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Related Experiment Video

Updated: Mar 12, 2026

Ultrasound Assessment of Endothelial Function: A Technical Guideline of the Flow-mediated Dilation Test
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Shock associated with endothelial dysfunction in omental microvessels.

Lewis B Somberg1, David D Gutterman2, Hiroto Miura2

  • 1Division of Trauma/Critical Care, Departments of Medicine and Surgery, Medical College of Wisconsin, Milwaukee, WI, USA.

European Journal of Clinical Investigation
|November 4, 2016
PubMed
Summary

Severe trauma and shock impair microvascular function by increasing reactive oxygen species (ROS) in omental arterioles. This endothelial dysfunction, linked to poor patient outcomes, can be improved by targeting ROS.

Keywords:
(III) tetrakis (4-benzoic acid) porphyrin chloride (MnTBAP)2', 7'-dichlorodihydrofluorescein diacetatedihydroethidineendothelial dysfunctionhaemorrhagic shockmicrovesselsomental fatreactive oxygen species

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Area of Science:

  • Vascular biology
  • Trauma research
  • Endothelial function

Background:

  • Impaired microvascular function is linked to adverse outcomes in various medical conditions.
  • The role of vasodilator responses to acetylcholine (Ach) in severe trauma-induced microvascular dysfunction is not well understood.

Purpose of the Study:

  • To investigate whether vasodilator responses to Ach are impaired in human omental arterioles from patients experiencing severe trauma and shock.
  • To assess the role of reactive oxygen species (ROS) in this dysfunction.

Main Methods:

  • Omental arterioles were obtained from trauma patients (first and second explorative laparotomy) and non-trauma controls.
  • Vasodilator responses to Ach were measured using videomicroscopy after endothelin-1-induced constriction.
  • Reactive oxygen species (ROS) production was quantified using dihydroethidine and DCF-DA fluorescence.
  • The impact of MnTBAP (a ROS scavenger) on Ach-induced vasodilation was evaluated.

Main Results:

  • Omental arterioles from trauma patients showed significantly reduced vasodilator responses to Ach compared to controls.
  • Microvessels from trauma patients exhibited markedly increased production of superoxide and peroxide-related ROS.
  • Pretreatment with MnTBAP significantly improved Ach-induced vasodilation in arterioles from trauma patients.

Conclusions:

  • Severe shock in trauma patients is associated with microvascular endothelial dysfunction and enhanced ROS production in omental tissues.
  • This altered vascular regulation may contribute to an imbalance between local blood supply and demand, worsening tissue perfusion and function.