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 (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 So₂levels 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.