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 Experiment Videos

Microvascular dysfunction in sepsis.

C W Lush1, P R Kvietys

  • 1Department of Physiology, University of Western Ontario, London, Canada.

Microcirculation (New York, N.Y. : 1994)
|May 10, 2000
PubMed
Summary

Sepsis causes microvascular dysfunction by affecting arterioles, capillaries, and venules. This review explores the mechanisms behind sepsis-induced inflammation in these critical circulatory components.

Related Concept Videos

You might also read

Related Articles

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

Sort by
Same author

Neutrophil-endothelial cell interactions during the development of tolerance to ischaemia/reperfusion in isolated cells.

Acta physiologica Scandinavica·2001
Same author

Peritonitis induces rat cardiac myocytes to promote polymorphonuclear leukocyte emigration and activate endothelial cells: effect of lipopolysaccharide pretreatment.

Critical care medicine·2001
Same author

Cardiac myocytes exposed to anoxia-reoxygenation promote neutrophil transendothelial migration.

American journal of physiology. Heart and circulatory physiology·2001
Same author

Neutrophil diapedesis: paracellular or transcellular?

News in physiological sciences : an international journal of physiology produced jointly by the International Union of Physiological Sciences and the American Physiological Society·2001
Same author

Endothelial E- and P-selectin expression in iNOS- deficient mice exposed to polymicrobial sepsis.

American journal of physiology. Gastrointestinal and liver physiology·2001
Same author

Role of endotoxin in the expression of endothelial selectins after cecal ligation and perforation.

American journal of physiology. Regulatory, integrative and comparative physiology·2000

Area of Science:

  • Cardiovascular Science
  • Inflammation Research
  • Sepsis Pathophysiology

Background:

  • Sepsis induces microvascular dysfunction impacting arterioles, capillaries, and venules.
  • Arterioles in sepsis exhibit hyporesponsiveness to vasoactive agents.
  • Capillary perfusion decreases, impairing oxygen diffusion, while venules show inflammatory responses like neutrophil infiltration and protein leakage.

Purpose of the Study:

  • To review emerging mechanisms of sepsis-induced microvascular dysfunction.
  • To analyze these mechanisms within the context of arterioles, capillaries, and venules.

Main Methods:

  • Literature review of emerging views on sepsis and microcirculation.
  • Focus on the three core elements: arterioles, capillaries, and venules.

Main Results:

  • Sepsis impairs arteriolar function, reduces capillary perfusion, and triggers venular inflammation.
  • Polymorphonuclear neutrophil (PMN)-endothelial interactions are observed in microvessels and capillaries of vital organs.
  • All microcirculatory components contribute to sepsis-induced inflammation.

Conclusions:

  • Microvascular dysfunction in sepsis is a complex process involving all three microcirculatory elements.
  • Understanding these mechanisms is crucial for developing targeted therapies for sepsis.

Related Experiment Videos