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1 Vascular Biology Program, Lawson Health Research Institute, London Health Sciences Centre, London, Ontario N6B 1B8; Departments of 2 Medical Biophysics and 3 Anesthesia, University of Western Ontario, London, Ontario N6A 5C1; 4 Department of Medicine, Sunnybrook and Woman's College Hospital, Toronto, Ontario, Canada M4N 3M5; and 5 Shackleton Department of Anesthesia, Southampton University Hospitals NHS Trust, Southampton SO16 6YD, United Kingdom
Inherent in the remote organ injury caused by sepsis is a profound maldistribution of microvascular blood flow. Using a 24-h rat cecal ligation and perforation model of sepsis, we studied O2 transport in individual capillaries of the extensor digitorum longus (EDL) skeletal muscle. We hypothesized that erythrocyte O2 saturation (SO2) levels within normally flowing capillaries would provide evidence of either a mitochondrial failure (increased SO2) or an O2 transport derangement (decreased SO2). Using a spectrophotometric functional imaging system, we found that sepsis caused 1) an increase in stopped flow capillaries (from 10 to 38%, P < 0.05), 2) an increase in the proportion of fast-flow to normal-flow capillaries (P < 0.05), and 3) a decrease in capillary venular-end SO2 levels from 58.4 ± 20.0 to 38.5 ± 21.2%, whereas capillary arteriolar-end SO2 levels remained unchanged compared with the sham group. Capillary O2 extraction increased threefold (P < 0.05) and was directly related to the degree of stopped flow in the EDL. Thus impaired O2 transport in early stage sepsis is likely the result of a microcirculatory dysfunction.
oxygen extraction; oxygen transport; microcirculation; video microscopy; peritonitis
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