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Involvement of nitric oxide (NO) and hydrogen sulfide (H2S) in endotoxic shock-associated anapyrexia

Grant number: 13/20266-5
Support type:Scholarships in Brazil - Scientific Initiation
Effective date (Start): January 01, 2014
Effective date (End): December 31, 2014
Field of knowledge:Biological Sciences - Physiology - General Physiology
Principal researcher:Luiz Guilherme de Siqueira Branco
Grantee:Rebeca Miranda de Araújo
Home Institution: Faculdade de Odontologia de Ribeirão Preto (FORP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil

Abstract

The gaseous messenger hydrogen sulfide (H2S) has been described as a modulator of systemic inflammation (SI). H2S basal levels in the preoptic area of the hypothalamus (POA) has been found altered in animal models of SI; moreover, endogenous preoptic H2S has been shown to modulate fever. Interestingly, when SI is severe, a state of shock happens, being called 'endotoxic' shock that one induced by administration of high dose of lipopolysaccharide (LPS). In endotoxic shock, fever is preceded by an adaptive thermoregulatory response: anapyrexia, a regulated fall in deep body temperature (Tb). By considering the fact that endogenous preoptic H2S is a modulator of fever, it seems plausible to hypothesize that this signaling molecule modulates anapyrexia in the medial POA (MPO). The MPO is hierarchically the most important area of the brain for elaborating adaptive thermoregulatory responses (fever and anapyrexia). Like H2S, NO (nitric oxide) has been demonstrated to be an important gaseous modulator not only of the cardiovascular system but also of fever and thermoregulation, acting peripherally or in the central nervous system. Studies have shown that peripheral production of NO favors the increase in body temperature induced by LPS; in contrast, NO central production, in the same conditions, has been shown to play an antipyretic role. However, the role of this gas during anapyrexia has been little studied. We will investigate, therefore, whether (I) central NO modulates anapyrexia; (II) central H2S modulates anapyrexia; and (III) during anapyrexia, NO and/or H2S basal levels are altered in the MPO. (AU)

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