本文選題：心肌 + 保護(hù)　； 參考：《浙江大學(xué)》2005年博士論文

【摘要】：缺血預(yù)處理(ischemic preconditioning,IPC)是一種強(qiáng)有力的內(nèi)源性心肌保護(hù)干預(yù),被眾多研究者所關(guān)注。已經(jīng)發(fā)現(xiàn)腺苷、乙酰膽堿、兒茶酚胺以及阿片肽類等物質(zhì)以及相關(guān)受體參與了IPC的心肌保護(hù)作用,但I(xiàn)PC如何介導(dǎo)保護(hù)的機(jī)理目前尚未明了。最近研究發(fā)現(xiàn),IPC的心肌保護(hù)作用與縫隙連接密切相關(guān),IPC具有使心肌在缺血期間電脫耦聯(lián)延遲作用,這具有很重要的意義,因?yàn)殡娒擇盥?lián)的出現(xiàn)是心肌不可逆損傷開始的標(biāo)志。但其它心肌保護(hù)措施或處理機(jī)制中是否也存在類似的電耦聯(lián)特性的改變,尚未見報(bào)道。我們認(rèn)為,心肌細(xì)胞間的電耦聯(lián)是心臟電生理學(xué)特性的基本元素,也是心肌細(xì)胞在遭受各種應(yīng)激后對抗損傷的關(guān)鍵機(jī)制,因此,我們推測,心肌電耦聯(lián)也很可能是各種心肌保護(hù)措施和藥物的作用靶點(diǎn)。本課題將應(yīng)用縫隙連接脫耦聯(lián)劑heptanol、非特異阿片受體激動(dòng)劑morphine和κ-阿片受體特異激動(dòng)劑U50,488H三種不同處理誘導(dǎo)心肌保護(hù)作用,觀察這三種具有不同特點(diǎn)的處理誘導(dǎo)的心肌保護(hù)中電耦聯(lián)特性的變化,發(fā)現(xiàn)心肌保護(hù)的一般規(guī)律,并探討心肌保護(hù)中電耦聯(lián)特性變化的內(nèi)在機(jī)制。 目的 1.使用縫隙連接脫耦聯(lián)劑heptanol分別在離體心臟水平和整體心臟水平缺血/復(fù)灌前進(jìn)行預(yù)處理,觀察heptanol對離體心臟或整體心臟缺血/復(fù)灌損傷所致的心律失常和梗死面
[Abstract]:Ischemic preconditioning (IPC) is a powerful endogenous myocardial protection intervention, which has been concerned by many researchers. Adenosine, acetylcholine, catecholamine, opioid peptides and related receptors have been found to be involved in the myocardial protection of IPC, but the mechanism of IPC mediated protection is not clear. Recently, it has been found that the myocardial protective effect of IPC is closely related to the gap junction. IPC has the effect of delaying the electrical decoupling of myocardium during ischemia, which is of great significance, because the appearance of electrical decoupling is a sign of the beginning of irreversible myocardial injury. However, it has not been reported whether there is a similar change in electrocoupler characteristics in other myocardial protective measures or mechanisms. We believe that electrical coupling between cardiomyocytes is a fundamental element of cardiac electrophysiology and a key mechanism for cardiomyocytes to resist damage after various stresses, so we conjecture, Electrocardial coupling is also likely to be the target of various myocardial protection measures and drugs. In this study, we used gap junction decoupling agent heptanol, non-specific opioid receptor agonist morphine and 魏 -opioid receptor specific agonist U50488H to induce myocardial protection. The changes of electrical coupling characteristics in myocardial protection induced by these three different treatments were observed, the general laws of myocardial protection were found, and the internal mechanism of the changes of electrical coupling characteristics in myocardial protection was discussed. Purpose 1. The gap junction decoupling agent (heptanol) was used to pretreat the arrhythmias and infarct surfaces of isolated heart and global heart before ischemia / reperfusion, respectively. The effects of heptanol on arrhythmias and infarct surface of isolated heart or whole heart were observed.
【學(xué)位授予單位】：浙江大學(xué)
【學(xué)位級別】：博士
【學(xué)位授予年份】：2005
【分類號】：R33

【參考文獻(xiàn)】

相關(guān)期刊論文 前5條

1 林樹新,范謹(jǐn)之,王復(fù)周;動(dòng)脈壁腦啡肽的含量、存在部位及作用途徑[J];生理學(xué)報(bào);1989年03期

2 張鵬,朱運(yùn)龍,王躍民,李明哲,畢輝,裴建明;к阿片受體選擇性激動(dòng)劑U50488H對大鼠心臟功能的影響[J];中國臨床康復(fù);2004年18期

3 周有林,沈岳良,陳瑩瑩,吳迅冬,夏強(qiáng);缺血預(yù)處理延緩大鼠心肌缺血引起的細(xì)胞間電脫耦聯(lián)[J];中國病理生理雜志;2004年01期

4 劉良明,盧儒權(quán),胡德耀,陳惠,孫陳艷,但飛君;μ,δ,κ阿片受體在創(chuàng)傷失血性休克大鼠心血管功能抑制中的作用[J];中華創(chuàng)傷雜志;1998年04期

5 沈岳良，，夏強(qiáng)，羅建根，陸源，黃德明;多次短暫缺血預(yù)處理的心肌保護(hù)作用[J];浙江醫(yī)科大學(xué)學(xué)報(bào);1995年06期

本文編號：1935362