OXIDATIVE STRESS AND PERFUSION IN SEPSIS

本子项目是利用由NIH/NCRR资助的中心赠款提供的资源的众多研究子项目之一。子项目和研究者（PI）可能已经从另一个NIH来源获得了主要资金，因此可以在其他CRISP条目中表示。列出的机构是中心的，不一定是研究者的机构。严重脓毒症是对感染的炎症反应，与氧化应激和微循环变化有关。过氧化脂质膜是氧化应激的重要产物，干扰细胞正常功能，可导致细胞死亡。虽然脂质过氧化在人类脓毒症中有描述，但对于脓毒症中脂质过氧化与血管舒缩功能障碍之间的关系知之甚少。这些研究人员假设氧化应激引起的脂质过氧化导致进行性内皮细胞损伤、不可逆的血管舒张功能障碍和微血管灌注受损，这对败血症治疗是难治性的。传统的血管舒缩功能测量需要专门的设备和人员，因此难以在研究中使用，例如败血症研究，当受试者无法安排时。这些研究人员设计了一项初步研究，以获得新的无创测量微血管灌注技术的经验。这些技术包括近红外光谱（NIRS）和侧流暗场（SDF）成像。他们将把这些测量结果与脂质过氧化、硒选择素以及器官功能障碍的测量结果进行比较。这些技术可以应用于旨在调查败血症中氧化应激、微血管功能障碍和器官损伤之间关系的正式研究。

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. Severe sepsis is an inflammatory response to infection that is associated with oxidative stress and microcirculatory changes. Peroxidized lipid membranes are an important product of oxidative stress, interfere with normal cell function, and can lead to cell death. Although lipid peroxidation has been described in human sepsis, little is known regarding the relationships between lipid peroxidation and vasomotor dysfunction in sepsis. These investigators hypothesize that lipid peroxidation from oxidative stress leads to progressive endothelial cell injury, irreversible vasomotor dysfunction, and impaired microvascular perfusion that is refractory to therapy sepsis. Traditional measures of vasomotor function require specialized equipment and personnel and are therefore difficult to employ in studies, such as those of sepsis, when subjects cannot be scheduled. These investigators have designed a pilot study to gain experience with new non-invasive techniques of measuring microvascular perfusion. These techniques include Near InfraRed Spectrometry (NIRS) and Sidestream DarkField (SDF) imaging. They will compare these measurements to measures of lipid peroxidation, sE-selectin, as well as organ dysfunction. These techniques can then be applied to formal studies designed to investigate the relationships between oxidative stress, microvascular dysfunction, and organ injury in sepsis.