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

R. L.Neville Navaratnam, Stephen E. Morris, Daniel L. Traber, John Flynn, Lee Woodson, Hugo Linares, David N. Herndon

Research output: Contribution to journalArticlepeer-review

90 Scopus citations


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 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 - Injury, Infection and Critical Care
Issue number9
StatePublished - Sep 1990

ASJC Scopus subject areas

  • Surgery
  • Critical Care and Intensive Care Medicine


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