【作者】 吕娇娇；

【导师】 黄强民；

【作者基本信息】 上海体育学院 ， 运动人体科学， 2011， 硕士

【摘要】 研究目的：日常生命活动或体育运动损伤后常常出现一些慢性疼痛后遗症状,这些疼痛往往会引起关节和脊柱周围疼痛,导致关节障碍。这些慢性疼痛大部分为骨骼肌疼痛,而肌筋膜疼痛触发点是导致骨骼肌疼痛的常见原因之一。临床上慢性肌筋膜疼痛综合症是以疼痛为主一组症候群,这种症候群表现为疼痛、牵涉痛、自主神经的和骨骼肌功能的障碍等症状。肌筋膜疼痛严重影响了人们的生活和工作,并成为消耗卫生资源的重要原因。目前认为受累肌内存在有骨骼肌或肌筋膜内的疼痛触发点。为了研究其发病机制,目前有关触发点的模型多为模拟模型或隐性触发点模型,无法代表活化触发点的全貌；因此无法说明触发点的自发肌电位和动作电位的真实变化,而且也无法说明到真实活化触发点的病理组织学的真实改变。本研究通过经济实惠的大鼠作为实验动物,采用股内侧肌打击结合离心运动的方法建立创伤性肌筋膜疼痛触发点的动物模型,在经历不同恢复时间后,检测触发点肌电图表现和观察触发点的病理组织学的改变,了解肌筋膜疼痛触发点的本质和发病特点,以推论触发点的可能发病机制。研究方法：32只七周龄雄性SD大鼠,平均体重220g-260g,随机分为ABCD四组,每组8只,A组为正常对照组,BCD三组为实验干预组。A组正常对照组在造模期与恢复期均正常喂养,不进行任何干预。实验干预组造模期每周第一天打击左下肢股内侧肌,打击后第二天配合离心运动,造模期为8周。实验干预组恢复期同对照组,不进行任何实验干预,正常喂养,其中B组恢复4周,C组恢复8周,D.组恢复12周。分别在不同时期分批对大鼠进行造模效果检查和取材,手术暴露大鼠股内侧肌,触摸打击处及周围肌肉的紧张带和收缩结节、针刺紧张带引起局部抽搐反应、记录紧张带处的自发性电位和记录结节数目。最后,对紧张带或结节处的局部组织进行组织活检取材：1.组织进行HE染色后,光镜下观察病理切片的结节数目、形态及大小等变化；2.使用透射电子显微镜超薄切片技术制作电镜标本,电镜观察触发点组织的肌丝排列、肌小节、线粒体等超微结构特点。将实验干预组和对照组所得结果进行比较分析,所用数据统计分析均采用SPSS17.0软件包进行分析。研究结果：A组对照组股内侧肌附近发现紧张带或触发点个数平均0.13个(1/8)；B、C、D组平均发现触发点个数分别为3.00个(24/8)、2.63个(21/8)、2.25个(18/8),紧张带或触发点在针刺时均出现局部抽搐反应。静息状态下,大鼠股内侧肌附测量肌肉的自发电位,A、B、C、D各组一分钟内出现自发电位的频数分别为2.75±2.87,172.57±102.88,151.63±65.37,168.14±64.53。对照组与实验组两两比较,P<0.01具有高度显著性差异,实验组之间两两比较P>0.05没有统计意义。A、B、C、D各组自发电位的波幅分别为26.06±16.67μV,33.08±18.40μV,93.26±163.18μV,78.27±161.68μV,其中A、B两组与C、D两组比较有显著性差异P＜0.05,而A、B组之间与C、D组之间不具有显著性差异。病理切片横切面显示,对照组肌细胞形态规则、大小均匀,未发现有大小不一、圆形、增大、深染的肌细胞,实验组横切面均发现增大、圆形深染的挛缩结节,实验组各组均出现炎细胞浸润和核内移(>10%)现象。纵切面,对照组表现为排列紧密而规律的纵向肌纤维。实验组B、C、D组均出现排列紊乱、中央膨大两端变细或相间出现粗细不等的梭形肌纤维。ABCD各组肌细胞直径分别为22.84±0.48μm,44.73±9.50μm,45.77±8.70μm,47.81±5.84μm,实验组与A组对照组比较具有高度显著差异性,P<0.01,而实验组之间无显著差异性。电子显微镜观察：对照组横切显示,粗细肌丝排列规则,大量线粒体存在,线粒体形态呈卵圆形并存在折叠嵴结构；纵切显示,肌原纤维排列整齐,明暗带交替出现。实验组横切均显示,线粒体数量明显减少,呈圆形且嵴结构减少或消失；纵切显示,肌原纤维排列紊乱、模糊不清,Z线呈水纹样改变。ABCD各组肌小节长度分别为1.95±0.02μm,1.92±0.08μm,1.53±0.06μm,1.48±0.07μm,实验组C、D组与A组对照组和B组实验组比较具有高度显著差异性,P<0.01,另外,C、D组之间比较无显著性差异,B组与A组比较无显著差异性,P>0.05。研究结论：1.紧张带或触发点,局部抽搐反应、自发电位等电生理特征和病理组织学改变证明打击结合离心运动方式建立的肌筋膜疼痛触发点大鼠模型成功。延长恢复期,肌筋膜疼痛触发点仍然存在,说明大鼠模型复制的MTrPs可长期存在,符合临床肌筋膜疼痛触发点的特征。2.恢复4周组肌筋膜疼痛触发点为早期触发点,存在明显炎症变化和肌肉损伤现象,恢复8周和恢复12周,肌筋膜疼痛触发点表现相似,为慢性触发点,说明触发点在恢复8周时已稳定存在,建立肌筋膜疼痛触发点模型时无需恢复12周即可复制稳定肌筋膜疼痛触发点。3.肌筋膜疼痛触发点产生的自发性电位是一种高频率的异常终板电位,说明肌筋膜触发点位于运动终板附近。4.病理组织学光镜观察受累骨骼肌触发点处聚集的圆形结节及膨大并相间出现的变细肌纤维结构,说明骨骼肌触发点存在异常收缩的收缩结节和因收缩而导致结节两端的变细,肌筋膜疼痛触发点是一种异常肌纤维改变。炎性浸润提示肌筋膜触发点存在慢性的炎症过程,核内移则提示可能存在神经肌肉接头功能异常现象。5.电镜观察肌小节排列紊乱,Z线水纹样改变,线粒体数量减少,结构异常,提示为受累肌肌筋膜疼痛触发点处存在能量危机现象,并且超微结构显示肌筋膜疼痛触发点肌纤维维存在损伤现象；肌小节显著性缩短进一步验证肌纤维存在异常收缩现象。更多还原

【Abstract】 Objective:Daily life activities or sports injury usually cause some chronic pain, which could lead to the pain at joint and spine or the disorders of skeletomuscular system. Most of this chronic pain is muscle pain, and myofascial pain is a common cause of muscle pain. Clinically, chronic myofascial pain syndrome has been characterized by pain, referred pain, autonomic nerve dysfunction and muscle disorders. Myofascial pain could seriously affect people’s living and work lead to an increase of the financial burden of society. Now it is believed that myofascial trigger points locate in skeletal