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(Referência obtida automaticamente do Web of Science, por meio da informação sobre o financiamento pela FAPESP e o número do processo correspondente, incluída na publicação pelos autores.)

Increased lipopolysaccharide-induced hypothermia in neurogenic hypertension is caused by reduced hypothalamic PGE(2)production and increased heat loss

Texto completo
Autor(es):
Amorim, Mateus R. [1, 2] ; Moreira, Diego A. [1] ; Santos, Bruna M. [3] ; Ferrari, Gustavo D. [3, 4] ; Nogueira, Jonatas E. [5] ; de Deus, Junia L. [1, 6] ; Alberici, Luciane C. [4] ; Branco, Luiz G. S. [1]
Número total de Autores: 8
Afiliação do(s) autor(es):
[1] Univ Sao Paulo, Dent Sch Ribeirao Preto, Ave Cafe S-N, BR-14040904 Ribeirao Preto, SP - Brazil
[2] Johns Hopkins Univ, Sch Med, Dept Med, Div Pulm & Crit Care Med, Baltimore, MD - USA
[3] Univ Sao Paulo, Med Sch Ribeirao Preto, Ribeirao Preto, SP - Brazil
[4] Univ Sao Paulo, Dept Biomol Sci, Sch Pharmaceut Sci Ribeirao Preto, Ribeirao Preto, SP - Brazil
[5] Univ Sao Paulo, Sch Phys Educ & Sports Ribeirao Preto, Ribeirao Preto, SP - Brazil
[6] Johns Hopkins Univ, Sch Med, Solomon H Snyder Dept Neurosci, Baltimore, MD - USA
Número total de Afiliações: 6
Tipo de documento: Artigo Científico
Fonte: JOURNAL OF PHYSIOLOGY-LONDON; AUG 2020.
Citações Web of Science: 0
Resumo

Key points The mechanisms involved in hypothermia and fever during systemic inflammation (SI) remain largely unknown. Our data support the contention that brain-mediated mechanisms are different in hypertension during SI. Considering that, clinically, it is not easy to assess all mechanisms involved in cardiovascular and thermoregulatory control during SI, the present study sheds light on these integrated mechanisms that may be triggered simultaneously in septic hypertensive patients. The result obtained demonstrate that, in lipopolysaccharide-induced SI, an increased hypothermia is observed in neurogenic hypertension, which is caused by reduced hypothalamic prostaglandin E(2)production and increased heat loss in conscious rats. Therefore, the results of the present study provide useful insight for clinical trials evaluating the thermoregulatory outcomes of septic patients with hypertension. Hypertension is a prevalent disease characterized by autonomic-induced elevated and sustained blood pressure levels and abnormal body core temperature (Tb) regulation. The present study aimed to determine the brain-mediated mechanisms involved in the thermoregulatory changes observed during lipopolysaccharide (LPS)-induced systemic inflammation (SI; at a septic-like model) in spontaneously hypertensive rats (SHR). We combined Tb and skin temperature (Tsk) analysis, assessment of prostaglandin (PG) E(2)levels (the proximal mediator of fever) in the anteroventral region of the hypothalamus (AVPO; an important site for Tb control), oxygen consumption analysis, cardiovascular recordings, assays of inflammatory markers, and evaluation of oxidative stress in the plasma and brain of male Wistar rats and SHR that had received LPS (1.5 mg kg(-1)) or saline. LPS induced hypothermia followed by fever in Wistar rats, whereas, in SHR, a maintained hypothermia without fever were observed. These thermoregulatory responses were associated with an increased heat loss in SHR compared to Wistar rats. We measured LPS-induced increased PGE(2)levels in the AVPO in Wistar rats, but not in SHR. The LPS-induced drop in blood pressure was higher in SHR than in Wistar rats. Furthermore, LPS-induced plasma and brain {[}regions involved in autonomic control: nucleus tractus solitarius (NTS) and rostral ventrolateral medulla (RVLM)] cytokine surges were blunted, whereas oxidative stress was higher in SHR. LPS-induced SI leads to blunted cytokine surges both systemically (plasma) and centrally (NTS and RVLM) and reduced hypothalamic PGE(2)production, which are all associated with increased hypothermia mediated by increased heat loss, but not by heat production, in SHR. (AU)

Processo FAPESP: 17/09878-0 - Efeito da estimulação vagal durante desafio imune por LPS em ratos normotensos e espontaneamente hipertensos
Beneficiário:Mateus Ramos Amorim
Linha de fomento: Bolsas no Brasil - Pós-Doutorado
Processo FAPESP: 16/17681-9 - Alterações fisiopatológicas durante a inflamação sistêmica
Beneficiário:Luiz Guilherme de Siqueira Branco
Linha de fomento: Auxílio à Pesquisa - Temático