Effect of a maldistribution of microvascular blood flow on capillary O2 extraction in sepsis

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 O 2 transport in individual capillaries of the extensor digitorum longus (EDL) skeletal muscle. We hypothesized that erythrocyte O 2 saturation (S O 2 ) levels within normally flowing capillaries would provide evidence of either a mitochondrial failure (increased S O 2 ) or an O 2 transport derangement (decreased S O 2 ). Using a spectrophotometric functional imaging system, we found that sepsis caused 1 ) an increase in stopped flow capillaries (from 10 to 38%, P