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不同缺血后調(diào)適方案對(duì)大鼠肢體骨骼肌缺血再灌注損傷影響的實(shí)驗(yàn)研究

發(fā)布時(shí)間:2018-10-25 09:58
【摘要】:目的:建立SD大鼠肢體骨骼肌缺血再灌注損傷的模型,研究不同缺血后調(diào)適方案對(duì)大鼠肢體骨骼肌缺血再灌注損傷是否具有保護(hù)作用并優(yōu)選最佳方案,為進(jìn)一步研究提供基礎(chǔ);并初步探討缺血后調(diào)適在肢體骨骼肌缺血再灌注損傷中的可能機(jī)制。方法:健康成年雄性SD大鼠隨機(jī)分為4組(n=9):缺血再灌注組(IRI組)和不同缺血后調(diào)適3個(gè)組(IpostA、IpostB、IpostC組)。各組大鼠均在右側(cè)股動(dòng)脈進(jìn)行缺血再灌注實(shí)驗(yàn)操作,并分離左側(cè)股動(dòng)脈作為自身假手術(shù)對(duì)照,其中缺血再灌注組給予右側(cè)股動(dòng)脈缺血4h再灌注24h;缺血后調(diào)適3個(gè)組(IpostA、IpostB、IpostC組)分別于右側(cè)4h缺血后立即施加4個(gè)循環(huán)分別為10s再灌/10s缺血、30s再灌/30s缺血、1min再灌/lmin缺血的后調(diào)適操作,再灌注24h。各組實(shí)驗(yàn)結(jié)束后抽血檢測(cè)乳酸脫氫酶(LDH),取樣腓腸肌測(cè)算濕干重(濕/干,W/D)比值、檢測(cè)髓過(guò)氧化物酶(MPO)和丙二醛(MDA),取樣脛前肌電鏡觀察骨骼肌病理變化。結(jié)果:IRI組實(shí)驗(yàn)側(cè)W/D值較假手術(shù)側(cè)明顯增加(P0.05);4個(gè)循環(huán)的30s再灌/30s缺血后調(diào)適IpostB組W/D值顯著低于IRI組(P0.05),其余2個(gè)缺血后調(diào)適組(IpostA、IpostC組)與IRI組差異不明顯(P0.05)。LDH值、MPO值、MDA值,缺血后調(diào)適3組均低于IRI組(P0.05),缺血后調(diào)適組間未見(jiàn)明顯差異。4個(gè)循環(huán)的30s再灌/30s缺血IpostB組電鏡下骨骼肌線粒體嵴的空泡變性程度、肌原纖維結(jié)構(gòu)清晰程度和細(xì)胞核完整性較缺血再灌注組均有明顯改善,其余2個(gè)缺血后調(diào)適組超微結(jié)構(gòu)較缺血再灌注組也有不同程度改善。結(jié)論:1、缺血后調(diào)適對(duì)大鼠肢體骨骼肌缺血再灌注損傷有保護(hù)作用,4個(gè)循環(huán)30s再灌/30s缺血方案的保護(hù)效果最明顯,可作為進(jìn)一步實(shí)驗(yàn)研究的基礎(chǔ)。2、缺血后調(diào)適在骨骼肌缺血再灌注損傷中發(fā)揮保護(hù)作用可能的機(jī)制是通過(guò)減少活性氧類(lèi)物質(zhì)的生成、減輕肌纖維水腫、中性白細(xì)胞聚集、能量代謝等發(fā)揮作用的。
[Abstract]:Objective: to establish a model of limb skeletal muscle ischemia-reperfusion injury in SD rats, and to study whether different ischemic conditioning schemes have protective effect on limb skeletal muscle ischemia-reperfusion injury and to select the best scheme for further study. To explore the possible mechanism of ischemic conditioning in limb skeletal muscle ischemia reperfusion injury. Methods: healthy adult male SD rats were randomly divided into 4 groups: ischemia reperfusion group (IRI group) and different ischemic conditioning group (IpostA,IpostB,IpostC group). All the rats in each group were subjected to ischemia-reperfusion experiment in the right femoral artery, and left femoral artery was separated as self-sham-operation control. The ischemia-reperfusion group was given right femoral artery ischemia reperfusion for 4 h and 24 h. Three groups (IpostA,IpostB,IpostC group) were subjected to 10 s reperfusion / 10 s ischemia, 30s reperfusion / 30s ischemia, 1min reperfusion / lmin ischemia and 24 h reperfusion immediately after right 4 h ischemia. After the experiment, lactate dehydrogenase (LDH),) was taken from gastrocnemius muscle to calculate wet dry weight (wet / dry, W / D) ratio, myeloperoxidase (MPO) and malondialdehyde (MDA),) were taken from tibial muscle to observe the pathological changes of skeletal muscle. Results: the W / D value of experimental side in IRI group was significantly higher than that in sham operation side (P0.05), the WR value in IpostB group after 30 s reperfusion / 30 s ischemia was significantly lower than that in IRI group (P0.05), there was no significant difference between the other two ischemic conditioning groups (IpostA,IpostC group) and IRI group (P0.05). LDH, MPO value, MDA value). The degree of vacuolar degeneration of mitochondrial crest of skeletal muscle was observed under electron microscope in 4 circulations of 30 s reperfusion / 30 s ischemia IpostB group, which was lower than that in IRI group (P0.05), and there was no significant difference between the three groups (P0.05). The structural clarity and nuclear integrity of myofibrils were improved significantly compared with those of ischemia reperfusion group, and the ultrastructure of the other two ischemic conditioning groups was improved to some extent than that of ischemia reperfusion group. Conclusion: 1.After-ischemic conditioning has protective effect on limb skeletal muscle ischemia-reperfusion injury, and the protective effect of four cycles for 30s reperfusion / 30s ischemia is the most obvious. 2. The possible protective mechanism of ischemic conditioning in skeletal muscle ischemia-reperfusion injury is to reduce muscle fiber edema and neutrophil aggregation by reducing the production of reactive oxygen species (Ros). Functioning in energy metabolism, etc.
【學(xué)位授予單位】:廣西醫(yī)科大學(xué)
【學(xué)位級(jí)別】:碩士
【學(xué)位授予年份】:2015
【分類(lèi)號(hào)】:R687

【參考文獻(xiàn)】

相關(guān)期刊論文 前1條

1 孫備;細(xì)胞凋亡與缺血-再灌注損傷的研究進(jìn)展[J];國(guó)外醫(yī)學(xué).外科學(xué)分冊(cè);1998年06期



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