title: Increased blood flow prevents intramucosal acidosis in sheep endotoxemia: a controlled study.
abstract: BACKGROUND
  Increased intramucosal-arterial carbon dioxide tension (PCO2) difference (DeltaPCO2) 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 DeltaPCO2.
  
  
  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 microg/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 DeltaPCO2 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 DeltaPCO2 (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.
authors.affiliation: Intensive Care Unit, Sanatorio Otamendi y Miroli, Buenos Aires, Argentina. arnaldodubin@speedy.com.ar
authors.forename: Arnaldo
authors.initials: A
authors.lastname: Dubin
authors.forename: Gastón
authors.initials: G
authors.lastname: Murias
authors.forename: Bernardo
authors.initials: B
authors.lastname: Maskin
authors.forename: Mario O
authors.initials: MO
authors.lastname: Pozo
authors.forename: Juan P
authors.initials: JP
authors.lastname: Sottile
authors.forename: Marcelo
authors.initials: M
authors.lastname: Barán
authors.forename: Vanina S Kanoore
authors.initials: VS
authors.lastname: Edul
authors.forename: Héctor S
authors.initials: HS
authors.lastname: Canales
authors.forename: Julio C
authors.initials: JC
authors.lastname: Badie
authors.forename: Graciela
authors.initials: G
authors.lastname: Etcheverry
authors.forename: Elisa
authors.initials: E
authors.lastname: Estenssoro
mesh_terms: D000136:Acid-Base Equilibrium; D000138:Acidosis / Q000378:metabolism / Q000517:prevention & control*; D000818:Animals; D002245:Carbon Dioxide / Q000097:blood / Q000378:metabolism; D003627:Data Interpretation, Statistical; D004195:Disease Models, Animal; D019446:Endotoxemia / Q000097:blood / Q000150:complications*; D004926:Escherichia coli; D004927:Escherichia coli Infections / Q000150:complications*; D007413:Intestinal Mucosa / Q000098:blood supply* / Q000378:metabolism*; D008070:Lipopolysaccharides / Q000008:administration & dosage; D017538:Mesenteric Artery, Superior / Q000502:physiology; D008643:Mesentery / Q000098:blood supply; D010100:Oxygen / Q000097:blood / Q000378:metabolism; D010101:Oxygen Consumption; D012756:Sheep
chemical_list: D008070:Lipopolysaccharides; D002245:Carbon Dioxide; D010100:Oxygen