目前敗血症仍為臨床醫療上的重大挑戰，它發生過程中常扮隨氧化壓力、發炎與一氧化氮增加等現象，同時氧化壓力所產生的自由基可傷害細胞膜或DNA，給予抗氧化劑是阻止它們傷害的方式之一，而臨床上常用的麻醉劑Propofol即具有抗氧化作用。
在本論文的第一部分中，我們研究了在大鼠中經由全身注射LPS下氧化傷害與一氧化氮所扮演的不同角色，我們發現氧化傷害是參與敗血症早期與晚期而一氧化氮則主要是在晚期參與心血管的抑制；Propofol做為一短效且快速恢復的麻醉劑，是經由抑制主動脈誘發型一氧化氮合成脢的活化而減少晚期敗血症一氧化氮的大量增加；我們也研究了propofol於敗血症中對血壓頻譜的影響與誘發型一氧化氮合成脢的角色，並得出在較低濃度propofol的給予下，誘發型一氧化氮合成脢產生一氧化氮是參予高頻血壓頻譜與低頻血壓頻譜的表現，但是一旦propofol濃度增加後，一氧化氮於血壓頻譜中的角色則不明顯。由於需要進一步探討propofol於細胞的保護機轉，我們以in vivo (大鼠注射LPS)與in vitro (H9C2,L2與NR8383分別來自大鼠心肌,肺與巨噬細胞株）的方法來探討propofol對敗血症中自由基有關的脢的影響，結果顯示propofol於肺臟上皮細胞(L2)中對誘發型一氧化氮合成脢、superoxide dismutase 與 p47 phox有抑制作用，而對心肌細胞與巨噬細胞則只抑制了誘發型一氧化氮合成脢，既使自由基皆被明顯抑制而減少。
缺血再灌流(IR)亦會產生大量的自由基與細胞激素並引起組織傷害，於臨床上亦不少見。我們以此不同於敗血症的模式來探討propofol對自由基與細胞激素的影響，並與另一種快速甦醒的麻醉劑sevoflurane做比較，豬主動脈夾放手術與豬單核球、兩種血管平滑肌細胞則分別用作in vivo與in vitro實驗模式，結果顯示propofol而非sevoflurane可於單核球細胞與冠狀血管平滑肌細胞中降低自由基的產生，但是於整體動物模式下則無此現象。
在敗血症與缺血再灌流模式下皆會產生大量的自由基與細胞激素，propofol可經由在不同器官的不同細胞中經由抑制不同的氧化脢來表現他的保護角色，然而作為一個麻醉劑，使用者必須十分小心來達到它最大的益處。

Sepsis, a great challenge to the physician, is characterized with massive oxidative stress of tissue, cytokine inflammation and increases in nitric oxide (NO) production. Meanwhile, free radical induced by oxidative stress also injures cell membrane or DNA. The way to terminate free radical chain reaction is to administer antioxidant. The commonly used anesthetic, propofol, was thought to be with antioxidant capacity.
In the first part of this thesis, we investigated the different role of oxidative injury and NO via systemic injection of LPS in rats. We demonstrated oxidative injury is associated with both early and late stage whereas NO is engaged primarily in late stage cardiovascular depression. Propofol, a rapid onset and fast recovery anesthetic, is attributed to protect anainst cardiovascular depression via attenuating the late stage NO surge in aorta by inhibition of iNOS upregulation. We also examine the influence of propofol on temporal changes in power density of frequency components of systemic arterial pressure (SAP) variability in rat with sepsis and the role of inducible NO synthase (iNOS). We have the conclusions that iNOS-induced NO might be involved in the manifestation of high-frequency and low-frequency components of the SAP spectrum during endotoxemia when low-dose propofol is used and the effect of NO is blunted when high-dose propofol is administered. Due to further investigation was needed to the cellular protective mechanisms of propofol, we delineate the effect of propofol to free radical related enzymel involved in sepsis via both in vivo and vitro studies with rats subjected to LPS (15 mg/kg) and H9C2, L2, NR8383 (derived from rat cardiac myocyte, lung, macrophage, respectively), respectively. Our results demonstrated that propofol may play the major protective role on iNOS, superoxide dismutase and p47 phox oxidative enzymes on lung epithelial cells. Propofol also provided protective effects on cardiac myocyte and macrophage with suppression of iNOS only although free radical production were all significantly suppressed.
Ischemia-reperfusion (IR) injury may also produce a lot of free radical and cytokines to cause tissue damage and is common in clinical. We investigated the effect of propofol on free radical and cytokine production via this different model and compared with another rapid recovery anesthesitc, sevoflurane. Aortic decalmping surgery in porcine and their monocyte, aortic and coronary smooth muscle cells were applied for in vivo and in vitro model, respectively. We also demonstrated that propofol but not sevoflurane suppressed the production of free radical and cytokine in monocyte and smooth muscle cells but not in vivo model.
In sepsis and IR model that produced a lot free radical and cytokines, propofol eliminated the free redical and cytokines via suppressed different kinds of oxidative enzymes in different cells of different organs to express its protective role. However, as an anesthetic, propofol must be used carefully to perform its maximal benefit.

封面……………………………………………………………………………….1
論文口試委員審定書……………………………………………………………..2
誌謝辭…………………………………………………………………..……..……3
論文提要
中文摘要…………………………………………………………………….4
Abstract(英文摘要)…………………………………………………….……6
目錄………………………………………………………………………..….……8
圖表目錄……………………………………………………………………….…10
論文正文
一、 Introduction ……………………………………….…………..………...12

二、Differential protection against oxidative stress and nitric oxide overproduction in cardiovascular and pulmonary systems by propofol during endotoxemia …..…………………………………………………18
1. Introduction
2. Materials and methods
3. Results
4. Discussion
三、The influence of propofol on blood pressure spectrum in sepsis and the role of inducible nitric oxide synthase……………………………………….36
1. Introduction
2. Materials and methods
3. Results
4. Discussion
四、The influence of propofol on the expression of various oxidative-related enzymes in sepsis model ……………………………………………….47
1. Introduction
2. Materials and methods
3. Results
4. Discussion
五、The effect of propofol and sevoflurane on antioxidant and proinflammatory cytoline in porcine ischemia-reperfusion model ….……………..……55
1. Introduction
2. Materials and methods
3. Results
4. Discussion
六、General discussion ………………………………………………………63

參考文獻……………………………………….……………………………………………………66

圖表與說明……………………………...………………………………………………………83

附錄(已發表論文) ……………………..…..………………………………………………….123

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