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Updated: Jun 27, 2026
11:53
Cecal Ligation Puncture Procedure
Published on: May 7, 2011
Thermoregulation and vasopressin secretion during polymicrobial sepsis
Gabriela Ravanelli Oliveira-Pelegrin1, Maria Ida Bonini Ravanelli, Luiz Guilherme Siqueira Branco
1Faculdade de Ciências Farmacêuticas, Universidade de São Paulo, Ribeirão Preto, Brazil.
Neuroimmunomodulation
|December 17, 2008
Summary
Experimental sepsis in rats caused hypothermia and altered arginine vasopressin (AVP) secretion. Impaired AVP replenishment, possibly due to nitric oxide (NO) formation, may explain late-phase sepsis dysfunction.
Area of Science:
- Physiology
- Endocrinology
- Sepsis Pathophysiology
Background:
- Sepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection.
- Thermoregulation, hydroelectrolytic balance, and neurohormonal axes are significantly impacted during sepsis.
Purpose of the Study:
- To investigate the temporal changes in thermoregulation, nitric oxide (NO) production, hydroelectrolytic balance, mean arterial pressure (MAP), and arginine vasopressin (AVP) secretion during experimental sepsis.
- To elucidate the relationship between these parameters and survival in a rat model of polymicrobial sepsis.
Main Methods:
- Male Wistar rats underwent cecal ligation and puncture (CLP) to induce sepsis or a sham operation.
- Measurements included survival rates, body temperature (Tb), MAP, and plasma/tissue AVP levels at various time points post-surgery.
- Neurohypophyseal and hypothalamic nuclei AVP content was analyzed.
Main Results:
- CLP induced high mortality, decreased MAP, and increased plasma NO.
- Body temperature initially dropped then increased, while plasma AVP levels showed biphasic increases.
- Neurohypophyseal AVP content depleted, contrasting with elevated AVP in specific hypothalamic nuclei.
Conclusions:
- Early AVP increase in sepsis may be linked to laparotomy and hypotension, potentially contributing to hypothermia.
- Impaired neurohypophyseal AVP replenishment, possibly mediated by elevated NO, may underlie AVP secretion deficits in severe sepsis.
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