Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Disorders of Leukocytes01:27

Disorders of Leukocytes

Leukocyte disorders can lead to either leukopenia, characterized by an abnormally low leukocyte count, or leukocytosis, marked by a very high leukocyte number.
Leukopenia may result from bone marrow disorders, autoimmune diseases, and infectious diseases. For example, conditions such as multiple myeloma and aplastic anemia can impair the bone marrow's ability to produce adequate leukocytes. Similarly, autoimmune diseases like lupus and viral infections such as HIV can prompt the immune system...
Inflammation01:38

Inflammation

Overview
Structure and Function of Leukocytes01:21

Structure and Function of Leukocytes

An adult in good health typically has between 4,500 and 11,000 leukocytes, or white blood cells, per microliter of blood, which constitutes about 1% of the total blood volume. Unlike red blood cells, white blood cells contain a nucleus and other cellular organelles but do not have hemoglobin. Most white blood cells reside in connective tissues, particularly in lymphatic organs such as the lymph nodes, with only a small fraction present in circulating blood.
White blood cells protect the body...
Acute Inflammation II: Cellular Phase01:26

Acute Inflammation II: Cellular Phase

The cellular phase of acute inflammation is a tightly orchestrated sequence of events that recruits leukocytes, primarily neutrophils, to sites of tissue injury or infection. Following the initial vascular changes, this phase ensures effective immune cell migration, activation, and function at the affected site to eliminate pathogens and initiate tissue repair.Leukocyte Recruitment CascadeLeukocyte recruitment happens in four steps: margination, adhesion, transmigration, and chemotaxis. Reduced...
Myocarditis I: Introduction01:21

Myocarditis I: Introduction

Myocarditis is inflammation of the myocardium, which is the muscular layer of the heart.EtiologyMyocarditis has a diverse etiology, including a wide range of infectious and non-infectious causes:Infectious CausesViral: Common viruses include Coxsackie A and B, adenovirus, parvovirus B19, enteroviruses, and influenza A.Bacterial: Examples include infections caused by Streptococcus, Staphylococcus, and Mycoplasma species.Rickettsial: Infections like Rocky Mountain spotted fever can result in...
Cytotoxic Edema: Pathophysiology01:21

Cytotoxic Edema: Pathophysiology

Cytotoxic edema is a form of cerebral edema characterized by intracellular swelling of neurons, astrocytes, and other glial cells. It develops when the mechanisms responsible for maintaining ionic gradients across the cell membrane become impaired. Under normal physiological conditions, the sodium–potassium ATPase actively transports sodium ions out of the cell and potassium ions into the cell, preserving osmotic balance and enabling electrical signaling. This pump requires a continuous supply...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

[A balance between surgical management and therapy in a patient with severe sternomediastinitis complicated by heart failure and refractory septic shock].

Khirurgiia·2024
Same author

[The use of autologous platelet-rich plasma in the treatment of chronic pharyngitis].

Vestnik otorinolaringologii·2024
Same author

[A new paradigm for the treatment of sternomediastinitis].

Khirurgiia·2023
Same author

Participation of NO-Dependent Mechanisms in the Effects of Increased Systemic Level of Interleukin-1β on Pial Microvessels under Conditions of Acute Hypoxia.

Bulletin of experimental biology and medicine·2020
Same author

Effects of Vascular Peptide Bioregulator on the Density of Microvascular Network in the Brain Cortex of Aged Rats.

Bulletin of experimental biology and medicine·2016
Same author

Effect of Hypothermia-Induced Respiratory Arrest on Cerebral Circulation in Rats.

Bulletin of experimental biology and medicine·2016

Related Experiment Video

Updated: Jul 16, 2026

Laminar Flow-based Assays to Investigate Leukocyte Recruitment on Cultured Vascular Cells and Adherent Platelets
08:50

Laminar Flow-based Assays to Investigate Leukocyte Recruitment on Cultured Vascular Cells and Adherent Platelets

Published on: April 9, 2018

Leukocytes as a cause of microcirculatory dysfunction.

K P Ivanov1, N N Mel'nikova

  • 1Laboratory for Physiology of Thermoregulation and Bioenergetics, I. P. Pavlov Institute of Physiology, Russian Academy of Sciences, St. Petersburg.

Bulletin of Experimental Biology and Medicine
|March 17, 2007
PubMed
Summary

This study used a special kind of microscopy to observe how white blood cells stick to blood vessels in the brains of rats with ischemic injury. The researchers found that these cells adhered strongly to the walls of pial veins, which are part of the brain's microcirculation. This adhesion was most noticeable in areas with reduced blood flow. The findings suggest that this sticking may be a response to the injury and could contribute to poor blood flow. The study does not claim that this is the only cause of microcirculatory dysfunction but highlights the need for further research to explore this link.

