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Related Concept Videos

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...
Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
Transient Ischemic Attack l: Introduction01:26

Transient Ischemic Attack l: Introduction

A transient ischemic attack (TIA) is a brief episode of neurological dysfunction caused by a temporary, focal reduction in cerebral blood flow. Although symptoms resemble those of an ischemic stroke, the interruption in perfusion is short-lived and does not cause permanent infarction. TIAs are clinically important because they often serve as early warning events for future stroke.Mechanisms of Transient Cerebral IschemiaTransient cerebral ischemia may arise through several mechanisms. One...
Hemorrhagic Stroke l: Introduction01:17

Hemorrhagic Stroke l: Introduction

A hemorrhagic stroke is an acute neurological event that occurs when a weakened cerebral blood vessel ruptures, allowing blood to accumulate within or around the brain. The sudden release of blood forms a focal hematoma that increases intracranial pressure, displaces neural tissue, and can obstruct cerebrospinal fluid pathways. These effects may be compounded by intraventricular extension of the hemorrhage, cerebral edema, or compression of adjacent structures, all of which contribute to...
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...
Cardiac Output II: Effect of Stroke Volume on Cardiac Output01:22

Cardiac Output II: Effect of Stroke Volume on Cardiac Output

Cardiac output (CO), the amount of blood the heart pumps per minute, is a parameter in cardiovascular physiology determined by stroke volume and heart rate. Stroke volume, the amount of blood pushed from one of the ventricles per heartbeat, is influenced by preload, afterload, and contractility.
Preload
Preload refers to the initial elongation of the cardiac myocytes before contraction and is related to the volume of blood filling the heart at the end of diastole, or end-diastolic volume. The...

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Related Experiment Video

Updated: May 17, 2026

A Mouse Model of Vascularized Heterotopic Spleen Transplantation for Studying Spleen Cell Biology and Transplant Immunity
08:04

A Mouse Model of Vascularized Heterotopic Spleen Transplantation for Studying Spleen Cell Biology and Transplant Immunity

Published on: June 11, 2019

A transient decrease in spleen size following stroke corresponds to splenocyte release into systemic circulation.

Hilary A Seifert1, Aaron A Hall, Cortney B Chapman

  • 1Department of Molecular Pharmacology and Physiology, School of Biomedical Sciences, Morsani College of Medicine, University of South Florida, Tampa, FL 33612, USA.

Journal of Neuroimmune Pharmacology : the Official Journal of the Society on Neuroimmune Pharmacology
|October 12, 2012
PubMed
Summary
This summary is machine-generated.

Following stroke, spleen cells (splenocytes) migrate to the brain, worsening neurodegeneration. Splenectomy may reduce this neural injury, but further research is needed to understand this splenic response to ischemic injury.

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Isolation and Flow Cytometric Analysis of Immune Cells from the Ischemic Mouse Brain
12:14

Isolation and Flow Cytometric Analysis of Immune Cells from the Ischemic Mouse Brain

Published on: February 12, 2016

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Last Updated: May 17, 2026

A Mouse Model of Vascularized Heterotopic Spleen Transplantation for Studying Spleen Cell Biology and Transplant Immunity
08:04

A Mouse Model of Vascularized Heterotopic Spleen Transplantation for Studying Spleen Cell Biology and Transplant Immunity

Published on: June 11, 2019

Isolation and Flow Cytometric Analysis of Immune Cells from the Ischemic Mouse Brain
12:14

Isolation and Flow Cytometric Analysis of Immune Cells from the Ischemic Mouse Brain

Published on: February 12, 2016

Area of Science:

  • Neuroscience
  • Immunology
  • Pathology

Background:

  • Stroke triggers a proinflammatory splenic response, exacerbating neurodegeneration.
  • Splenectomy has shown potential in reducing neural injury in stroke models.
  • The precise mechanisms of the splenic response to ischemic injury remain unclear.

Purpose of the Study:

  • To investigate splenocyte migration following ischemic stroke.
  • To understand the role of splenocytes in exacerbating neurodegeneration.
  • To utilize in vivo labeling techniques to track cell movement.

Main Methods:

  • Middle cerebral artery occlusion (MCAO) model in rats to induce ischemic stroke.
  • Carboxyfluorescein diacetate succinimidyl ester (CFSE) labeling of splenocytes in vivo.
  • Monitoring spleen size, splenocyte counts in circulation, and brain infiltration.

Main Results:

  • Spleen size significantly decreased 24-48 hours post-MCAO, returning to normal by 96 hours.
  • Increased numbers of labeled lymphocytes, monocytes, and neutrophils were found in blood 48 hours post-MCAO.
  • CFSE-labeled splenocytes, including NK cells, T cells, and monocytes, migrated to the brain vasculature post-MCAO.

Conclusions:

  • Splenocytes enter circulation and migrate to the brain after ischemic injury, contributing to neurodegeneration.
  • The spleen's role in stroke pathology involves releasing immune cells that impact the brain.
  • Targeting splenocyte migration could be a therapeutic strategy for stroke recovery.