Endotoxin (LPS) increases mesenteric vascular resistance (MVR) and bacterial translocation (BT)

R. L N Navaratnam, S. E. Morris, D. L. Traber, J. Flynn, L. Woodson, H. Linares, David Herndon

Research output: Contribution to journalArticle

88 Citations (Scopus)

Abstract

Endotoxemia is responsible for many of the pathophysiologic alterations that occur with Gram-negative sepsis. We utilized a chronic ovine model to determine the hemodynamic disturbances in the gastrointestinal tract during endotoxemia. Sheep with indwelling arterial, venous, and pulmonary arterial catheters were used. An ultrasonic flow probe was placed on the cephalic mesenteric artery. The animals were subjected to: 1) Ringer's lactate infusion (sham n = 6); or 2) 1.5 mcg/kg E. coli endotoxin (n = 6) over a period of one half hour and were monitored for 48 hours. They were then sacrificed and specimens of mesenteric lymph node, liver, spleen, kidney, and lung obtained for bacteriologic cultures and histologic analysis. Sheep receiving endotoxin showed more than 50% reduction in the mesenteric blood flow. Mesenteric vascular resistance increased while non-mesenteric systemic vascular resistance decreased. The increase in the total systemic vascular resistance, noted during endotoxemia, was thus likely due to the increase in the mesenteric vascular resistance. At autopsy there were positive cultures for microorganism in the mesenteric lymph nodes in six out of six sheep with endotoxemia as compared to one out of six of control. Thus the vasoconstriction in the mesenteric areas may have resulted in bacterial translocation from the GI tract.

Original languageEnglish (US)
Pages (from-to)1104-1115
Number of pages12
JournalJournal of Trauma
Volume30
Issue number9
StatePublished - 1990

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Bacterial Translocation
Endotoxemia
Endotoxins
Vascular Resistance
Sheep
Gastrointestinal Tract
Lymph Nodes
Lung
Mesenteric Arteries
Vasoconstriction
Ultrasonics
Autopsy
Sepsis
Spleen
Catheters
Hemodynamics
Head
Escherichia coli
Kidney
Liver

ASJC Scopus subject areas

  • Surgery

Cite this

Navaratnam, R. L. N., Morris, S. E., Traber, D. L., Flynn, J., Woodson, L., Linares, H., & Herndon, D. (1990). Endotoxin (LPS) increases mesenteric vascular resistance (MVR) and bacterial translocation (BT). Journal of Trauma, 30(9), 1104-1115.

Endotoxin (LPS) increases mesenteric vascular resistance (MVR) and bacterial translocation (BT). / Navaratnam, R. L N; Morris, S. E.; Traber, D. L.; Flynn, J.; Woodson, L.; Linares, H.; Herndon, David.

In: Journal of Trauma, Vol. 30, No. 9, 1990, p. 1104-1115.

Research output: Contribution to journalArticle

Navaratnam, RLN, Morris, SE, Traber, DL, Flynn, J, Woodson, L, Linares, H & Herndon, D 1990, 'Endotoxin (LPS) increases mesenteric vascular resistance (MVR) and bacterial translocation (BT)', Journal of Trauma, vol. 30, no. 9, pp. 1104-1115.
Navaratnam RLN, Morris SE, Traber DL, Flynn J, Woodson L, Linares H et al. Endotoxin (LPS) increases mesenteric vascular resistance (MVR) and bacterial translocation (BT). Journal of Trauma. 1990;30(9):1104-1115.
Navaratnam, R. L N ; Morris, S. E. ; Traber, D. L. ; Flynn, J. ; Woodson, L. ; Linares, H. ; Herndon, David. / Endotoxin (LPS) increases mesenteric vascular resistance (MVR) and bacterial translocation (BT). In: Journal of Trauma. 1990 ; Vol. 30, No. 9. pp. 1104-1115.
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