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

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.

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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.