muscle or fascia muscularis. In order to study the pathogenesis of the myofascial trigger points, most of current models are simulation models of latent trigger points models which can not represent the whole characters of myofascial trigger points. Therefore, all of these models couldn’t explain real changes of trigger points’ spontaneous electrical activity (SEA) and histopathological changes. In this study, we will use rats as experimental animals. During experiment, rats were dealt with striking and eccentric exercise to produce the myofascial trigger points in rats. After different longed recovery time, the EMG and histopathological changes at trigger points will be inspected on the nature and pathological character of myofascial trigger points which could infer the possible pathogenesis of myofascial trigger points.Methods:32 male SD rats seven week-old, average weight of 220g-260g, were randomly divided into 4 groups which were A group, B group, C group and D group. There were 8 rats in every group. A group was control group and B group, C group and D groups were experimental groups. A group:During periods of modeling and recovery, all rats in A group weren’t given any intervention. Experimental groups:in the first day of every week during modeling period, all rats in experimental groups were stroked at the left vastus medialis, and the next day, all rats were taken to eccentric exercise for 90 min. The modeling period lasted 8 weeks. During recovery periods, without any experimental intervention and normal feeding, all experimental rats were dealt as the control group. The recovery periods of BCD group separately lasted 4,8 and 12 weeks. After recovery period, all groups were detected taut band, contraction knots, local twitch response (LTR) and SEA. Finally, diagnose myofascial trigger points and make muscle biopsy:1.After HE staining, use microscope to record the modules number and observe the shape and size of modules; 2.Using transmission electron microscope (TEM), observe arrangement of myoneme, sarcomere, mitochondria, etc. All the results of experimental groups and control group were compared and analyzed by SPSS17.0 software package.Results:The average number of myofascial trigger points or taut band of A group was 0.13(1/8) and that of B, C, D group was respectively 3.00 (24/8),2.63 (21/8),2.25 (18/8). When acupunctured, all taut band or nodules could be induced LTR. During resting state, the frequency of SEA in a minute of A, B, C, D group was respectively 2.75±2.87,172.57±102.88,151.63±65.37,168.14±64.53. When the control group was compared with every experimental group, P<0.01 which has highly significant difference; while each experimental group was compared, P> 0.05 which didn’t have statistical significance. The amplitude of each group’s SEA was 26.06±16.67μV,33.08±18.40μV,93.26±163.18μV,78.27±161.68μV. When A, B group and C, D group were compared, there was significant difference, P<0.05, while there was no significant difference between A group and B group and between C