Increased intestinal permeability in endotoxic pigs. Mesenteric hypoperfusion as an etiologic factor
M. P. Fink, J. B. Antonsson, H. L. Wang and H. R. Rothschild
Department of Surgery, University of Massachusetts Medical Center, Worcester 01655.
Infusing pigs with lipopolysaccharide (LPS) decreases superior mesenteric
artery blood flow (Qsma), suggesting that mesenteric hypoperfusion may be
responsible for LPS-induced alterations in gut mucosal permeability. To
test this hypothesis, we studied four groups of anesthetized swine. Group 1
animals (N = 6) were infused with LPS (250 micrograms/kg over 1 hour
beginning at 60 minutes) and continuously resuscitated with Ringer's
lactate (48 mL/kg per hour). In group 2 (N = 5), Qsma was decreased by 50%
by means of a mechanical occluder to mimic the LPS-induced alterations in
Qsma observed in group I. Group 3 (N = 5) was included to document our
ability to detect ischemia/reperfusion-induced alterations in mucosal
permeability; in these pigs, Qsma was decreased in steps to zero flow (at
150 to 210 minutes) and then perfusion was restored (at 210 to 270
minutes). Pigs in group 4 (N = 6) served as normal controls; these animals
were resuscitated with Ringer's lactate at the same rate as in group 1 but
were not infused with LPS. To assess mucosal permeability, we measured
plasma-to-lumen clearances for two markers, chromium 51-labeled edetic acid
monohydrate (EDTA) and urea. Loading and maintenance infusions of the
markers were given intravenously, and a 20-cm isolated segment of small
intestine was continuously perfused at 2 mL/min with Ringer's lactate at 37
degrees C. Results were expressed as the ratio of the clearances for the
two probes (CEDTA/CUREA). In group 3, CEDTA/CUREA was 999% +/- 355% of
baseline at 270 minutes. In group 1, CEDTA/CUREA was 572% +/- 235% of
baseline at 270 minutes. In groups 2 and 4, however, CEDTA/CUREA did not
change significantly from the baseline value over the duration of the
study. These data suggest that increased mucosal permeability after LPS is
due to factors other than (or in addition to) mesenteric hypoperfusion.
Changes in small intestinal nutrient transport and barrier function after lipopolysaccharide exposure in two pig breeds
Albin et al.
J ANIM SCI 2007;85:2517-2523.
ABSTRACT
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Review article: Organ perfusion/permeability-related effects of norepinephrine and vasopressin in sepsis: [Expose de synthese : Les effets relies a la perfusion et a la permeabilite organique de la norepinephrine et de la vasopressine durant le "sepsis"].
Farand et al.
Canadian J. Anesthesia 2006;53:934-946.
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Serotonin stimulates endotoxin translocation via 5-HT3 receptors in the rat ileum
Yamada et al.
Am. J. Physiol. Gastrointest. Liver Physiol. 2003;284:G782-G788.
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Enteral feeding decreases gut apoptosis, permeability, and lung inflammation during murine endotoxemia
Alscher et al.
Am. J. Physiol. Gastrointest. Liver Physiol. 2001;281:G569-G576.
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The Effects of Olprinone (a Phosphodiesterase III Inhibitor) on Hepatic Vascular Bed in a Porcine Model of Endotoxemia
Nagata et al.
Anesth. Analg. 2001;92:676-680.
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Milrinone improves intestinal villus blood flow during endotoxemia
Schmidt et al.
Canadian J. Anesthesia 2000;47:673-679.
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Mesenteric dysfunction after cardiopulmonary bypass: role of complement C5a
Tofukuji et al.
Ann. Thorac. Surg. 2000;69:799-807.
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DOES STEROID PRETREATMENT INCREASE ENDOTOXIN RELEASE DURING CLINICAL CARDIOPULMONARY BYPASS?
Wan et al.
J. Thorac. Cardiovasc. Surg. 1999;117:1004-1008.
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Increased Intestinal Permeability Is Associated with the Development of Multiple Organ Dysfunction Syndrome in Critically Ill ICU Patients
DOIG et al.
Am. J. Respir. Crit. Care Med. 1998;158:444-451.
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A murine model for studying endotoxemia and the efficacy of anti-LPS agents in an immunocompromised host
Neely et al.
Innate Immunity 1995;2:115-120.
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