本文關(guān)鍵詞：模擬高原環(huán)境大腦皮質(zhì)及血腦屏障的病理變化與AQP4的相關(guān)性實(shí)驗(yàn)研究　出處：《第三軍醫(yī)大學(xué)》2005年碩士論文　論文類型：學(xué)位論文

  更多相關(guān)文章： 高原反應(yīng) 水通道蛋白-4 星形膠質(zhì)細(xì)胞 血腦屏障

【摘要】：人或動(dòng)物從低海拔急進(jìn)高原,暴露于低壓低氧寒冷環(huán)境可能發(fā)生系列病理反應(yīng),表現(xiàn)為頭痛、惡心、嘔吐、失眠、疲乏、頭昏眼花、共濟(jì)失調(diào)等,稱高山反應(yīng),也稱急性高原病(acute mountain sickness,AMS)。有報(bào)道說人進(jìn)入2,500 米以上高原就可能發(fā)生高原反應(yīng)。AMS 重者發(fā)生高原肺水腫(high altitude pulmonary edema,HAPE)或高原腦水腫(high altitude cerebral edema,HACE),表現(xiàn)為呼吸困難、精神智力障礙以至昏迷。HACE 是急性高原病的極端嚴(yán)重情況,如不及早預(yù)防和救治,危及患者生命�，F(xiàn)代交通和旅游業(yè)的發(fā)達(dá),社會(huì)交流的增多,有越來越多的人進(jìn)入高原地區(qū),因此,高原病的防治愈加重要和迫切。 已有研究認(rèn)為,急性高原病和HACE 的主要病變是血管源性腦水腫和顱內(nèi)高壓,但到目前為止對(duì)高原腦水腫發(fā)生的細(xì)胞和分子機(jī)制仍知之甚少。膠質(zhì)細(xì)胞足板是血腦屏障(blood brain barrier,BBB)的重要結(jié)構(gòu)成分,近年在創(chuàng)傷、缺血、腫瘤性腦水腫的研究中發(fā)現(xiàn),膠質(zhì)細(xì)胞(及其突起、膠質(zhì)足)形態(tài)學(xué)變化先于神經(jīng)元,認(rèn)為是最早的病理反應(yīng),但膠質(zhì)細(xì)胞在AMS 和HACE 中的反應(yīng)變化還未見研究報(bào)告。水通道蛋白是水分子跨膜運(yùn)動(dòng)的主要分子基礎(chǔ),在調(diào)節(jié)腦水平衡中起著關(guān)鍵作用,認(rèn)為在病理生理過程中也發(fā)揮主要作用,是目前研究的熱點(diǎn),AQP4在AMS 和HACE 發(fā)生中的作用值得探討。 在高原反應(yīng)、AMS 和HACE 情況下BBB 的病理變化、膠質(zhì)細(xì)胞反應(yīng)、AQP4及其mRNA 的表達(dá)變化,以及他們之間的相互關(guān)系還未見研究報(bào)道,本實(shí)驗(yàn)通過急進(jìn)高原5000m 大鼠動(dòng)物模型,觀察4h~4w 這些指標(biāo)的改變,以探索高原反應(yīng)/AMS 和HACE 的發(fā)病機(jī)制。 實(shí)驗(yàn)結(jié)果如下: 1.一般情況:實(shí)驗(yàn)組大鼠4h~72h 活動(dòng)度減少,蛛網(wǎng)膜、肺組織、胃腸明顯充血。以后活動(dòng)增加,進(jìn)食有所增加,組織充血減輕至接近正常。 2.光鏡觀察:實(shí)驗(yàn)組24h、48h 及72h 蛛網(wǎng)膜輕度充血,腦組織微血管周圍間隙增寬。2w、4w 時(shí)膠質(zhì)細(xì)胞有增生現(xiàn)象,有膠質(zhì)結(jié)節(jié)形成。
[Abstract]:People or animals from low altitude into the plateau, exposure to low pressure hypoxia cold environment may occur a series of pathological reactions, such as headache, nausea, vomiting, insomnia, fatigue, dizziness, ataxia, and so on, known as mountain reaction. Also known as acute high altitude disease (AMS). It has been reported that people enter 2. High altitude pulmonary edema may occur in patients with high altitude reaction. Hape) or high altitude cerebral HACEE showed dyspnea. Mental retardation and even coma. HACE is an extremely serious condition of acute altitude disease, such as early prevention and treatment, endangering the life of patients, the development of modern transportation and tourism, and the increase of social communication. More and more people enter plateau area, therefore, the prevention and cure of altitude disease is more and more important and urgent. It has been suggested that the main lesions of acute high altitude disease and HACE are vasogenic brain edema and intracranial hypertension. But up to now, little is known about the cellular and molecular mechanism of high altitude brain edema. Glial cell foot plate is the blood-brain barrier brain barrier. The important structural components of BBB have been found in recent years in the study of trauma, ischemia, tumorous brain edema, glial cells (and their processes, glial foot) morphological changes before neurons, thought to be the earliest pathological response. However, the changes of glial cell reaction in AMS and HACE have not been reported. Aquaporins are the main molecular basis of water molecule transmembrane movement, and play a key role in regulating brain water balance. It is suggested that AQP4 plays a major role in the pathophysiological process, and the role of AQP4 in the pathogenesis of AMS and HACE is worthy of discussion. The pathological changes of BBB and the expression of AQP4 and its mRNA in glial response were observed under high altitude reaction (AMS) and HACE. And the relationship between them has not been reported yet. In this experiment, we observed the changes of these indexes in 4hs and 4w by using the animal model of 5000m rats at high altitude. To explore the pathogenesis of high altitude reaction / AMS and HACE. The results are as follows: 1. General conditions: the rats in the experimental group showed decreased activity at 72h, obvious congestion in arachnoid, lung and gastrointestinal tract, and increased activity, food intake and hyperemia to nearly normal level. 2. Light microscope observation: the experimental group had slight hyperemia in arachnoid at 24 h and 72 h, and glial cell proliferation and glial nodule formation in the brain tissue after 4 weeks of widening the space around the microvessel.
【學(xué)位授予單位】：第三軍醫(yī)大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2005
【分類號(hào)】：R363

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