本文選題：心臟 + 缺血后處理��； 參考：《浙江大學(xué)》2006年碩士論文

【摘要】：背景: 20世紀(jì)80年代中期,Murry等首次提出心肌在經(jīng)受多次短暫缺血復(fù)灌后能在隨后的長時(shí)間缺血中延遲并減輕心肌損傷,即缺血預(yù)處理(ischemic preconditioning,IP)的心肌保護(hù)作用。但由于這種預(yù)處理需在缺血前施與,而在臨床實(shí)踐中,患者往往在出現(xiàn)嚴(yán)重缺血導(dǎo)致心肌梗塞后就診,使其臨床應(yīng)用價(jià)值受限。2003年Vinten-Johansen實(shí)驗(yàn)室首次提出了缺血后處理的概念。缺血后處理是指在心肌長時(shí)間缺血后,于復(fù)灌初期立即給予心肌反復(fù)多次的短暫的復(fù)灌/停灌,具有明顯的對(duì)抗心臟缺血/復(fù)灌損傷的保護(hù)作用。但缺血后處理的心肌保護(hù)作用機(jī)制尚未完全清楚。研究表明,心臟阿片受體參與缺血預(yù)處理的心肌保護(hù)作用。根據(jù)阿片的生物學(xué)與藥理學(xué)特性,可分為三種受體,分別為Mu(μ)、Kappa(κ)及Delta(δ)三種類型。對(duì)成年大鼠心室肌組織的功能性和轉(zhuǎn)錄水平的研究都表明心室僅有δ和κ阿片受體,而無μ阿片受體。這些受體的激活可產(chǎn)生急性和慢性心臟保護(hù)作用,其中涉及的信號(hào)途徑包括Gi/o蛋白、蛋白激酶C、酪氨酸激酶、絲裂原活化蛋白激酶和ATP敏感性鉀通道等。研究證實(shí),阿片受體的激活導(dǎo)致了線粒體鈣激活鉀通道(mitochondrial calcium activated potassium channel,mKCa)通道開放而發(fā)揮心肌保護(hù)作用。mKCa通道是心肌線粒體膜上存在的通道,已知它的開放是心肌缺血預(yù)處理保護(hù)作用的觸發(fā)機(jī)制之一。因此,我們假設(shè)阿片受體和mKCa通道的開放可能均參予缺血后處理的心肌保護(hù)作用。本實(shí)驗(yàn)旨在探討缺血后處理與缺血預(yù)處理聯(lián)合在嚴(yán)重缺血心臟損傷中的作用,mKCa通道和阿片受體是否參予心肌的缺血后處理的保護(hù)作用。
[Abstract]:Background: in the mid-1980s, Murry et al first proposed that myocardial injury can be delayed and alleviated during subsequent long periods of ischemia after several short periods of ischemia and reperfusion. This is the myocardial protective effect of ischemic preconditioning IP. However, because this kind of preconditioning needs to be applied before ischemia, and in clinical practice, patients often go to hospital after myocardial infarction due to severe ischemia, which limits the clinical application value. In 2003, Vinten-Johansen laboratory first put forward the concept of ischemic post-processing. Post-ischemic treatment is a kind of protection against myocardial ischemia / reperfusion injury, which is given immediately after a long period of ischemia and immediately after reperfusion for several times. However, the mechanism of myocardial protection after ischemic treatment has not been fully understood. Studies have shown that cardiac opioid receptors participate in the myocardial protection of ischemic preconditioning. According to the biological and pharmacological characteristics of opioids, they can be divided into three types: mu (渭) Kappa (魏) and Delta (未). The functional and transcriptional levels of ventricular myocytes in adult rats showed that there were only 未 and 魏 opioid receptors, but no 渭 opioid receptors in the ventricle. The activation of these receptors can produce acute and chronic cardioprotective effects. The signal pathways involved include Giro protein, protein kinase C, tyrosine kinase, mitogen-activated protein kinase and ATP-sensitive potassium channel. It has been demonstrated that the activation of opioid receptors leads to the opening of mitochondrial calcium activated potassium channel (mitochondrial calcium activated potassium channel mKCa) channel, which may play a role in myocardial protection. Its opening is known to be one of the trigger mechanisms of myocardial ischemic preconditioning. Therefore, we hypothesized that the opening of opioid receptor and mKCa channel may be involved in myocardial protection after ischemia. The purpose of this study was to investigate the role of combination of ischemic postconditioning and ischemic preconditioning in the pathogenesis of severe ischemic heart injury and the role of mKCa channel and opioid receptor in the protection of myocardial ischemic postconditioning.
【學(xué)位授予單位】：浙江大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2006
【分類號(hào)】：R363

【引證文獻(xiàn)】

相關(guān)碩士學(xué)位論文 前1條

1 趙麗;舒芬太尼后處理對(duì)大鼠腸缺血再灌注后肝細(xì)胞凋亡的影響[D];山西醫(yī)科大學(xué);2011年

，

本文編號(hào)：2102432