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Differential intestinal microvascular dysfunction occurs during bacteremia

D A Spain1, M A Wilson, R J Krysztopik

  • 1Department of Surgery, University of Louisville School of Medicine, Kentucky, USA.

The Journal of Surgical Research
|January 1, 1997
PubMed
Summary
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Early sepsis rapidly impairs intestinal arteriole function, affecting vasomotion and smooth muscle responses. These microvascular changes precede significant relaxation alterations and may cause gut ischemia.

Area of Science:

  • Vascular Physiology
  • Sepsis Pathophysiology
  • Microcirculation Research

Background:

  • Septic shock is characterized by altered vascular responsiveness, often linked to nitric oxide (NO) overproduction.
  • While large arteries show hyporeactivity in established sepsis, early microvascular changes in visceral arterioles remain unclear.

Purpose of the Study:

  • To investigate early microvascular functional changes in rat intestinal arterioles during acute bacteremia.
  • To assess endothelial-dependent relaxation, vasomotion, and vascular smooth muscle responses in early sepsis.

Main Methods:

  • In vivo microscopy of rat small intestine arterioles.
  • Evaluation of responses to acetylcholine (endothelial-dependent), nitroprusside (endothelial-independent), and norepinephrine (smooth muscle).

Related Experiment Videos

  • Comparison between normal and Escherichia coli-bacteremic rats.

    • Main Results:

    • Acute bacteremia severely impaired arteriole vasomotion, particularly in A1 and A3 vessels.
    • Endothelial-dependent and -independent relaxation (mean diameter) remained unaltered.
    • Norepinephrine response was impaired in A1 arterioles, while A3 arterioles showed altered vasoconstriction sensitivity.

    Conclusions:

    • Bacteremia rapidly induces differential impairment of endothelial-dependent vasomotion and vascular smooth muscle function in intestinal microcirculation.
    • These early microvascular dysfunctions may contribute to sepsis-induced intestinal mucosal ischemia.
    • Findings highlight critical early changes in microvascular tone regulation during sepsis.