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Related Experiment Videos

Coronary vascular dysfunction associated with direct current shock injury.

Christine L Oltman1, Craig B Clark, Neal L Kane

  • 1The Cardiovascular Center, University of Iowa, Iowa City, IA, USA. christine-oltman@uiowa.edu

Basic Research in Cardiology
|October 14, 2003
PubMed
Summary

Direct current (DC) shocks impair coronary vascular reactivity by causing endothelial dysfunction. Pretreatment with antioxidant enzymes or a nitric oxide synthase inhibitor protected against this damage, suggesting a free radical mechanism.

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Area of Science:

  • Cardiovascular Science
  • Physiology
  • Biochemistry

Background:

  • Direct current (DC) shocks are used for cardioversion and defibrillation.
  • Myocardial injury following DC shocks may involve free radical mechanisms.
  • The impact of DC shocks on coronary vascular reactivity is not fully understood.

Purpose of the Study:

  • To investigate if cardiac injury from DC shocks impairs coronary vascular reactivity.
  • To explore the role of free radicals and nitric oxide synthase in DC shock-induced endothelial dysfunction.

Main Methods:

  • 36 dogs underwent thoracotomy and received either sham or DC shock treatment.
  • Animals were pretreated with antioxidant enzymes (superoxide dismutase and catalase) or a nitric oxide synthase inhibitor (N(G)-nitro-L-arginine).

Related Experiment Videos

  • Epicardial microvessels and conduit arteries were studied in vitro to assess responses to various vasodilators, including acetylcholine.

    • Main Results:

    • DC shocks resulted in impaired dilation to acetylcholine in canine coronary arteries.
    • Treatment with superoxide dismutase/catalase improved acetylcholine-induced dilation, suggesting a role for superoxide radicals.
    • Pretreatment with N(G)-nitro-L-arginine also improved vascular function after DC shock.

    Conclusions:

    • DC shocks induce endothelial dysfunction in canine coronary arteries, characterized by impaired acetylcholine-mediated dilation.
    • Free radicals, potentially involving endothelial nitric oxide synthase (eNOS), contribute to this dysfunction.
    • Antioxidant enzymes and nitric oxide synthase inhibition offer protection against DC shock-induced vascular injury.