BIOLOGICAL VARIATIONS OF REACTIVE HYPEREMIA IN CRITICALLY ILL PATIENTS

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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. Reactive hyperemia (RH) refers to arterial dilation in response to temporary stagnant ischemia, and is mediated in part through release of nitric oxide from endothelial cells. Near Infra-Red Spectroscopy (NIRS) can detect capillary hemoglobin concentration as well as capillary hemoglobin oxygen saturation. Tissue oxygen saturation falls during stagnant ischemia, and rises when flow returns; the rate of increase in tissue oxygen saturation represents reactive hyperemia. Our initial work has shown tht microvascular responses to reactive hyperemia are impaired in some critically ill patients. What is not known is the anatomic variation of these findings, and whether invasive catheters alter the blood flow response distal to the catheter. Furthermore, literature suggests that locally released soluble factors may be responsible for the microvascular responses in reactive hyperemia. We propose a pilot study to examine the anatomic and iatrogenic associated variation of microvascular reactive hyperemia in critically ill patients that have clinically indicated radial arterial catheters. Subjects will have NIRS measurements of reactive hyperemia in three locations, including one leg and both left and right forearms. Blood will be collected (ICU subjects only) before and during reactive hyperemia, simultaneously from arterial and venous catheters that demarcate the monitored tissue bed, and analyzed for candidate soluble factors purported to be associated with reactive hyperemia.