Keywords:
Leukocyte adhesionCerebral microcirculationIschemic injuryVital microscopy

Frequently Asked Questions

More Related Videos

A Microphysiological System to Study Leukocyte-Endothelial Cell Interaction during Inflammation
12:55

A Microphysiological System to Study Leukocyte-Endothelial Cell Interaction during Inflammation

Published on: December 9, 2021

Assessing Leukocyte-endothelial Interactions Under Flow Conditions in an Ex Vivo Autoperfused Microflow Chamber Assay
09:01

Assessing Leukocyte-endothelial Interactions Under Flow Conditions in an Ex Vivo Autoperfused Microflow Chamber Assay

Published on: December 30, 2014

Related Experiment Videos

Last Updated: Jul 16, 2026

Laminar Flow-based Assays to Investigate Leukocyte Recruitment on Cultured Vascular Cells and Adherent Platelets
08:50

Laminar Flow-based Assays to Investigate Leukocyte Recruitment on Cultured Vascular Cells and Adherent Platelets

Published on: April 9, 2018

A Microphysiological System to Study Leukocyte-Endothelial Cell Interaction during Inflammation
12:55

A Microphysiological System to Study Leukocyte-Endothelial Cell Interaction during Inflammation

Published on: December 9, 2021

Assessing Leukocyte-endothelial Interactions Under Flow Conditions in an Ex Vivo Autoperfused Microflow Chamber Assay
09:01

Assessing Leukocyte-endothelial Interactions Under Flow Conditions in an Ex Vivo Autoperfused Microflow Chamber Assay

Published on: December 30, 2014

Area of Science:

  • Neurovascular physiology
  • Inflammatory response mechanisms
  • Cerebral microcirculation

Background:

It was already known that leukocytes can interact with blood vessel walls during injury. However, the extent of their adhesion in pial veins during brain ischemia remained unclear. Prior research has shown that such adhesion may contribute to impaired blood flow. No prior work had resolved the specific role of leukocytes in microcirculatory dysfunction. This gap motivated the use of vital microscopy to observe real-time interactions. Researchers sought to determine if leukocyte adhesion correlates with reduced perfusion. The study aimed to clarify whether this adhesion is a cause or a consequence of ischemic damage. Understanding this could help identify new approaches to manage cerebral ischemia.

Purpose Of The Study:

The researchers aimed to investigate the role of leukocyte adhesion in microcirculatory dysfunction following brain ischemia. They focused on pial veins in rats to assess the extent of adhesion. The study's goal was to determine if this adhesion correlates with impaired blood flow. By using vital microscopy, they could observe dynamic interactions in real time. The motivation was to clarify whether leukocyte adhesion is a direct contributor to ischemic injury. This could help distinguish between cause and effect in microcirculatory failure. The study also aimed to quantify the degree of adhesion in ischemic conditions. These findings could inform future strategies to mitigate microcirculatory dysfunction.

Main Methods:

The study used vital microscopy to observe live tissue in real time. Researchers focused on pial veins in rats with induced brain ischemia. They tracked leukocyte behavior in response to ischemic injury. The method allowed for direct visualization of adhesion events. No invasive procedures were used beyond the initial injury induction. The setup enabled continuous monitoring of microcirculatory changes. The researchers recorded adhesion frequency and distribution patterns. This approach provided insights into the dynamics of leukocyte-endothelium interactions.

Main Results:

The study found significant leukocyte adhesion to pial vein endothelium in ischemic rats. Adhesion was most prominent in regions with reduced blood flow. The extent of adhesion correlated with the severity of ischemic injury. Vital microscopy captured real-time adhesion events with high precision. No spontaneous detachment was observed during the monitoring period. The adhesion was localized primarily to post-capillary venules. The findings suggest a direct link between adhesion and microcirculatory dysfunction. These results support the hypothesis that leukocyte adhesion contributes to impaired perfusion.

Conclusions:

The authors propose that leukocyte adhesion to pial veins may contribute to microcirculatory dysfunction. Their findings suggest a correlation between adhesion and reduced blood flow. The study supports the idea that this adhesion is a response to ischemic injury. The results do not establish causation but suggest a potential mechanism. The researchers emphasize the need for further studies to confirm these findings. They suggest that adhesion may be a key factor in post-ischemic perfusion deficits. The study does not claim that leukocyte adhesion is the sole cause of dysfunction. The authors recommend additional research to explore therapeutic interventions.

The study found that leukocytes adhere to pial vein endothelium in rats with brain ischemia.

They used vital microscopy to visualize adhesion in real time in live animals.

Pial veins are part of the cerebral microcirculation and are accessible for microscopic observation.

Adhesion may indicate impaired blood flow and a response to ischemic injury.

No spontaneous detachment was observed during the monitoring period.

The authors suggest that leukocyte adhesion may contribute to microcirculatory dysfunction.