European surgical research. Europaische chirurgische Forschung. Recherches chirurgicales europeennes · 2014
Portal cytokine response and metabolic markers in the early stages of abdominal sepsis in pigs.
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Haugen O, Ovrebø K K, Elvevoll B, Skutlaberg D H, Syre H, Husby P
Аннотация
BACKGROUND: The portal vein could play a major role in disseminating the local inflammation of acute bacterial peritonitis since it is responsible for the venous drainage of the gastrointestinal tract. We hypothesized that after peritoneal exposure to Escherichia coli, a gradient between the portal and systemic levels of cytokines would be expected.
METHODS: Acute peritonitis was induced by depositing 200 ml of broth with live E. coli in the peritoneal cavity of the animals in the B-group (n = 7). They were then observed for 4 h and compared with a control group (C-group, n = 7). Tumour necrosis factor alpha (TNF-α), interleukin (IL)-6, IL-10 and vascular endothelial growth factor were measured repeatedly in the portal vein and the femoral artery. Portal vein metabolic markers (microdialysis), haemodynamics, biochemistry, plasma volume (PV), fluid shifts and total tissue water content were recorded or calculated.
RESULTS: The intervention led to PV contraction, increased fluid extravasation, increased pulmonary vascular resistance and reduced urinary output in the B-group as compared with the C-group. The levels of glucose in the portal vein were reduced in both study groups with no between-group differences. The levels of TNF-α and IL-6 increased markedly in the portal vein as well as in the systemic circulation of the B-group, but no gradient was seen between them. The corresponding levels of TNF-α and IL-6 remained low and stable in the C-group.
CONCLUSION: The portal vein appears to play a minor role in supplying TNF-α and IL-6 to the systemic circulation after peritoneal exposure to a substantial dose of E. coli.
METHODS: Acute peritonitis was induced by depositing 200 ml of broth with live E. coli in the peritoneal cavity of the animals in the B-group (n = 7). They were then observed for 4 h and compared with a control group (C-group, n = 7). Tumour necrosis factor alpha (TNF-α), interleukin (IL)-6, IL-10 and vascular endothelial growth factor were measured repeatedly in the portal vein and the femoral artery. Portal vein metabolic markers (microdialysis), haemodynamics, biochemistry, plasma volume (PV), fluid shifts and total tissue water content were recorded or calculated.
RESULTS: The intervention led to PV contraction, increased fluid extravasation, increased pulmonary vascular resistance and reduced urinary output in the B-group as compared with the C-group. The levels of glucose in the portal vein were reduced in both study groups with no between-group differences. The levels of TNF-α and IL-6 increased markedly in the portal vein as well as in the systemic circulation of the B-group, but no gradient was seen between them. The corresponding levels of TNF-α and IL-6 remained low and stable in the C-group.
CONCLUSION: The portal vein appears to play a minor role in supplying TNF-α and IL-6 to the systemic circulation after peritoneal exposure to a substantial dose of E. coli.