Renin-angiotensin system activation correlates with microvascular dysfunction in a prospective cohort study of clinical sepsis.
Renin-angiotensin system activation correlates with microvascular dysfunction in a prospective cohort study of clinical sepsis.
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DOI：
10.1186/cc8887
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发表时间：
2010
期刊：
影响因子：
--
通讯作者：
Ashare A
中科院分区：
文献类型：
--
作者：
Doerschug KC;Delsing AS;Schmidt GA;Ashare A
以血管反应低下和血流不均匀为特征的微血管失调与脓毒症器官衰竭的发病机制有关。肾素-血管紧张素系统（RAS）影响微血管系统，但RAS与临床脓毒症器官损伤之间的关系仍不清楚。我们检验了我们的假设，即系统性 RAS 介质与临床严重脓毒症中的微血管失调和器官衰竭有关。我们研究了 30 名患有严重败血症的受试者和 10 名健康对照受试者。分析血浆的血浆肾素活性（PRA）和血管紧张素II浓度（Ang II）。使用近红外光谱，我们测量了诱导前臂缺血五分钟后鱼际微血管血红蛋白氧饱和度的增加率。在此过程中，我们评估了反应性充血期间大量微血管血红蛋白流入组织的情况。我们在器官衰竭发生后 24 小时对所有受试者进行了研究。我们在另一个时间点（即识别器官衰竭（早期败血症）后八小时）对 12 名受试者的子集进行了研究。 24小时复苏至临床定义的前负荷和动脉压终点后，脓毒症受试者的Ang II和PRA升高，升高程度与反应性充血期间微血管复氧率呈负相关。早期 RAS 介质与微血管功能障碍相关。早期 Ang II 还与脓毒症第一天器官衰竭的程度相关。 RAS 在临床严重脓毒症中被激活。全身 RAS 介质与微血管失调和器官衰竭的测量相关。
Microvascular dysregulation characterized by hyporesponsive vessels and heterogeneous bloodflow is implicated in the pathogenesis of organ failure in sepsis. The renin-angiotensin system (RAS) affects the microvasculature, yet the relationships between RAS and organ injury in clinical sepsis remain unclear. We tested our hypothesis that systemic RAS mediators are associated with dysregulation of the microvasculature and with organ failure in clinical severe sepsis. We studied 30 subjects with severe sepsis, and 10 healthy control subjects. Plasma was analyzed for plasma renin activity (PRA) and angiotensin II concentration (Ang II). Using near-infrared spectroscopy, we measured the rate of increase in the oxygen saturation of thenar microvascular hemoglobin after five minutes of induced forearm ischemia. In so doing, we assessed bulk microvascular hemoglobin influx to the tissue during reactive hyperemia. We studied all subjects 24 hours after the development of organ failure. We studied a subset of 12 subjects at an additional timepoint, eight hours after recognition of organ failure (early sepsis). After 24 hours of resuscitation to clinically-defined endpoints of preload and arterial pressure, Ang II and PRA were elevated in septic subjects and the degree of elevation correlated negatively with the rate of microvascular reoxygenation during reactive hyperemia. Early RAS mediators correlated with microvascular dysfunction. Early Ang II also correlated with the extent of organ failure realized during the first day of sepsis. RAS is activated in clinical severe sepsis. Systemic RAS mediators correlate with measures of microvascular dysregulation and with organ failure.
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DOI：
10.1152/ajplung.00141.2005
发表时间：
2005-09-01
影响因子：
4.9
作者：
Bechara, RI;Pelaez, A;Guidot, DM
通讯作者：
Guidot, DM
DOI：
10.1164/rccm.200109-016oc
发表时间：
2002-07-01
影响因子：
24.7
作者：
De Backer, D;Creteur, J;Vincent, JL
通讯作者：
Vincent, JL
DOI：
10.1046/j.1365-201x.2000.00713.x
发表时间：
2000-04-01
期刊：
ACTA PHYSIOLOGICA SCANDINAVICA
影响因子：
--
作者：
Boushel, R;Piantadosi, CA
通讯作者：
Piantadosi, CA
影响因子：
5.5
作者：
Itoh, T;Kajikuri, J;Mabuchi, Y
通讯作者：
Mabuchi, Y
影响因子：
8.8
作者：
Levy, MM;Fink, MP;Ramsay, G
通讯作者：
Ramsay, G