OXIDATIVE STRESS AND PERFUSION IN SEPSIS

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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.