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Desmopressin improves intestinal functional capillary density and decreases leucocyte activation in experimental endotoxemia in the rat

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Critical Care201115 (Suppl 1) :P256

  • Published:


  • Vasopressin
  • Desmopressin
  • Microvascular Perfusion
  • Functional Capillary Density


The vasopressin analogue desmopressin (DDAVP), a selective agonist of the vasopressin V2 receptor, is known to cause vasodilatation in addition to its haemostatic effects. To verify whether desmopressin could be beneficial in sepsis we investigated its effects on intestinal microcirculation in experimental endotoxemia in rats.


In Lewis rats (six groups, 10 animals each) the effects of vasopressin (VAS) (0.06 U/340 g/minute) and DDAVP (1 μg/kg/ml) on the terminal ileum microcirculation 2 hours after introducing endotoxemia (5 mg/kg lipopolysaccharide (LPS), i.v.) were examined using intravital fluorescence microscopy.


Although desmopressin administration (DES-group) increased the number of rolling leucocytes in V3 venules (P < 0.05 vs. CON-group), the number of firmly adhering leucocytes in V1 venules of the LPS-group was significantly reduced (LPS-group: 259 ± 25.7 vs. LPS+DES-group: 203 ± 17.2 n/mm2; P < 0.05) (Figure 1). Additionally, DDAVP treatment improved impaired functional capillary density (FCD) following LPS in all examined intestinal layers (P < 0.001 vs. LPS-group), while the density of nonfunctional capillaries was significantly reduced (P < 0.001 vs. LPS-group). Vasopressin administration deteriorated FCD in endotoxemic and non-endotoxemic rats (P < 0.05 vs. CON-group or LPS-group). Three hours after LPS challenge, TNFα levels were reduced in both DDAVP-treated and vasopressin-treated LPS-groups (LPS-group: 429 ± 119; LPS+DES-group: 262 ± 21.9; LPS+VAS-group: 249 ± 46.5 pg/ml; P < 0.05).
Figure 1
Figure 1

Number of adherent leucocytes in venules ( n /mm 2 ). *P < 0.001 for all LPS vs. all controls; #P < 0.05 for LPS+DES vs. LPS.


Desmopressin administration improved microvascular perfusion and reduced inflammatory response in experimental endotoxemia.

Authors’ Affiliations

Greifswald University, Greifswald, Germany
Dalhousie University, Halifax, Canada


© Wagner et al. 2011

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.