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Related Experiment Videos

Endothelial dysfunction in trauma patients: a preliminary communication.

Mali Mathru1, John D Lang

  • 1Department of Anesthesiology, University of Texas Medical Branch, Galveston, Texas, USA. mamathru@uab.edu

Shock (Augusta, Ga.)
|September 2, 2005
PubMed
Summary

Trauma resuscitation impairs nitric oxide (NO)-mediated endothelial function in humans. Flow-mediated dilation (FMD) was significantly reduced in trauma patients despite adequate fluid resuscitation, indicating impaired NO bioavailability.

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Area of Science:

  • Cardiovascular Physiology
  • Trauma and Resuscitation Medicine
  • Endothelial Function

Background:

  • Global ischemia and reperfusion generate reactive metabolites, decreasing nitric oxide (NO) bioavailability.
  • Previous studies in animal models show impaired endothelium-dependent relaxation after trauma and resuscitation.
  • The effect on human endothelial function following traumatic hemorrhage and crystalloid resuscitation remains unclear.

Purpose of the Study:

  • To investigate whether endothelium-dependent vasodilation is impaired in human trauma patients after crystalloid resuscitation.
  • To test the hypothesis that impaired endothelium-dependent relaxation occurs despite adequate fluid resuscitation.

Main Methods:

  • Examined NO-mediated, endothelium-dependent flow-mediated dilation (FMD) of the brachial artery.

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  • Compared resuscitated trauma victims (n=13) with normal controls (n=12).
  • Measured baseline brachial artery diameter, FMD induced by reactive hyperemia, and endothelium-independent dilation via nitroglycerin.

    • Main Results:

    • Baseline brachial artery diameter was similar between trauma patients and controls.
    • Brachial artery FMD was significantly impaired in trauma patients (0.8 +/- 1.7 mm) compared to controls (5.7 +/- 0.8 mm).
    • Endothelium-independent dilation induced by nitroglycerin showed no significant difference between groups.

    Conclusions:

    • Endothelium-dependent vasodilation, assessed by FMD, is significantly impaired in trauma patients post-resuscitation.
    • This impairment suggests reduced NO bioavailability despite stable hemodynamics achieved through crystalloid resuscitation.
    • Findings highlight a specific deficit in endothelial function following trauma and resuscitation in humans.