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Updated: Jun 25, 2026
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A Low Mortality Rat Model to Assess Delayed Cerebral Vasospasm After Experimental Subarachnoid Hemorrhage
Published on: January 17, 2013
Alcohol does not modulate the augmented acetylcholine-induced vasodilatory response in hemorrhaged rodents
Miguel F Molina1, Annie Whitaker, Patricia E Molina
1Department of Physiology and Alcohol and Drug Abuse Center of Excellence, LSU Health Sciences Center, New Orleans, Louisiana 70112, USA.
Shock (Augusta, Ga.)
|February 7, 2009
Summary
Acute alcohol intoxication does not impair blood vessel reactivity to vasoactive agents. However, increased vasodilation may contribute to shock progression in alcohol-intoxicated individuals.
Area of Science:
- Physiology
- Pharmacology
- Toxicology
Background:
- Acute alcohol intoxication (AAI) is known to decrease blood pressure and impair hemodynamic compensation during hemorrhagic shock.
- Previous research suggests AAI may blunt neuroendocrine activation or impair vascular responsiveness.
Purpose of the Study:
- To investigate the effects of AAI, hemorrhagic shock, and resuscitation on the reactivity of isolated blood vessels.
- To determine if impaired vascular responsiveness contributes to hemodynamic instability in AAI.
Main Methods:
- Rats received alcohol or dextrose infusions, followed by sham procedure, hemorrhage, or hemorrhage with resuscitation.
- Thoracic aorta and mesenteric artery ring segments were isolated and tested for reactivity to phenylephrine and acetylcholine using myography.
Main Results:
- AAI alone did not significantly alter pressor or dilator responses in aortic or mesenteric artery rings.
- Hemodynamic counterregulation during hemorrhagic shock in AAI is not attributable to decreased vasopressor responsiveness.
Conclusions:
- Impaired vascular responsiveness is not the primary cause of hemodynamic dysfunction in AAI during hemorrhagic shock.
- Accentuated vasodilatory responses may play a significant role in the progression to decompensatory shock in alcohol-intoxicated individuals.
