The OVLT initiates the fall in arterial pressure evoked by high dose lipopolysaccharide: evidence that dichotomous, dose-related mechanisms mediate endotoxic hypotension

J Neuroimmunol. 2015 Aug 15:285:94-100. doi: 10.1016/j.jneuroim.2015.05.023. Epub 2015 May 28.

Abstract

This study tested the hypothesis that lipopolysaccharide (LPS) lowers arterial pressure through two different mechanisms depending on the dose. Previously, we found that a low hypotensive dose of LPS (1mg/kg) lowers arterial pressure by activating vagus nerve afferents. Here we report that hypotension evoked by high dose LPS (15mg/kg) can be prevented by injecting lidocaine into the OVLT but not by vagotomy or inactivation of the NTS. The hypotension produced by both LPS doses was correlated with elevated extracellular norepinephrine concentrations in the POA and prevented by blocking alpha-adrenergic receptors. Thus, initiation of endotoxic hypotension is dose-related, mechanistically.

Keywords: Endotoxin; Lipopolysaccharide; OVLT; Preoptic area; Septic shock.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Arterial Pressure / drug effects
  • Arterial Pressure / physiology*
  • Dose-Response Relationship, Drug
  • Endotoxemia / chemically induced
  • Endotoxemia / physiopathology*
  • Hypotension / chemically induced
  • Hypotension / physiopathology*
  • Lipopolysaccharides / administration & dosage*
  • Lipopolysaccharides / toxicity*
  • Male
  • Organum Vasculosum / drug effects
  • Organum Vasculosum / physiology*
  • Rats
  • Rats, Sprague-Dawley

Substances

  • Lipopolysaccharides