【摘要】：目的:發(fā)展一種適合穴位敏化現(xiàn)象研究的動(dòng)物模型,觀察心肌缺血導(dǎo)致的體表穴位處力敏變化,探討穴位敏化的現(xiàn)象及發(fā)生機(jī)制。方法:新西蘭家兔隨機(jī)分成對(duì)照組和模型組,每組10只。模型組采用改進(jìn)的氣囊阻塞可控心肌缺血模型。在造模前后檢測(cè)心肌缺血引起的Ⅱ?qū)?lián)變化,通過心肌2,3,5-三苯基氯化四氮唑(TTC)染色確定心肌壞死程度。分別在心肌缺血模型制備過程第8、14、20天檢測(cè)清醒家兔不同體表部位機(jī)械痛閾值。結(jié)果:可控心肌缺血模型制備過程中模型組Ⅱ?qū)?lián)變化一致,在氣囊充氣阻塞左冠狀動(dòng)脈前降支(心肌缺血)時(shí)ST段抬高(P0.05),氣囊放氣后ST段恢復(fù),表明家兔心肌缺血刺激可控。心肌TTC染色示模型組心肌壞死程度為(9.37±0.19)%。3個(gè)檢測(cè)階段模型組與對(duì)照組家兔在足底及"太溪"穴處均無明顯機(jī)械痛閾值改變(P0.05);心肌缺血刺激14d后模型組"內(nèi)關(guān)"處及心肌缺血刺激20d后模型組"神門"和"內(nèi)關(guān)"處機(jī)械痛閾均顯著低于對(duì)照組(P0.01)。結(jié)論:改進(jìn)的家兔可控心肌缺血模型適用于疾病前后穴位敏化現(xiàn)象的力敏研究。心肌缺血可導(dǎo)致"神門"和"內(nèi)關(guān)"處力敏降低,內(nèi)臟疾病可導(dǎo)致相關(guān)臨床治療穴位發(fā)生敏化。
[Abstract]:Aim: to develop an animal model suitable for the study of acupoint sensitization, to observe the changes of acupoint sensitivity induced by myocardial ischemia, and to explore the phenomenon and mechanism of acupoint sensitization. Methods: new Zealand rabbits were randomly divided into two groups: control group (n = 10) and model group (n = 10). The model group was treated with improved balloon occlusion controlled myocardial ischemia model. Myocardial necrosis was determined by 2,3,5-triphenyl tetrazolium chloride (TTC) staining. The threshold of mechanical pain in different parts of the body surface of conscious rabbits was measured on the 8th, 14th and 20th day during the preparation of myocardial ischemia model. Results: the changes of lead 鈪，

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