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Volume 17 Supplement 4

Sepsis 2013

  • Poster presentation
  • Open Access

Vasopressin secretion in sepsis-surviving animals following dehydration

  • 1,
  • 1 and
  • 1
Critical Care201317 (Suppl 4) :P103

  • Published:


  • Vasopressin
  • Serum Sodium
  • Sham Animal
  • Cecal Ligation
  • Posterior Pituitary Gland


Vasopressin (AVP) plasma levels increase in the early phase of sepsis but remain at basal levels in the late phase of sepsis [1]. It is also known that one-half of septic patients do not properly respond to an osmotic challenge, one of the strongest stimuli for AVP secretion [2]. However, whether these AVP secretion changes persist in sepsis survivors is not known. This study investigated the possible alterations in plasma AVP levels in sepsis-surviving animals.

Materials and methods

Male Wistar rats were separated into two groups: sepsis induced by cecal ligation and puncture (CLP), or sham animals. They received saline solution (50 mg/ml; s.c) immediately and 12 hours after CLP, and also ceftriaxone (30 mg/kg; s.c.) and clyndamicin (25 mg/kg; s.c.) after every 6 hours for 3 days. Sham animals received the volume of saline corresponding to antibiotic administration. After 10 days, the animals were dehydrated or left as control. After 2 days, the animals were decapitated, and the serum and plasma collected for sodium, hematocrit and hormone determination. The posterior pituitary glands were removed for hormone stock analysis.


Sepsis-surviving animals presented a higher serum sodium even without the osmotic stimulus (147.8 ± 0.97 SEM vs. 151.4 ± 0.6 SEM mmol/l CLP; P < 0.001). Following dehydration, as expected, there was an increase of serum sodium in CLP animals (151.4 ± 0.6 SEM vs. 155.71 ± 0.47 SEM mmol/l; P < 0.001) and sham animals (147.8 ± 0.97 SEM vs. 154 ± 0.26 SEM mmol/l dehydrated; P < 0.001) with difference between the groups (154 ± 0.26 SEM vs. 155.71 ± 0.47 SEM mmol/l CLP; P < 0.041). Hematocrit also increased in both CLP (42.63 ± 1.58 SEM vs. 50.17 ± 1.67% SEM dehydrated; P = 0.002) and sham (mean: 41.8 ± 1.43 SEM vs. 49.5 ± 1.0% SEM; P = 0.003) groups but without difference between the groups. The animals responded with an increase in the AVP plasma levels (6.12 ± 0.68 SEM vs. 6.16 ± 0.94 SEM pg/ml CLP, P > 0.05), and a decrease in AVP neurohypophysis stocks (4.0 ± 1.02 SEM vs. 1.91 ± 0.67 SEM ng/μg CLP; P = 0.107), with no difference between the groups.


The results suggest that sepsis-surviving animals do not present alterations in secretion of AVP in relation to volemia. However, serum sodium results suggest that AVP secretion is impaired in sepsis-surviving animals.



Fazal Wahab, Nilton Nascimento dos Santos Junior, Nadir Martins Fernandes, José Antunes Rodrigues and Milene M. Lopes.

Authors’ Affiliations

Department of Morphology, Physiology and Basic Pathology, Faculty of Dentistry of Ribeirão Preto - USP, Ribeirão Preto, Brazil


  1. Correa PB, Pancoto JA, De Oliveira-Pelegrin GR, Carnio EC, Rocha MJ: Participation of iNOS-derived NO in hypothalamic activation and vasopressin release during polymicrobial sepsis. J Neuroimmunol 2007, 183: 17-25. 10.1016/j.jneuroim.2006.10.021View ArticlePubMedGoogle Scholar
  2. Siami S, Bailly-Salin J, Polito A, Porcher R, Blanchard A, Haymann JP, Laborde K, Maxime V, Boucly C, Carlier R, Annane D, Sharshar T: Osmoregulation of vasopressin secretion is altered in the postacute phase of septic shock. Crit Care Med 2010, 38: 1962-1969.PubMedGoogle Scholar


© Tazinafo et al.; licensee BioMed Central Ltd. 2013

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. The Creative Commons Public Domain Dedication waiver ( applies to the data made available in this article, unless otherwise stated.