發(fā)布時(shí)間：2018-02-27 06:06

  本文關(guān)鍵詞： 高壓氧 低氧 低氧耐受 一氧化氮 一氧化氮合酶　出處：《第二軍醫(yī)大學(xué)》2006年碩士論文　論文類(lèi)型：學(xué)位論文

【摘要】：低氧是多種疾病如心、肺疾病、中風(fēng)及腫瘤的主要病理生理反應(yīng)。經(jīng)典的誘導(dǎo)低氧耐受的方法為低氧預(yù)適應(yīng)。大量研究表明,高壓氧(hyperbaric oxygen,HBO)和低氧適應(yīng)性暴露都可增強(qiáng)機(jī)體抗氧化損傷的能力、預(yù)防動(dòng)物慢性氧中毒、減輕中樞神經(jīng)系統(tǒng)(central nervous system,CNS)缺血性損傷、提高CNS對(duì)HBO的敏感性。同時(shí),我們研究發(fā)現(xiàn),HBO適應(yīng)性暴露可提高機(jī)體耐受低氧損傷的能力,但其誘導(dǎo)機(jī)制尚不清楚。 一氧化氮(nitric oxide,NO)是一種高生物活性的氣體分子,在體內(nèi)發(fā)揮多種生物學(xué)效應(yīng),如神經(jīng)調(diào)節(jié)、舒張血管、細(xì)胞再生,尤其是在改善腦血流、神經(jīng)保護(hù)方面發(fā)揮重要作用,對(duì)腦缺血缺氧具有保護(hù)作用。一氧化氮合酶(nitric oxide synthase,NOS)在體內(nèi)可催化精氨酸生成NO和胍氨酸,NOS的含量及活性直接影響體內(nèi)NO的含量。 NOS活性增強(qiáng),NO生成增多可能通過(guò)以下幾種途徑發(fā)揮對(duì)缺血缺氧腦組織損傷的保護(hù)作用:(1)舒張血管:NO通過(guò)與血管平滑肌細(xì)胞內(nèi)可溶性鳥(niǎo)苷酸環(huán)化酶(soluble guanylyl cyclase,sGC)結(jié)合,引起細(xì)胞內(nèi)環(huán)磷酸鳥(niǎo)苷(cyclic GMP,cGMP)增加并進(jìn)一步激活其下游信號(hào)轉(zhuǎn)導(dǎo)途徑而最終引起血管舒張。同時(shí),NO還能阻止去甲腎上腺素和5-羥色胺等物質(zhì)所引發(fā)的腦動(dòng)脈收縮反應(yīng)。(2)信息傳遞:腦動(dòng)脈由非腎上腺素能非膽堿能(NANC)神經(jīng)支配,NANC神經(jīng)末梢釋放的NO在NANC神經(jīng)與腦血管平滑肌之間的信息傳遞中起著重要的作用。(3)維持血管正常結(jié)構(gòu):主要通過(guò)抑制血管平滑肌增殖,抑制血小板、白細(xì)胞的粘附和聚集,保護(hù)腦血管內(nèi)皮而發(fā)揮作用。(4)與低氧誘導(dǎo)因子-1(hypoxia-inducible factor-1,
[Abstract]:Hypoxia is the main pathophysiological response of many diseases such as heart, lung, stroke and tumor. The classical method of inducing hypoxia tolerance is hypoxic preconditioning. Hyperbaric oxygen (HBO) and hypoxic adaptive exposure can enhance the ability of antioxidant injury, prevent chronic oxygen poisoning in animals, alleviate central nervous system central nervous system ischemic damage, and enhance the sensitivity of CNS to HBO. We found that adaptive exposure to HBO can improve the ability of tolerance to hypoxia injury, but the mechanism of its induction is not clear. Nitric oxide nitric oxide (no) is a highly bioactive gas molecule that plays many biological effects in the body, such as nerve regulation, vasodilation, cell regeneration, especially in improving cerebral blood flow and neuroprotection. Nitric oxide synthase (NOS) can catalyze arginine to produce no and guanidine acid. The enhancement of NOS activity and the increase of no production may play a protective role against ischemic and hypoxic brain tissue injury in the following ways: 1) vasodilator 1) vasodilator: no binds to soluble guanylyl cyclase in vascular smooth muscle cells (VSMCs). It also increases and further activates its downstream signal transduction pathway and eventually results in vasodilation. At the same time, no can prevent the contractility of cerebral artery induced by norepinephrine and serotonin, and other substances, such as norepinephrine and serotonin. (2) Information transduction: the cerebral artery innervated by non-adrenergic, non-cholinergic, NANC- (no) released from the nerve endings of the NANCs plays an important role in the transmission of information between the NANC nerve and the vascular smooth muscle. Mainly by inhibiting the proliferation of vascular smooth muscle, Inhibiting the adhesion and aggregation of platelets, leukocytes, and protecting cerebrovascular endothelium. 4) and hypoxia-inducible factor-1, a hypoxia-inducible factor-1, a hypoxia-inducible factor-1, and hypoxia-inducible factor-1.
【學(xué)位授予單位】：第二軍醫(yī)大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2006
【分類(lèi)號(hào)】：R363

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本文編號(hào)：1541468