nerve filament which produced an intrafusal contraction.4. At the initial length, the firing rate of spindles in the twitch muscle was greatly increased by the motor tetanus. There was little further increase in the response during and following stretch of the muscle.5. While the spindles in the slow muscle were only moderately excited by the motor tetanus at the initial length of the muscle, a large increase was recorded during the dynamic component of the stretch. At the new length, the steady-state firing continued at a rate well above that for the initial length.6. The effect of the motor tetanus on the response to stretch of muscle spindles in the slow muscle could be mimicked by adding succinyl choline (5 mug/ml.) to the perfusion solution. Spindles in the twitch muscle did not show a sustained sensitivity to the drug.7. It is suggested that while the different effects of motor stimulation on the responses to stretch of spindles in slow and twitch muscle can be explained by propositions based on the sliding filament theory of contraction, the sustained elevation, at the new length, of firing frequencies of spindles in slow muscle might require an additional explanation.     

The mechanical properties of cat soleus muscle during controlled lengthening and shortening movements

1. By supplying pulses to different subdivisions of the ventral nerve roots in rotation, it was possible to obtain smooth contractions of cat soleus with low rates of stimulation.2. After contracting isometrically the muscle was subjected to constant velocity lengthening or shortening movements.3. During shortening the tension always fell below the isometric value. The fall in tension was usually greatest when low rates of stimulation were used.4. The effect of lengthening on tension depended on the rate of stimulation. At high rates of stimulation the tension during lengthening always rose above the isometric tension. At lower rates of stimulation (5-15 pulses/sec) the tension rose at the beginning of an extension, but decreased later in the movement to a level that was often less than the isometric tension corresponding to that muscle length. At these stimulus rates the tension during isometric contraction was usually higher than during a sustained movement in either direction.5. At low rates of stimulation longitudinal vibratory movements of more than 0.1 mm also reduced the tension far below the isometric value, whereas the reduction was quite slight when the rate of stimulation was high.6. The isometric tension during smooth contractions at low stimulus rates was remarkable in the following respects: it developed rather slowly, it was higher than the tension during or immediately after movements, and it was only slowly regained after movement had ceased.7. The results are discussed in relation to the sliding filament theory of muscle contraction, which, with certain assumptions, provides an explanation for many of the findings.     

Histological study and LYVE-1 immunolocalization of mouse mesenteric lymph nodes with "In Vivo Cryotechnique"

The "in vivo cryotechnique" (IVCT) is a powerful tool to directly freeze living animal organs in order to maintain biological components in frozen tissues, reflecting their native states. In this study, mesenteric lymph nodes of living mice were directly frozen with IVCT, and we did morphological studies and immunohistochemical analyses on a hyaluronic acid receptor, LYVE-1. In lymph nodes, widely open lymphatic sinuses were observed, and many lymphocytes adhered to inner endothelial cells along subcapsular sinuses. The LYVE-1 was clearly immunolocalized at inner endothelial cells of subcapsular sinuses, as well as those of medullary sinuses. Conventional pre-embedding electron microscopy also showed LYVE-1 immunolocalization along both the apical and basal sides of cell membranes of inner endothelial cells. By triple-immunostaining for LYVE-1, smooth muscle actin, and type IV collagen, the LYVE-1 was immunolocalized only in the inner endothelial cells, but not in outer ones which were surrounded by collagen matrix and smooth muscle cells. Thus, the functional morphology of lymph nodes in vivo was demonstrated and LYVE-1 immunolocalization in inner endothelial cells of subcapsular sinuses suggests hyaluronic acid incorporation into lymph node parenchyma.     

Neurophysiological and technical considerations for the design of an implantable phrenic nerve stimulator

Sequential stimulation during one muscle contraction of several compartments of a motor nerve, using multiple-electrodes, allows individual nerve-muscle compartments to be stimulated at fairly low frequencies. This provides time for recovery even during muscle contraction. However, the whole muscle is stimulated at near to its optimum fusion frequency, which provides smooth muscle contraction. This stimulation system imitates the natural activation of skeletal muscle. The new phrenic nerve stimulator described utilises the principle of sequential motor nerve stimulation. It also incorporates a sigh function. The sigh current recruits additional axons at certain intervals and thus creates and keeps available a reserve of conditioned muscle. Clinical advantages result: the conditioning phase after the beginning of long-term phrenic nerve stimulation for electroventilation is shortened and muscle fatigue is delayed. A need of increase of gas exchange can be answered by increasing tidal volume instead of respiration rate alone.     

