Abstract
IntroductionIncreased intramucosal–arterial carbon dioxide tension (PCO2) difference (ΔPCO2) is common in experimental endotoxemia. However, its meaning remains controversial because it has been ascribed to hypoperfusion of intestinal villi or to cytopathic hypoxia. Our hypothesis was that increased blood flow could prevent the increase in ΔPCO2.MethodsIn 19 anesthetized and mechanically ventilated sheep, we measured cardiac output, superior mesenteric blood flow, lactate, gases, hemoglobin and oxygen saturations in arterial, mixed venous and mesenteric venous blood, and ileal intramucosal PCO2 by saline tonometry. Intestinal oxygen transport and consumption were calculated. After basal measurements, sheep were assigned to the following groups, for 120 min: (1) sham (n = 6), (2) normal blood flow (n = 7) and (3) increased blood flow (n = 6). Escherichia coli lipopolysaccharide (5 μg/kg) was injected in the last two groups. Saline solution was used to maintain blood flood at basal levels in the sham and normal blood flow groups, or to increase it to about 50% of basal in the increased blood flow group.ResultsIn the normal blood flow group, systemic and intestinal oxygen transport and consumption were preserved, but ΔPCO2 increased (basal versus 120 min endotoxemia, 7 ± 4 versus 19 ± 4 mmHg; P < 0.001) and metabolic acidosis with a high anion gap ensued (arterial pH 7.39 versus 7.35; anion gap 15 ± 3 versus 18 ± 2 mmol/l; P < 0.001 for both). Increased blood flow prevented the elevation in ΔPCO2 (5 ± 7 versus 9 ± 6 mmHg; P = not significant). However, anion-gap metabolic acidosis was deeper (7.42 versus 7.25; 16 ± 3 versus 22 ± 3 mmol/l; P < 0.001 for both).ConclusionsIn this model of endotoxemia, intramucosal acidosis was corrected by increased blood flow and so might follow tissue hypoperfusion. In contrast, anion-gap metabolic acidosis was left uncorrected and even worsened with aggressive volume expansion. These results point to different mechanisms generating both alterations.
Highlights
Increased intramucosal–arterial carbon dioxide tension (PCO2) difference (∆PCO2) is common in experimental endotoxemia
Our results suggest that intramucosal acidosis is related mainly to local hypoperfusion, because the only difference between our groups, in terms of PCO2 difference determinants, was the level of blood flow
Volume expansion prevented the increase in ∆PCO2, implying that intramucosal acidosis is related mainly to local hypoperfusion
Summary
Increased intramucosal–arterial carbon dioxide tension (PCO2) difference (∆PCO2) is common in experimental endotoxemia. Sheep were assigned to the following groups, for 120 min: (1) sham (n = 6), (2) normal blood flow (n = 7) and (3) increased blood flow (n = 6). In experimental models of sepsis, animals with spontaneous elevation of oxygen transport present improved survival [3]. The intramucosal minus arterial carbon dioxide tension (PCO2) gradient (∆PCO2) is considered a sensitive marker of regional gut perfusion [5] and is frequently found in human sepsis and in experimental endotoxemia. Because intramucosal acidosis can appear with normal or increased blood flow, it has been ascribed to a defect in cellular metabolism, namely cytopathic hypoxia [6]. Vasodilators might correct these microcirculatory deficits [8,9,10], but volume expansion or inotropic drugs have often failed to reverse intramucosal acidosis [11,12,13,14]
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