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頁籤選單縮合
題名 | 精氨酸--一氧化氮路徑:從基礎到臨床應用=L-Arginine-NO Pathways: From Bench to Bedside |
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作者 | 林廷燦; Lin, Mike; |
期刊 | 內科學誌 |
出版日期 | 20020400 |
卷期 | 13:2 2002.04[民91.04] |
頁次 | 頁51-78 |
分類號 | 415.121 |
語文 | chi |
關鍵詞 | 一氧化氮; 一氧化氮合成酶; 內皮功能失全; 非對稱性雙甲基精氨酸; 精氨酸一氧化氮路徑; Nitric oxide; Nitric oxide synthase; Endothelial dysfunction; Asymmetrical dimethylarginine; L-arginine-NO pathway; |
中文摘要 | 精氯酸--一氧化氮路徑之發現對於生命科學之影響巨大深遠 , 此點無庸置疑。 1987 年發現一氧化氮是從左旋精氯酸形成更是石破天驚 , 不管是脊椎動物或是人類 , 一氧化氮之"蹤影", 無所不在。事實上 , 一氧化氮可持續在血管內皮 , 腦 部合成 , 而且它在人類疾病之進展上也扮演相當主要之角色 , 包括感染發炎皆會 改變一氧化氮之合成。更由於一氧化氮合成酉每分佈於全身主要器官系統 , 因此 一氧化氮自然扮演多重生理功能之角色。正常人類內皮細胞可持續分泌一氧化氮以維持血管恆定舒張。它可降低切應力 , 減低血管阻力 , 改善局部血流。一旦內皮依賴型血管擴張受損 , 可見於傳統的心 血管危險因子 ( 甚至在無動脈硬化時業可見到 ) 。目前血管超音波之進步 , 可使吾人評估內皮功能益發容易。事實上 , 內皮功能失全與高膽固醇血症、高齡、抽 煙、高血壓、糖尿病以及高同恍氯酸血症習習相關。吾人已知內皮功能失全可發生於早期甚至兒童皆可見到 , 甚至一頓高脂飲食皆可 誘發內皮功能失全。嚴重的內皮功能失全甚至可預估心血管事件之發生 , 連無明 顯狹窄之冠心病人皆可發生。因此內皮功能測試應是心血管評估中一項深具顯著 預估價值 , 此點臨床應用應不能忽略。另外非對稱性雙甲基精氯酸濃度也可誘發 內皮功能失全 , 許多科學証據指陳一氧化氮合成酉每之異常也可導致動脈硬化之 發生。因此吾人歸納內皮受傷機轉如下表:(I) 一氧化氮合成酉每結構及表現異常 (II) 是一氧化氮合成酉每功能異常;(III) 是一氧化氮過量破壞或退化。 (IV)是一氧化氮敏感度降低。 總之本篇旨在介紹精氯酸一一氧化氮路徑之來龍去脈以及發展緣由 , 以及科學根 據 , 那就是改變路徑會影響眾多之生理功能 , 包括內皮功能失全、動脈硬化、免 疫功能以及宿主防禦機轉。 希冀本篇回溯性論文能幫我們完全了解 : 精氯酸-一氧化氮此路徑在預防醫學、 內科醫學以及分子生物學方面全方位基礎臨床應用。 |
英文摘要 | The discovery of the L-arginine-nitric oxide pathway has had many profound impacts on biological science. The enzymatic synthesis of nitric oxide (NO) from L-arginine, which was only discovered in 1987, appears to be very important in nearly every type of vertebrate as well as in human beings. NO is synthesized continually in vascular endothelium and the brain, and many disease processes-particularly those involving infection and inflammation, are associated with altered nitric oxide synthesis. Moreover, the widespread distribution of NO synthase (NOS) enzyme has led to considerable interests in the multiphysiological roles of NO. Normal human endothelial cells continuously produce NO and maintain the vascular system in a basal state of vasodilations. NO reduces shear stress, minimized vascular resistance and optimized regional blood flow. Impaired endothelium-mediated, NO-dependent vasodilatation is associated with traditional cardiovascular risk factors even in the absence of atherosclerosis. The development of noninvasive methods to assess endothelial function has allowed many studies of healthy subjects and also has confirmed independent associations of endothelial dysfunction (ED) with hypercholesteronemia, old age, cigarette smoking, hypertension, diabetes mellitus, and hyperhomocysteinemia. ED occurs early and can be detected even in children or after a single high-fat meal. Further, three major studies also showed that those with severe ED in the absence of obstructive CAD were also at increased risk of any ischemic events. Thus, any ED evaluation remained a significant predictor of any cardiovascular events. As raised ADMA levels appear to cause ED, many scientific observations strengthen the views that derangement of NOS pathway lead to atherogenesis. Thus, we categorized them as follows: (1) NOS structure / expression abnormality; (2) NOS functional impairment; (3) NO excessive destruction or degradation, and (4) NO sensitivity reduction. In summary, this review article is intended as an introduction to this subject describing the rapid development and understanding of the L-arginine-NO system and focusing on many scitific evidences that altered concentration of L-arginine affect NO synthesis and, thereby, affect a wide range of biological functions, including ED, atherogenesis, immune responses and host defenses. We hope this review will help us understand the novel pictures of L-arginive-NO pathway in the field of preventive medicine, internal medicine, and molecular biology. (J Intern Med Taiwan 2002;13:51-78 ) |
本系統之摘要資訊系依該期刊論文摘要之資訊為主。