group and D group.The cross-section of pathological section showed:A group had regular muscle cell and uniform size, and was not found different sized, round, augmented and deeply stained muscle cell; All experimental groups were found augmented, round and deeply stained contracture nodules, and also found inflammatory cell infiltration and nuclear transfer phenomena (>10%). The Longitudinal section of pathological section showed:the control group showed a tightly and regular arrangement of longitudinal muscle fibers; all experimental groups were appeared disorganized shuttle-shaped muscle fibers which were swollen in central and thin at both ends. The average muscle cell diameter in each group were 22.84±0.48μm,44.73±9.50μm,45.77±8.70μm,47.81±5.84μm. There was a highly significant difference between experimental groups and the control group, P<0.01, while there was no significant difference between experimental groups.The observation of TEM showed:cross-section of the control group showed regularly arranged thin filament and thick filament, a large number of mitochondria which were ovoid and had whole ridge structures; the longitudinal section shows regularly arranged myofibrils with alternating light band and dark band. The cross-section of experimental groups all showed significantly decreased mitochondria which were round and had less ridge structures or abnormal ones; the longitudinal section showed disordered myofibrils which were blurred and whose Z lines had a water-patterns-like changing. The main sarcomere length in each groups were 1.95±0.02μm,1.92±0.08μm,1.53±0.06μm,1.48±0.071μm, there was a highly significant difference between C, D group and A group,p<0.01, while there was no significant difference between A group and B group and between C group and D group,p>0.05.Conclusions:1. All founds of the experiment which conclude taut band or myofascial trigger points, LTR, SEA and pathological changes demonstrate that myofascial trigger points rat model though striking and eccentric exercise is successful. When the recovery period was extended, myofascial trigger points did not disappeared and could prove that myofacial trigger points can exist in the long time, which is in accordance with the characteristics of clinical MTrPs.2.The SEA generated in MTrPs is a kind of abnormal end plate potential with high frequency and low amplitude, which could prove that MTrPs locate near motor end plate.3.The pathological observation of microscopy illustrate that there are abnormally contracted nodules in myofascial trigger points and MTrPs is a kind of abnormal muscle fiber. Inflammatory infiltration suggests that there may be a inflammatory process during the pathogenesis of MTrPs, and the nuclear transfer may point out a muscle repairing process or muscle that is lost of neural control.4.The observation of TEM suggests that muscle with MTrPs has a energy crisis and injury phenomenon; significantly shorten sarcomere can further prove that the muscle fibers near MTrPs are abnormally contracted fiber.更多还原