RENIN-ANGIOTENSIN SYSTEM AND VASCULAR REACTIVITY IN SEVERE SEPSIS

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 脓毒症是对感染的全身性炎症反应，并且当存在器官功能障碍时被分类为严重脓毒症。 在严重脓毒症中，微血管对缺血的反应性受损，并且可能导致灌注改变和器官衰竭。 在脓毒症中，肾素-血管紧张素系统被激活，并且有越来越多的证据表明，它有助于动物模型中脓毒症的发病机制。 由于血管紧张素II是一种强血管收缩剂，它可能会导致微血管反应性受损。 这是一项初步研究，旨在评价严重脓毒症受试者中肾素-血管紧张素系统与微血管功能之间的关系。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Sepsis is a systemic inflammatory response to infection, and is classified as severe sepsis when there is organ dysfunction. Microvascular reactivity to ischemia is impaired in severe sepsis, and is likely causal to altered perfusion and organ failure. The renin-angiotensin system is activated in sepsis, and there is mounting evidence that it contributes to the pathogenesis of sepsis in animal models. Because angiotensin II is a strong vasoconstrictor, it may contribute to impaired microvascular reactivity. This is a pilot study to evaluate the relationship between the renin-angiotensin system and microvascular function in human subjects with severe sepsis.