Thermoregulation and vasopressin secretion during polymicrobial sepsis.
OBJECTIVE
We investigated the time course of thermoregulation, nitric oxide (NO) formation and hydroelectrolytic alterations, as well as mean arterial pressure and arginine vasopressin (AVP) secretion, in experimental sepsis induced by cecal ligation and puncture (CLP).


METHODS
Male Wistar rats submitted to CLP or a sham operation were divided into 4 groups, as follows: group 1, for survival rate evaluation for 24 h; group 2, for body temperature (Tb) analysis; group 3, for mean arterial pressure registration, and group 4, for blood collection and processing of the neurohypophysis and hypothalamic nuclei 0, 2, 4, 6 and 24 h after surgery. AVP levels and content were measured in plasma, neurohypophysis and the hypothalamic paraventricular and supraoptic nuclei.


RESULTS
Animals which underwent CLP showed high mortality, a progressive decrease in mean arterial pressure and an increase in plasma NO. Tb dropped during the first 4 h and showed a progressive increase 6 h after surgery. Plasma AVP levels increased immediately after CLP surgery and again at 6 h, before returning to basal levels at 24 h. This was followed by a depletion of neurohypophyseal AVP content at 4 h that continued until 24 h. AVP content in the supraoptic nucleus was elevated 24 h after CLP surgery, while in the paraventricular nucleus, an increase was observed at 6 h and 24 h.


CONCLUSIONS
In the present study, laparotomy and hypotension may have been responsible for the increase in plasma AVP in the initial phase of polymicrobial sepsis, and this may have contributed to the observed hypothermia. Moreover, an apparently impaired replenishment of AVP content in the neurohypophysis, possibly due to increased NO formation, may explain the impaired AVP secretion in the late phase of severe sepsis.
Oliveira-Pelegrin
Gabriela Ravanelli
GR
Faculdade de Ciências Farmacêuticas, Universidade de São Paulo, Ribeirão Preto, Brazil.
Ravanelli
Maria Ida Bonini
MI
Branco
Luiz Guilherme Siqueira
LG
Rocha
Maria José Alves
MJ
D000818:Animals; D001127:Arginine Vasopressin / Q000097:blood / Q000378:metabolism*; D001794:Blood Pressure / Q000502:physiology; D001833:Body Temperature Regulation / Q000502:physiology*; D004195:Disease Models, Animal; D018450:Disease Progression; D007022:Hypotension / Q000209:etiology / Q000503:physiopathology; D007031:Hypothalamus / Q000378:metabolism*; D007813:Laparotomy / Q000009:adverse effects; D008297:Male; D009026:Mortality; D009569:Nitric Oxide / Q000096:biosynthesis / Q000097:blood; D010286:Paraventricular Hypothalamic Nucleus / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D018805:Sepsis / Q000097:blood* / Q000382:microbiology / Q000503:physiopathology*; D012772:Shock, Septic / Q000097:blood / Q000382:microbiology / Q000503:physiopathology; D013495:Supraoptic Nucleus / Q000378:metabolism; D015854:Up-Regulation / Q000502:physiology
D001127:Arginine Vasopressin; D009569:Nitric Oxide