Related Experiment Video

Updated: Jul 16, 2026

Two-vessel Occlusion Mouse Model of Cerebral Ischemia-reperfusion
07:34

Two-vessel Occlusion Mouse Model of Cerebral Ischemia-reperfusion

Published on: March 1, 2019

Peripheral inflammation exacerbates damage after global ischemia independently of temperature and acute brain

Sarah J Spencer1, Abdeslam Mouihate, Quentin J Pittman

  • 1Hotchkiss Brain Institute and Institute of Infection, Immunity and Inflammation, Department of Physiology and Biophysics, Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada. spences@ucalgary.ca

Stroke
|March 31, 2007
PubMed
Abstract

Insights

Concomitant infection worsens brain damage after ischemia. However, lipopolysaccharide-induced damage in rats is independent of fever and acute brain inflammation, suggesting a novel mechanism.

Area of Science:

  • Neuroscience
  • Immunology
  • Pathophysiology

Background:

  • Concomitant infections can worsen cerebral ischemia damage.
  • The roles of fever and inflammation in immune response exacerbation are unclear.

Purpose of the Study:

  • Investigate the interaction between febrile and inflammatory responses post-cerebral ischemia.
  • Determine the relative importance of these components in exacerbating ischemic damage.

Main Methods:

  • Male Sprague-Dawley rats underwent 2-vessel occlusion with hypotension.
  • Rats received intraperitoneal lipopolysaccharide or saline immediately after occlusion.

Main Results:

  • Lipopolysaccharide exacerbated hippocampal cell loss and anxiety-related behaviors.
  • These effects were not linked to body temperature changes.
  • No differences were observed in hippocampal pro-inflammatory cytokine or microglial activation.

Conclusions:

  • Lipopolysaccharide-induced damage after global ischemia is dissociated from temperature and acute brain immune response.
  • The mechanism for enhanced lipopolysaccharide damage is independent of hippocampal cytokine and temperature in this model.

More Related Videos

A Preclinical Controlled Cortical Impact Model for Traumatic Hemorrhage Contusion and Neuroinflammation06:50

A Preclinical Controlled Cortical Impact Model for Traumatic Hemorrhage Contusion and Neuroinflammation

Published on: June 10, 2020

Related Concept Videos

Acute Inflammation III: Local and Systemic Effects01:25

Acute Inflammation III: Local and Systemic Effects

Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...
Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
Bacterial Meningitis II: Pathophysiology01:26

Bacterial Meningitis II: Pathophysiology

Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...
Secondary Spinal Cord Injury llI: Pathophysiology01:25

Secondary Spinal Cord Injury llI: Pathophysiology

Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...
Inflammation01:38

Inflammation

Overview
Acute Inflammation I: Inflammatory Response01:26

Acute Inflammation I: Inflammatory Response

Acute inflammation is a rapid, short-lived physiological response to tissue injury or infection, designed to eliminate harmful agents and initiate repair. This tightly regulated process typically lasts from minutes to several days and is triggered by factors such as microbial invasion, physical trauma, or chemical injury.Recognition and Mediator ReleaseThe inflammatory response begins when resident immune cells—such as mast cells, macrophages, and dendritic cells—detect damage-associated...