THE PREOPTIC ANTERIOR HYPOTHALAMIC AREA MEDIATES INITIATION OF THE HYPOTENSIVE RESPONSE INDUCED BY LPS IN MALE RATS

Autor: William R. Millington, Carlos Feleder, Mustafa Sertac Yilmaz
Přispěvatelé: Uludağ Üniversitesi/Tıp Fakültesi/Farmakoloji ve Klinik Farmakoloji Anabilim Dalı., Yılmaz, Mustafa Sertaç, AAH-1571-2021
Rok vydání: 2008
Předmět:
Lipopolysaccharides
Male
Lidocaine
Lateral hypothalamus
Blood Pressure
Critical Care and Intensive Care Medicine
Animal tissue
Rats
Sprague-Dawley

Nitric-oxide
Endotoxin
Mediator release
Septic shock
Medicine
Regulatory mechanism
Anterior hypothalamicnucleus
Sickness behavior
Inhibition
Arterial pressure
Hematology
Brain
Neural mechanism
Peripheral
Emergency Medicine
Hypotension
Halothane
Animal cell
medicine.drug
endocrine system
medicine.medical_specialty
Fever
Hypothalamus
Periaqueductal gray
Lipopolysaccharide
Nucleus
Article
Internal medicine
Animals
Critical care medicine
Illness Behavior
Leukocyte Endogenous Mediator
Antipyretics
Animal model
Animal experiment
Endotoxic shock
Inflammation
Systemic inflammation
Tumor necrosis factor alpha
Tumor Necrosis Factor-alpha
business.industry
medicine.disease
Cardiovascular function
Rats
Blockade
Cardiovascular system & cardiology
Blood pressure
Endocrinology
Stimulation
Peripheral vascular disease
Rat
Surgery
Alpha-msh
General & internal medicine
Preoptic area
Anterior Hypothalamic Nucleus
business
Controlled study
Zdroj: Shock. 29:232-237
ISSN: 1073-2322
DOI: 10.1097/shk.0b013e3180caac7e
Popis: The mechanism responsible for the initiation of endotoxic hypotension is not fully understood, although it is often attributed to a direct effect of LPS and other vasoactive mediators on the vasculature. Alternatively, recent evidence raises the possibility that endotoxic hypotension may be initiated through a central mechanism. Previous studies have shown that LPS initiates fever, sickness behavior, and other aspects of the inflammatory response through a neural pathway that sends peripheral inflammatory signals to the preoptic anterior hypothalamic area (POA). It is also well known that the POA plays a role in the regulation of cardiovascular function, but its involvement in LPS-induced hypotension has not been examined previously. Therefore, the aim of the present paper was to investigate whether the initial abrupt fall in arterial pressure evoked by LPS in septic shock is mediated by the POA. LPS (1 mg/kg, im.) administration to halothane-anesthetized or conscious rats lowered arterial blood pressure by 24.8 +/- 2.9 and 25.1 +/- 5.8 mmHg, respectively. Bilateral lidocaine (2%; 1 mu L) injection into the POA, but not the lateral hypothalamus, prevented the hypotension evoked by LPS entirely in both anesthetized and conscious animals. Remarkably, this blockade significantly inhibited the second, delayed fall in arterial pressure induced by LPS, and simultaneously decreased TNF-alpha plasma levels. Together, these data indicate that the initial phase of endotoxic hypotension is mediated by the POA and suggest that the initiation of the hypotensive response induced by LPS can be essential for the development of the late fall in blood pressure.
Databáze: OpenAIRE