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  • Poster presentation
  • Open Access

Hydroxyethyl starch but not crystalloid resuscitation improves impairment of intestinal microvascular perfusion during normotensive sepsis

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  • 1,
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  • 2
Critical Care20048 (Suppl 1) :P129

  • Published:


  • Fluid Resuscitation
  • Hydroxyethyl Starch
  • Intravital Microscopy
  • Intestinal Injury
  • Mucosal Atrophy


During sepsis the impairment of gut microvascular perfusion and activation of leukocytes lead to mucosal damage and aggravation of systemic inflammation. Recently, hydroxyethyl starch (HES) has been shown to attenuate deterioration of skin microcirculation in endotoxic hamsters [1]. This study investigates the effects of fluid resuscitation with HES or isotonic saline solution (NaCl) on intestinal microvascular perfusion in a rat model of normotensive endotoxemia.


In anaesthetized rats (n = 7 per group), normotensive sepsis was induced by a continuous infusion of lipopolysaccharide (LPS) (1.5 mg/kg/hour). After 1 hour of LPS infusion, HES 130/0.4 (16 ml/kg) or NaCl (66 ml/kg) were infused for a 1 hour period. Using intravital microscopy, the functional capillary density and erythrocyte velocity were measured in the mucosa of the terminal ileum at baseline, after 1 hour of endotoxemia and 3 hours after fluid resuscitation. Intestinal injury was assessed histologically. In another set of experiments the leukocyte–endothelium interaction was determined in mesenteric venules 3 hours after fluid resuscitation.


Functional capillary density was significantly higher in animals that received HES (994/mm2 vs NaCl 826/mm2, P ≤ 0.001), whereas erythrocyte velocity was not altered considerably in either group. Histologic grading revealed severe mucosal atrophy in the NaCl but not in the HES group (P < 0.001). The number of rolling leukocytes was notably higher in NaCl as compared with HES animals (26/min vs 50/min, P ≤ 0.05).


The results show beneficial effects of HES on microvascular perfusion and mucosal cellular integrity of the gut. A possible mechanism may be the inhibition of the leukocyte–endothelium interaction in the mesenteric circulation.

Authors’ Affiliations

Charité Campus Benjamin Franklin, Berlin, Germany
Klinikum Darmstadt, Germany


  1. Anesthesiology 2002, 97: 460-470. 10.1097/00000542-200208000-00025Google Scholar


© BioMed Central Ltd. 2004