Persistent villi hypoperfusion explains intramucosal acidosis in sheep endotoxemia.
OBJECTIVE
To test the hypothesis that persistent villi hypoperfusion explains intramucosal acidosis after endotoxemic shock resuscitation.


METHODS
Controlled experimental study.


METHODS
University-based research laboratory.


METHODS
A total of 14 anesthetized, mechanically ventilated sheep.


METHODS
Sheep were randomly assigned to endotoxin (n = 7) or control groups (n = 7). The endotoxin group received 5 microg/kg endotoxin, followed by 4 microg x kg(-1) x hr(-1) for 150 mins. After 60 mins of shock, hydroxyethylstarch resuscitation was given to normalize oxygen transport for an additional 90 mins.


RESULTS
Endotoxin infusion decreased mean arterial blood pressure, cardiac output, and superior mesenteric artery blood flow (96 +/- 10 vs. 51 +/- 20 mm Hg, 145 +/- 30 vs. 90 +/- 30 mL x min(-1) x kg(-1), and 643 +/- 203 vs. 317 +/- 93 mL x min(-1) x kg(-1), respectively; p < .05 vs. basal), whereas it increased intramucosal-arterial PCO2 (deltaPCO2) and arterial lactate (3 +/- 3 vs. 14 +/- 8 mm Hg, and 1.5 +/- 0.5 vs. 3.7 +/- 1.3 mmol/L; p < .05). Sublingual, and serosal and mucosal intestinal microvascular flow indexes, and the percentage of perfused ileal villi were reduced (3.0 +/- 0.1 vs. 2.3 +/- 0.4, 3.2 +/- 0.2 vs. 2.4 +/- 0.6, 3.0 +/- 0.0 vs. 2.0 +/- 0.2, and 98% +/- 3% vs. 76% +/- 10%; p < .05). Resuscitation normalized mean arterial blood pressure (92 +/- 13 mm Hg), cardiac output (165 +/- 32 mL x min(-1) x kg(-1)), superior mesenteric artery blood flow (683 +/- 192 mL x min(-1) x kg(-1)), and sublingual and serosal intestinal microvascular flow indexes (2.8 +/- 0.5 and 3.5 +/- 0.7). Nevertheless, deltaPCO2, lactate, mucosal intestinal microvascular flow indexes, and percentage of perfused ileal villi remained altered (10 +/- 6 mm Hg, 3.7 +/- 0.9 mmol/L, 2.3 +/- 0.4, and 78% +/- 11%; p < .05).


CONCLUSIONS
In this model of endotoxemia, fluid resuscitation corrected both serosal intestinal and sublingual microcirculation but was unable to restore intestinal mucosal perfusion. Intramucosal acidosis might be due to persistent villi hypoperfusion.
Dubin
Arnaldo
A
Facultad de Ciencias Médicas, Universidad Nacional de La Plata, La Plata, Argentina. arnaldodubin@speedy.com.ar
Edul
Vanina Siham Kanoore
VS
Pozo
Mario Omar
MO
Murias
Gastón
G
Canullán
Carlos Manuel
CM
Martins
Enrique Francisco
EF
Ferrara
Gonzalo
G
Canales
Héctor Saul
HS
Laporte
Mercedes
M
Estenssoro
Elisa
E
Ince
Can
C
D000138:Acidosis / Q000209:etiology* / Q000503:physiopathology; D000818:Animals; D019446:Endotoxemia / Q000150:complications* / Q000503:physiopathology / Q000628:therapy; D007082:Ileum / Q000098:blood supply*; D007413:Intestinal Mucosa / Q000098:blood supply*; D008833:Microcirculation / Q000502:physiology; D009060:Mouth Floor / Q000098:blood supply; D012039:Regional Blood Flow / Q000502:physiology; D012151:Resuscitation; D012756:Sheep; D012772:Shock, Septic / Q000150:complications* / Q000503:physiopathology / Q000628:therapy; D013361:Sublingual Gland / Q000098:blood supply