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目的:观察肌筋膜疼痛触发点模型鼠股内侧肌触发点能量代谢(腺苷酸、乳酸)的含量以及针刀干预后的变化,探讨针刀治疗肌筋膜疼痛综合征的生物学机制。方法:打击结合离心运动法建立触发点大鼠模型,通过电生理观察大鼠触发点病理学变化;通过高效液相色谱法和比色法观察触发点部腺苷酸、乳酸表达情况,进而统计分析各组间的差异。结果:造模8周后模型组腺苷酸含量降低,乳酸含量显著升高(P<0.05),针刀治疗3次后,针刀组的腺苷酸含量升高,乳酸含量降低,与模型组比较,差异有统计学意义(P<0.01),与空白组比较,差异有统计学意义(P<0.05)。结论:针刀可能通过松解活化触发点来增加局部腺苷酸的释放,抑制乳酸分泌,从而改善肌肉的持续收缩状态,减少代谢产物的蓄积,以打破恶性循环,最终达到治疗肌筋膜疼痛综合征的目的。
OBJECTIVE: To observe the changes of energy metabolism (adenosine and lactic acid) and the changes after acupuncture intervention at the trigger point of myofascial pain triggering point to explore the biological mechanism of acupotome treatment of myofascial pain syndrome. Methods: The rat model of triggering point was established by combing centrifugation and the pathological changes of triggering point were observed by electrophysiology. The expression of adenylate and lactate at triggering point was observed by HPLC and colorimetric method, and then statistical Analysis of differences between groups. Results: After 8 weeks, the content of adenylate decreased and the content of lactate increased significantly (P <0.05). After acupuncture treatment for 3 times, the content of adenylate increased and the content of lactate decreased in model group The difference was statistically significant (P <0.01), compared with the blank group, the difference was statistically significant (P <0.05). Conclusion: The acupotomist may release the release of local adenylate by releasing the activation trigger point, inhibit the secretion of lactate, so as to improve the sustained contractility state of the muscle and reduce the accumulation of metabolites in order to break the vicious cycle and eventually achieve the treatment of myofascial pain The purpose of the syndrome.