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Related Experiment Videos

Cocaine and cardiovascular toxicity.

C W Schindler1

  • 1Preclinical Pharmacology Laboratory, National Institutes of Health/National Institute on Drug Abuse, Division of Intramural Research, Addiction Research Center, Baltimore 21224, USA. cschindl@helix.nih.gov

Addiction Biology
|January 1, 1996
PubMed
Summary

Cocaine acutely increases heart rate and blood pressure via sympathetic nervous system activation and coronary vasoconstriction. Chronic use can lead to tolerance or sensitization, with pathological heart changes contributing to lethal cardiovascular events.

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Area of Science:

  • Cardiovascular Pharmacology
  • Neuropharmacology

Background:

  • Cocaine significantly impacts cardiovascular function through various mechanisms.
  • Understanding these effects is crucial for managing cocaine toxicity.

Purpose of the Study:

  • To review the cardiovascular effects of cocaine.
  • To elucidate the mechanisms underlying cocaine's cardiac toxicity.

Main Methods:

  • Review of existing literature on cocaine's cardiovascular effects.
  • Analysis of acute and chronic administration studies.
  • Examination of cocaine's impact on the sympathetic nervous system and cardiac electrophysiology.

Main Results:

  • Acute cocaine administration increases blood pressure and heart rate via sympathetic activation, suppresses baroreflex, and causes coronary vasoconstriction.

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  • Higher doses depress ventricular function and slow conduction due to local anesthetic properties, unaffected by anesthesia or acute tolerance.
  • Chronic use may lead to tolerance or sensitization, alongside pathological changes like myocardial necrosis and hypertrophy.

    • Conclusions:

    • Cocaine induces a range of cardiovascular effects, from acute functional changes to chronic pathological alterations.
    • These cardiac effects, exacerbated by metabolites and drug interactions, can result in life-threatening events.