Department of Intensive Care, ICU Research Office, Austin Hospital, 145 Studley Road, Heidelberg, Victoria 3084, Australia.
Department of Medicine, University of Melbourne, Austin Health, Austin Hospital, 145 Studley Road, Heidelberg, Victoria 3084, Australia.
Crit Care Clin. 2019 Apr;35(2):213-227. doi: 10.1016/j.ccc.2018.11.002. Epub 2019 Jan 28.
Classic and nonclassic renin-angiotensin systems (RAS) are 2 sides of an ubiquitous endocrine/paracrine cascade regulating blood pressure and homeostasis. Angiotensin II and angiotensin-converting enzyme (ACE) levels are associated with severity of disease in the critically ill, and are central to the physiology and the pathogenesis of circulatory shock. Angiotensin (1-7) and ACE2 act as an endogenous counterregulatory arm to the angiotensin II/ACE axis. The tissue-based RAS has paracrine effects dissociated from those of the circulating RAS. Exogenous angiotensin II or ACE2 may improve the outcome of septic shock and acute respiratory distress syndrome, respectively.
经典和非经典肾素-血管紧张素系统（RAS）是调节血压和体内平衡的普遍内分泌/旁分泌级联反应的两个方面。血管紧张素 II 和血管紧张素转换酶（ACE）水平与危重病患者的疾病严重程度相关，并且是循环性休克的生理学和发病机制的核心。血管紧张素（1-7）和 ACE2 作为血管紧张素 II/ACE 轴的内源性拮抗性臂发挥作用。基于组织的 RAS 具有与循环 RAS 分离的旁分泌作用。外源性血管紧张素 II 或 ACE2 分别可能改善脓毒性休克和急性呼吸窘迫综合征的预后。
