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博碩士論文 etd-0722116-213743 詳細資訊
Title page for etd-0722116-213743
論文名稱
Title
氧化壓力,發炎反應與自律神經在各種中風後急性期與慢性期所扮演的角色
The role of oxidative stress, inflammatory and autonomic reflex in acute and convalescent stage of stroke
系所名稱
Department
畢業學年期
Year, semester
語文別
Language
學位類別
Degree
頁數
Number of pages
107
研究生
Author
指導教授
Advisor
召集委員
Convenor
口試委員
Advisory Committee
口試日期
Date of Exam
2016-07-14
繳交日期
Date of Submission
2016-08-22
關鍵字
Keywords
氧化壓力、發炎反應、自律神經、中風
oxidative stress, stroke, autonomic function, inflammation
統計
Statistics
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The thesis/dissertation has been browsed 5726 times, has been downloaded 26 times.
中文摘要
中風與腦缺血的診斷,在近幾十年影像的發展後,已經有了很大的進展,功能性與結構性的影像使診斷的正確性提高了許多,但是對於治療的成果仍然有許多的進步空間,中風是造成死亡與失能的因子當中非常重要的疾病之一,因此了解其中的病理機轉是非常重要的課題。許多的研究已經知道,中風與腦缺血的區域,有顯著的發炎反應,這些發炎反應伴隨著壞疽的腦損傷,因此了解發炎反應的機轉變成要治療中風非常重要的機轉之一,許多的化學物質和氧化壓力的平衡也都參與了這其中的細胞機轉。
學術研究顯示,缺血性腦中風會有許多的氧化物質產生,而這些氧化物質又進一步的造成了腦部的破壞,了解氧化壓力的濃度與機轉,可以知道哪些病人需要針對氧化壓力提升來做治療,進一步的可以提供病患更確切的治療,要在人體腦缺血的細胞旁邊測得氧化壓力是有其局限性的,因此很多的生化物質變成了可能可以代表氧化壓力的生物指標,而脂質的氧化代謝物是其中最重要的氧化壓力生物標記之一。
對於發生在腦缺血旁局部的發炎反應,中樞神經會有三種不同的路徑因應這樣的發炎反應,第一種是局部的反應,是第一線的局部反應,透過的方式是局部的末梢神經所釋放的神經傳導物質。第二種是區域性乃至全身性的反應,牽涉到自律神經反射,自律神經功能越好,越能夠抑制過多的發炎反應,因為交感神經的末稍有觸及免疫器官,這些免疫器官像是骨髓,胸線都會因為交感神經旺盛而釋放成熟的免疫細胞,副交感神經越強,越能夠避免過多的發炎反應,最後一種全身性的反應,是經由下視丘-腦下垂體-腎上腺體的路徑來作用的,使腎上腺體的皮質分泌皮質醇,這樣的皮質醇也能夠抑制過多的免疫反應。
因此這邊博士學位的研究當中,我們證實了自律神經與氧化壓力和發炎反應的關聯性,並且發現了某些腦區域對於全身自律神經的強度有相關性,可能是有調控的作用。
Abstract
Stroke is an important cause of morbidity and mortality. Although tremendous achievements in the ability to diagnose stroke has been witnessed in the past several decades, the treatment is still not precisional and not satisfactory. It has been demonstrated that brain ischemic change is accompanied by significance of inflammatory response and necrotic brain injury.
Oxidative stress plays one of the important roles in inflammatory pathway. Free radical substances are increased in ischemic stroke and increased oxidative stress is considered as important cause contributes to brain damage.
Central nervous system provides systemic, regional and local routes to modulate the immediate inflammatory response. In local routes, the peripheral nervous system release neuropeptides to participate local inflammation. In regional routes, the autonomic nervous system innervates immune organs such as thymus and bone marrow to modulate inflammation. In systemic routes, hypothalamic-pituitary-adrenal axis release glucocorticoids to control inflammation at a systemic level.
In this study, we observe that there are relationship between autonomic dysfunction and inflammatory titer and there is central autonomic network which may play a role in modulate autonomic function.
