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Related Experiment Videos

Nicotine-induced calcium overload during postischemic reperfusion.

S Panagiotopoulos1, W G Nayler

  • 1Department of Medicine, University of Melbourne, Austin Hospital, Heidelberg, Victoria, Australia.

Journal of Cardiovascular Pharmacology
|December 1, 1987
PubMed
Summary

Nicotine worsens calcium (Ca2+) overload in rat hearts during reperfusion after ischemia. This effect was reduced by calcium channel blockers, suggesting a potential therapeutic target for reducing heart damage.

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Area of Science:

  • Cardiovascular Physiology
  • Pharmacology

Background:

  • Excessive calcium (Ca2+) gain during heart reperfusion after ischemia contributes to cell death.
  • Nicotine from cigarette smoke may impact cardiac reperfusion injury.

Purpose of the Study:

  • To investigate if nicotine alters reperfusion-induced Ca2+ gain in isolated rat hearts.
  • To determine the mechanisms underlying nicotine's effect on Ca2+ gain.

Main Methods:

  • Isolated rat hearts were perfused and subjected to normothermic ischemia followed by reperfusion.
  • Nicotine was administered at a concentration mimicking plasma levels after smoking.
  • Calcium (Ca2+) content was measured, and effects of calcium channel blockers (anipamil, verapamil) were assessed.

Main Results:

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  • Nicotine (0.15 microgram/ml) increased Ca2+ gain during reperfusion after 30 or 60 minutes of ischemia.
  • This effect was independent of norepinephrine release, reflow area, heart rate, contractility, or resting tension.
  • Pretreatment with anipamil or verapamil attenuated the nicotine-induced exacerbation of Ca2+ gain.

Conclusions:

  • Nicotine exacerbates reperfusion-induced Ca2+ gain in the heart.
  • This exacerbation is mediated, at least in part, by calcium channels.
  • Nicotine's detrimental effect on cardiac reperfusion injury may be mitigated by calcium channel blockers.