Batalhao, Marcelo E.
Fernandes, Marcia H. M. R.
Komegae, Evilin N.
Buqui, Gabriela A.
Lopes, Norberto P.
Gargaglioni, Luciane H.
Carnio, Evelin C.
Steiner, Alexandre A.
Bicego, Kenia C.
Número total de Autores: 10
Afiliação do(s) autor(es):
 Sao Paulo State Univ, Dept Anim Morphol & Physiol, Coll Agr & Vet Sci, Sao Paulo - Brazil
 Natl Inst Sci & Technol Comparat Physiol INCT Fis, Sao Paulo - Brazil
 Univ Sao Paulo, Nursing Sch Ribeirao Preto, Sao Paulo - Brazil
 Sao Paulo State Univ, Dept Anim Sci, Coll Agr & Vet Sci, Sao Paulo - Brazil
 Univ Sao Paulo, Inst Biomed Sci, Dept Immunol, Sao Paulo, SP - Brazil
 Univ Sao Paulo, Fac Pharmaceut Sci Ribeirao Preto, Dept Chem & Phys, Nucleo Pesquisa Prod Nat & Sintet, Sao Paulo - Brazil
Número total de Afiliações: 6
Tipo de documento:
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY;
MAY 15 2016.
Citações Web of Science:
Nitric oxide (NO) plays a role in thermogenesis but does not mediate immune-to-brain febrigenic signaling in rats. There are suggestions of a different situation in birds, but the underlying evidence is not compelling. The present study was designed to clarify this matter in 5-day-old chicks challenged with a low or high dose of bacterial LPS. The lower LPS dose (2 mu g/kg im) induced fever at 3-5 h postinjection, whereas 100 mu g/kg im decreased core body temperature (T-c) (at 1 h) followed by fever (at 4 or 5 h). Plasma nitrate levels increased 4 h after LPS injection, but they were not correlated with the magnitude of fever. The NO synthase inhibitor (NG-nitro-L-arginine methyl ester, L-NAME; 50 mg/kg im) attenuated the fever induced by either dose of LPS and enhanced the magnitude of the Tc reduction induced by the high dose in chicks at 31-32 degrees C. These effects were associated with suppression of metabolic rate, at least in the case of the high LPS dose. Conversely, the effects of L-NAME on Tc disappeared in chicks maintained at 35-36 degrees C, suggesting that febrigenic signaling was essentially unaffected. Accordingly, the LPS-induced rise in the brain level of PGE(2) was not affected by L-NAME. Moreover, L-NAME augmented LPS-induced huddling, which is indicative of compensatory mechanisms to run fever in the face of attenuated thermogenesis. Therefore, as in rats, systemic inhibition of NO synthesis attenuates LPS-induced fever in chicks by affecting thermoeffector activity and not by interfering with immune-to-brain signaling. This may constitute a conserved effect of NO in endotherms. (AU)