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Related Experiment Videos

Coronary vasomotor dysfunction following hemorrhagic shock.

R J Dignan1, A S Wechsler, E J DeMaria

  • 1Department of Surgery, Medical College of Virginia, Virginia Commonwealth University, Richmond 23298.

The Journal of Surgical Research
|April 1, 1992
PubMed
Summary

Hemorrhagic shock (HS) impairs coronary artery function. This study found that HS reduced both contraction and relaxation in isolated coronary arteries, including endothelium-dependent relaxation.

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Area of Science:

  • Cardiovascular Physiology
  • Hemorrhagic Shock Research
  • Vascular Biology

Background:

  • Myocardial dysfunction and ischemia occur during hemorrhagic shock (HS).
  • In vitro studies of coronary reactivity post-hemorrhage were limited.
  • HS may negatively impact coronary artery function.

Purpose of the Study:

  • To test if in vitro coronary artery contraction and relaxation are impaired by hemorrhagic shock (HS).
  • To investigate the effects of HS on isolated coronary arterial smooth muscle function.

Main Methods:

  • Hemorrhagic shock (HS) induced in awake rats by bleeding to 50 mm Hg for 2 hours.
  • Coronary arterial ring segments analyzed using a small vessel myograph.
  • Comparison of reactivity in HS rats versus control groups (normal, cannulated, non-hypotensive hemorrhage).

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Main Results:

  • HS rats showed impaired coronary smooth muscle contraction to potassium chloride (KCl).
  • Maximum smooth muscle relaxation was significantly lower in HS rats.
  • Endothelium-dependent relaxation was significantly impaired in HS rats compared to controls.

Conclusions:

  • Hemorrhagic shock (HS) is associated with diminished coronary arterial smooth muscle contraction.
  • HS impairs both maximum and endothelium-dependent relaxation in coronary arteries.
  • These findings highlight vascular dysfunction in coronary arteries following HS, independent of neurohumoral factors.