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

Abstract

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 (So 2) levels within normally flowing capillaries would provide evidence of either a mitochondrial failure (increased So 2) or an O2 transport derangement (decreased So 2). 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 So 2 levels from 58.4 ± 20.0 to 38.5 ± 21.2%, whereas capillary arteriolar-end So 2levels 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.