Research

Increased blood flow prevents intramucosal acidosis in sheep endotoxemia: a controlled study

Arnaldo Dubin¹ , Gastón Murias² , Bernardo Maskin³ , Mario O Pozo² , Juan P Sottile⁴ , Marcelo Barán⁵ , Vanina S Kanoore Edul⁴ , Héctor S Canales⁶ , Julio C Badie⁴ , Graciela Etcheverry⁷ and Elisa Estenssoro⁸

¹Medical Director, Intensive Care Unit, Sanatorio Otamendi y Miroli, Buenos Aires Argentina

²Staff Physician, Intensive Care Unit, Clinicas Bazterrica y Santa Isabel, Buenos Aires, Argentina

³Medical Director, Intensive Care Unit, Hospital Posadas, Buenos Aires, Argentina

⁴Research Fellow, Cátedra de Farmacología, Facultad de Ciencias Médicas, Universidad Nacional de La Plata, Argentina

⁵Medical Director, Renal Transplantation Unit, CRAI Sur, CUCAIBA, Argentina

⁶Staff Physician, Intensive Care Unit, Hospital San Martin de la Plata, Argentina

⁷Staff Physician, Clinical Chemistry Laboratory, Hospital San Martin de La Plata, Argentina

⁸Medical Director, Intensive Care Unit, Hospital San Martin de la Plata, Argentina

author email corresponding author email

Critical Care 2005, 9:R66-R73doi:10.1186/cc3021

Published:	11 January 2005

See related commentary http://ccforum.com/content/9/2/149

Abstract

Introduction

Increased 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.

Methods

In 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.

Results

In 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).

Conclusions

In 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.