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

Inherent in remote organ injury caused by sepsis is a profound maldistribution of microvascular blood flow [1]. Using a 24-hour rat cecal ligation and perforation model of sepsis, we studied oxygen transport in individual capillaries of the extensor digitorum longus (EDL) skeletal muscle. We hypothesized that erythrocyte oxygen saturation (SO₂) levels within normally flowing capillaries would provide evidence of either a mitochondrial failure (increased SO₂) or an oxygen transport derangement (decreased SO₂). Using a spectrophotometric functional imaging system [2] 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%, while capillary arteriolar-end SO₂ levels remained unchanged compared to sham group. Capillary oxygen extraction increased three-fold (P < 0.05) and was directly related to the degree of stopped flow in the EDL. Our results support the hypothesis that tissue capacity to increase O₂ extraction in early sepsis is impaired by a maldistribution of O₂ delivery and not a failure to utilize O₂.