敗血性休克的致病機轉和治療之探討：生理、生化、藥物和藥理的角度

Investigation of Pathogenesis and Treatment of Septic Shock: Different Approaches from Physiology, Biochemistry, Drugs and Pharmacology

吳錦楨(Chin-Chen Wu) ； 陸翔寧(Hsiang-Ning Luk) ； 黃旭山(Hsu-Shan Huang) ； 闕小輝(Sheau-Huei Chueh) ； 林正一(Cheng-I Lin) ； 顏茂雄(Mao-Hsiung Yen)

《Journal of Medical Sciences》 19卷3期 (1998/12) Pp. 135-140

摘要

「敗血性休克（septic shock）」是「敗血症（sepsis）」末期所常見到的一主要症狀，其在臨床上的症狀除了血壓下降（因血管周邊阻力降低），血管對內生性和外給性血管收縮劑有低反應性外;尚有心肌功能降低（心衰竭），周邊組織血流量減少（器官壞死）等現象。它的形成主要是因宿主受到葛蘭氏陰性菌感染，而且往往由於治療不當或不易控制而進一步惡化而來，此一問題是全世界軍陣醫學所重視的主要課題，也是平常為各醫院加護病房中所常見的病例。本綜合論述在扼要的介紹最近十年來，生物醫學界對此課題的了解和研究概況，以作為國內研究此相關課題的參考;其中又以「一氧化氮（nitric oxide, NO）」與敗血性休克間的關係為討論主題。

關鍵字

敗血症 ； 敗血性休克 ； 一氧化氮 ； 活性氧化物

並列摘要

Septic shock is a final common syndrome in the late stage of sepsis. Systemic hypotension associated with the circulatory dysfunction produced by Gram-negative lipopolysaccharide (LPS [endotoxin]) is an important determinant of the morbidity and mortality incurred during the hypo dynamic phase of Gram-negative sepsis. This circulatory failure is also a major cause of death in patients with sepsis and its prognosis is poor in spite of aggressive medical treatment. Clinically septic shock is characterized by a precipitous fall in blood pressure which is not or only temporarily responsive to vasoconstricting catecholamines. In addition preclinical studies have concluded that vascular responsiveness to a variety of vasoconstrictors such as norepinephrine angiotensin Il vasopressin serotomn calimycin and potassium chloride is reduced in tissues treated with endotoxin or from endotoxin-treated animals. This life-threatening clinical occurrence has been associted with a multitude or physiological and pathological abnormalitie, however, the pathogenesis of which is not yet fully understood. Endotoxin, tumor necrosis factor. interleukin-I, platlet activating factor, eicosanoids and nitric oxide (NO) have been reported to be involved in the pathogenesis of septic shock. It has now been proposed that LPS and its endogenous hiological response modifiers promote the release of NO, with the latter hearing responsibility for expressing the hypotensive actions of the former. This hypothesis is based on different lines of evidence, including observations that pharmacological inhibition of the NO synthase enzyme (1) improved blood pressure in patients with septic shock and (2) antagonized the hypotensive response to LPS in laboratory animals. Therefore, this review is focusing the relationship of NO and septic shock in the past decade. This review may be able to raise attention of our medical researcher to study septic shock or sepsis more efficiently.

並列關鍵字

sepsis ； septic shock ； nitric oxide ； reactive nitrogen species