目次 Table of Contents
目 錄
論文審定書……………………………………………………………….i
誌謝………………………………………………………………………ii
中文摘要………………………………………………………….……..iii
英文摘要………………………………………..……………………….iv
第 一 章 引言…………………………………………………….….1
1.1 Inflammation …………………………………………………..5
1.2 Oxidative stress ………………………………………………. 10
1.3 Autonomic function evaluation ……………………………… 14
第 二 章 假說………………………………………………………..18
第 三 章 如何探討自律神經,發炎反應與氧化壓力之變化的方法……………………………………………………………………….21
2.1 study design……………………………………………...........22
2.2 Inclusion of internal carotid occlusion patients………………..22
3.3 Subject enrollment……………………………………………..23
3.4 Cardiovascular autonomic function testing…………………….23
3.5 Brain imaging acquisition, processing, and analysis…………..27
3.6 Inflammatory biomarkers………………………………………32
3.7 Oxidative stress and antioxidant biomarkers…………………..33
第 四 章 結果……………………………………………………......34
3.1 Central autonomic network modulating autonomic function……………………………………………..........................35
3.2 Relationship between autonomic function and inflammatory biomarkers………………………………………………………….40
3.3 Relationship between autonomic function and oxidative stress………………………………………………………………..43
第 五 章 討論………………………………………………………..44
4.1 Relationship between brain and cardiovascular function……………………………………………..........................45
4.2 Central autonomic network modulating cardiac function and BRS…………………………………………………………………46
4.3 Relationship between autonomic function and inflammation….51
4.4 Interaction between brain, autonomic function and inflammatory response…………………………………………………………….54
4.5 Relationship between autonomic function and oxidative stress………………………………………………………………..57
4.6 Reactive oxidative stress involved in central autonomic network……………………………………………………………..59
第 六 章 可能的限制………………………………………………..60
第 七 章 未來方向與展望……………………………………………64
參考文獻……………………………………………………….……….68
附錄……………………………………………………………………..83
圖 次
圖1-1 發炎反應與氧化壓力和自律神經系統與血管病變的關係…………………3
圖1-2 發炎反應在血管硬化當中的機轉……………………………………………9
圖1-3 氧化壓力的連續反應與代寫產物…………………………………………..11
圖1-4 因應發炎反應不同神經反應的機轉………………………………………..17
圖1-5 圖解所假設的氧化壓力與發炎反應和自律神經對於中風預後的影響…..19
圖2-1 HR_DB反應的案例………………………………………………………….25
圖2-2 Frequency domain of R-R interval案例………………………………………26
圖2-3 Non-linear transformation of R-R interval 案例……………………………..26
圖2-4 ICAO病患之ASL的表現和中樞自律神經控制區域………………………28
圖2-5 影像定位圈選amygdala位置之過程……………………………………….29
圖2-6影像定位圈選insula位置之過程……………………………………………30
圖2-7影像定位圈選anterior cingulate cortex 位置之過程……………………….31
圖3-1 HRV與BRS_VM之關聯性…………………………………………………40
圖3-2 HRV與Vr之關聯性…………………………………………………………41
圖3-3 HRV與BRS_seq之關聯性…………………………………………………..41
圖3-4 HRV與ICAM之關聯性……………………………………………………..42
圖3-5 HRV與VCAM之關聯性…………………………………………………….42
圖3-5 HRV與TBARS之關聯性…………………………………………………….43
圖4-1 Insula 位置圖………….…………………………………………………….46
圖4-2 Central autonomic network 位置圖………….…………………………….47
圖4-3 Central autonomic network 功能連結圖….……………………………….48
圖4-4 Central autonomic network與自律神經所控制之器官的關聯性圖….…….49
圖4-5 BRS與central autonomic network, HRV與發炎反應的關聯性圖..……….56
圖4-6 氧化壓力與自律神經異常的互為因果圖.………………………………….58
圖4-6 氧化壓力影響central autonomic network圖解…………………………….59
表 次
表1-1 各種發炎反應的功能與特色……...………………………………………4
表1-2 各種氧化壓力的功能與特色……...………………………………………4
表1-3 自律神經反應的臨床意義……...…………………………………………16
表3-1 ICAO 病患與對照組及風險對照組的臨床資料…………………………35
表3-2 ICAO 病患與對照組及風險對照組的自律神經功能有顯著差異………37
表3-3 ICAO 病患預後好壞之間自律神經功能的差別…………………………38
表3-4 ICAO 病患自律神經功能與中央自律神經網絡血流的關聯性…………39
符號說明
ASL Arterial Spin Labeling
BRS Baroreceptor reflex sensitivity
CAM Cell adhesion molecule
HNE 4-hydroxy-2-nonenal
HR_DB Heart Rate Response to Deep Breathing
HRV Heart rate variability
ICAM Intercellular Adhesion Molecule
ICAO Internal carotid arterial occlusion
IL Interleukin
MDA Malondialdehyde
TBARS Thiobarbituric acid reactive substances
TNF Tissue necrotic factor
VCAM Vascular cell adhesion molecule
Vr Valsalva ratio
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