机械按压对大鼠肌筋膜激痛点能量代谢及线粒体超微结构的影响

Effects of Mechanical Compression on Energy Metabolism and Mitochondrial Ultra-structure of Rat Myofascial Trigger Points

目的观察机械按压对大鼠肌筋膜激痛点(myfascial trigger points,MTrPs)三磷酸腺苷(adenosine triphosphate,ATP)、乳酸、肌糖原含量及线粒体超微结构的影响,初步探讨机械按压对大鼠MTrPs能量代谢的影响及其机制。方法48只雄性SD大鼠随机分为空白组、模型组、按压组和利多卡因组,每组12只。采用钝性打击结合离心运动法复制MTrPs大鼠模型。按压组予MTrPs按压治疗,每次7.5 min,隔天1次,共治疗7次;利多卡因组予MTrPs局部注射利多卡因治疗,6 d 1次,共治疗3次;模型组和空白组不做治疗。治疗结束后采用比色法检测MTrPs骨骼肌组织ATP、肌糖原和乳酸含量,采用透射电镜观察MTrPs骨骼肌线粒体超微结构。结果与空白组比较,模型组大鼠MTrPs肌组织ATP和肌糖原含量下降,乳酸含量上升(P<0.05);电镜下线粒体数量减少、畸形,体积变小,嵴断裂变形。与模型组比较,按压组和利多卡因组大鼠ATP和肌糖原含量上升,乳酸含量下降(P<0.05);电镜下,按压组大鼠线粒体数量增多,外形大小基本正常,嵴尚可见;利多卡因组大鼠线粒体数量增多,形态较规整,可见少量肿胀线粒体。与利多卡因组比较,按压组大鼠肌糖原升高(P<0.05),电镜下两组线粒体数量相当,但按压组形态较规整,未见肿胀线粒体。结论机械按压可缓解MTrPs骨骼肌能量代谢危机,其机制可能与改善线粒体超微结构,促进线粒体损伤修复有关。

Objective To explore the effect of mechanical compression on adenosine triphosphate(ATP),lactic acid,muscle glycogen and ultra-structure of mitochondria in rat myfascial trigger points(MTrPs),and to explore the effects of mechanical compression on the energy metabolism of MTrPs and its mechanism.Methods 48 male SD rats were randomly divided into blank group,model group,compression group and lidocaine group,with 12 rats in each group.The rat model of MTrPs was established by blunt shock combined with centrifugal motion.The compression group was treated with mechanical compression,7.5 minutes each time,once every other day,for a total of 7 times.The lidocaine group was treated with local injection of lidocaine at the MTrPs,once every 6 days,for 3 times in total.The model group and the blank group did not receive treatment.After treatment,ATP,glycogen and lactic acid content in muscle were detected by colorimetry.The ultrastructure of skeletal muscle mitochondria in MTrPs was observed by transmission electron microscopy.Results Compared with the blank group,ATP and muscle glycogen content decreased,and lactic acid accumulated in the rat MTrPs of model group(P<0.05).Under electron microscope,the number of mitochondria decreased,malformed,the volume became smaller,and the mitochondrial cristal fracture was deformed in the model group.Compared with the model group,the content of ATP and muscle glycogen in compression group and lidocaine group increased,while the content of lactic acid decreased(P<0.05).Under electron microscope,the number of mitochondria in compression group increased,the shape and size were basically normal,and the mitochondrial cristae were still visible.In lidocaine group,the number of mitochondria increased and the morphology was relatively regular,with a small amount of swollen mitochondria.Compared with lidocaine group,muscle glycogen was increased in compression group(P<0.05).The number of mitochondria in the two groups was similar under electron microscope,but the morphology of mitochondria in compression group was regular and no swelling was observed.Conclusion Mechanical compression can alleviate the energy metabolism crisis of MTrPs skeletal muscle,and its mechanism may be related to improving mitochondrial ultra-structure and promoting mitochondrial repair.