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Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học quốc tế cung cấp cho các bạn kiến thức về ngành y đề tài: Renin-angiotensin system activation correlates with microvascular dysfunction in a prospective cohort study of clinical sepsis. | Doerschug et al. Critical Care 2010 14 R24 http ccforum.eom content 14 1 R24 c CRITICAL CARE RESEARCH Open Access Renin-angiotensin system activation correlates with microvascular dysfunction in a prospective cohort study of clinical sepsis Kevin C Doerschug1 Angela S Delsing1 Gregory A Schmidt1 Alix Ashare2 Abstract Introduction 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. Methods 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 . Results 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. Conclusions RAS is activated in clinical severe sepsis. Systemic RAS mediators correlate with measures of .
