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Effects of morphine on atrial preparations obtained from nonfailing and failing human hearts

F Llobel1, M L Laorden

  • 1Department of Anaesthesiology, University School of Medicine, Murcia, Spain.

Insights

Morphine inhibits auricular myocardium in both healthy and failing human hearts. The failing heart shows significantly reduced responses to morphine, indicating non-opioid receptor involvement in these cardiac effects.

Area of Science:

  • Cardiology
  • Pharmacology
  • Cardiac Physiology

Background:

  • Morphine is an opioid analgesic with known cardiovascular effects.
  • The impact of morphine on human auricular myocardium, particularly in failing hearts, requires further investigation.
  • Understanding drug responses in failing hearts is crucial for patient management.

Purpose of the Study:

  • To investigate the effects of morphine on auricular myocardium from non-failing and failing human hearts.
  • To determine if naloxone antagonizes morphine-induced responses in the myocardium.
  • To compare the sensitivity and maximal response to morphine between failing and non-failing heart preparations.

Main Methods:

  • Myocardial preparations from human non-failing and failing hearts were utilized.
  • Concentration-response curves for morphine were generated.
  • The effect of naloxone on morphine responses was assessed.
  • IC30 values and maximal responses were calculated and compared.

Main Results:

  • Morphine induced inhibition in both non-failing and failing auricular myocardium.
  • Naloxone did not antagonize the observed inhibitory effects of morphine.
  • Preparations from failing hearts exhibited a significant rightward shift in morphine concentration-response curves (P < 0.001).
  • A decreased maximal response to morphine was noted in failing heart preparations.

Conclusions:

  • The cardiac effects of morphine in the auricular myocardium are not mediated by opioid receptors.
  • Failing human hearts demonstrate significantly diminished responsiveness to morphine.
  • These findings highlight altered drug sensitivity in cardiac failure.

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