慢性电刺激神经后背阔肌纤维的组织化学和超微结构改变

８只成年杂种犬，低频电刺激胸背神经４、６、１２、１４周后，观察了背阔肌纤维的组织化学和超微结构的变化。电刺激后酸预孵育ｍＡＴＰａｓｅ反应，所有肌纤维均染成深黑色；碱预孵育ｍＡＴＰａｓｅ反应，随着刺激时间的延长，深染纤维逐渐减少，浅染纤维增多。说明电刺激后含快肌球蛋白的快缩肌纤维逐步转变成含慢肌球蛋白的慢缩肌纤维。电镜观察显示，电刺激后肌纤维内的肌原纤维、横小管和肌浆网系统减少，线粒体含量明显地多于     

Early effects of cervical sympathetic stimulation on cerebral,ocular and cochlear blood flow

Autoregulatory mechanisms may be expected to modify effects of vasomotor nerve stimulation in many tissues. Attempts were made to reveal a distinct early, but transient effect of cervical sympathetic stimulation on cerebral, retinal and cochlear blood flow. The labelled microsphere method was used to determine regional blood flow during electrical stimulation of the cervical sympathetic chain for 15–25 s and 5 min. At a frequency of 6 Hz there was a 5% reduction in cerebral flow at 15–25 s and 7% at 5 min. In the choroid plexus the mean reduction was 22% at 15–25 s but decreased to 10% after 5 min. In the cerebellum, optic nerve and retina, sympathetic stimulation had no appreciable effect on the blood flow. In the cochlea and iris, the blood flow reductions were 25 and 32%, respectively, on both occasions. In the choroid, vasoconstriction increased with time, whereas in the masseter muscle there was a decrease. Thus in the present experiments no indication was found of an autoregulatory escape phenomenon in the brain, the eye or the cochlea. Some escape was noted in the masseter muscle.     

Fatigue and recovery of phosphorus metabolites and pH during stimulation of rat skeletal muscle: an evoked electromyography and in vivo31P-nuclear magnetic resonance spectroscopy study

³¹P-nuclear magnetic resonance spectroscopy and evoked electromyography were applied to rat skeletal muscle to examine the mechanism of muscle fatigue and the recovery of muscle phosphorus metabolites and pH during fatigue. When the sciatic nerve was electrically stimulated at 1 Hz, the contraction force of the gastrocnemius muscle decreased gradually to 46% of the maximal force, accompanied by a decrease in phosphocreatine (PCr) and a corresponding increase in inorganic phosphate (P_i) and diprotonated inorganic phosphate (H₂PO₄ ^–). Neither the amplitudes of compound muscle action potentials (CMAP) nor muscle pH changed significantly. At 10-Hz stimulation, contraction force rapidly decreased to 26% of maximal force, accompanied by a decrease in PCr and increases in P_i and H₂PO₄ ^–. Muscle pH decreased for a few minutes, then gradually recovered during continued stimulation. The amplitude of the CMAP also decreased for a few minutes and then reached steady values. At 100-Hz stimulation, the contraction force decreased to 6% of the maximal force and there was a decrease in the amplitude of the CMAP. However, the changes in the phosphorus metabolites and pH were transient and recovered to the control value during the stimulation. These results indicated that fatigue at 1 and 100-Hz stimulation was mainly caused by the change in phosphorus metabolite concentrations and electrical failure, respectively, and that fatigue at 10-Hz stimulation might have been due to both of the these factors. These results also indicated that electrical failure might have been the cause of the recovery of the phosphorus metabolites and pH during 100-Hz stimulation and of pH during 10-Hz stimulation.     

肌肉磁刺激脑诱发电位传入机制的研究

目的：研究磁刺激肌肉脑诱发电位（ＭＭＳＥＰ）的传入机制。方法：对肌松弛下腓肠肌ＭＭ－ＳＥＰ及电刺激踝部胫后神经体感诱发电位（ＳＥＰ）进行配对对比研究。结果：（１）肌松弛无肌收缩时仍可记录到ＭＭＳＥＰ；（２）配对腓肠肌ＭＭＳＥＰ与胫后神经ＳＥＰＰ４０潜伏期差值伴与不伴肌收缩相差显著；（３）伴肌收缩时，ＭＭＳＥＰ较配对ＳＥＰＰ４０潜伏期显著延长，不伴肌收时则相差不显著。结论：正常伴肌收缩时，磁刺激很可能先兴奋肌肉运动神经末梢致肌肉运动，间接兴奋肌肉Ｉａ纤维或（和）肌肉深部感受器；由此可解释ＭＭＳＥＰ较电刺激同等水平ＳＥＰＰ４０潜伏期长。