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Related Experiment Videos

Vasoactive mediators and splanchnic perfusion

P M Reilly1, G B Bulkley

  • 1Department of Surgery, Johns Hopkins Medical Institutions, Baltimore, MD.

Critical Care Medicine
|February 1, 1993
PubMed
Summary
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Circulatory shock causes mesenteric vasoconstriction via the renin-angiotensin axis. While beneficial in mild shock, severe shock can lead to gut barrier dysfunction and organ failure, with angiotensin II playing a key role.

Area of Science:

  • Physiology
  • Hemodynamics
  • Gastroenterology

Background:

  • Circulatory shock triggers complex physiological responses.
  • The splanchnic circulation's role in shock is critical for organ perfusion.
  • Understanding splanchnic hemodynamic changes is vital for managing shock.

Purpose of the Study:

  • To provide an overview of the splanchnic hemodynamic response to circulatory shock.
  • To elucidate the role of the renin-angiotensin axis in splanchnic vasoconstriction during shock.
  • To examine the consequences of splanchnic hypoperfusion in severe shock.

Main Methods:

  • Literature review of studies on splanchnic hemodynamics in shock.
  • Inclusion of both clinical and animal model studies.

Related Experiment Videos

  • Data abstraction from relevant published articles.

    • Main Results:

    • Splanchnic shock response involves mesenteric vasoconstriction mediated by the renin-angiotensin axis.
    • Mild-to-moderate shock benefits from this vasospasm, preserving vital organ perfusion.
    • Severe shock can lead to gut barrier compromise, hemorrhagic gastritis, ischemic colitis, and hepatitis.

    Conclusions:

    • Angiotensin II is a primary mediator of splanchnic vasoconstriction in shock.
    • This effect contributes to decreased mesenteric perfusion and potential organ failure post-cardiac surgery.
    • Splanchnic hypoperfusion is linked to multiple organ failure syndrome in 1-5% of cardiac surgery patients.