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Related Experiment Videos

Opiate action in the pulmonary circulation.

T S Hakim1, M M Grunstein, R P Michel

  • 1Department of Surgery, SUNY Health Science Center, Syracuse 13210.

Pulmonary Pharmacology
|September 1, 1992
PubMed
Summary
This summary is machine-generated.

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Morphine causes pulmonary venoconstriction through histamine release, potentially explaining acute pulmonary edema linked to narcotic abuse. This effect is blocked by naloxone pretreatment.

Area of Science:

  • Pharmacology
  • Pulmonary Medicine
  • Toxicology

Background:

  • Narcotic abuse is associated with acute pulmonary edema.
  • The direct mechanisms linking morphine and pulmonary edema require elucidation.

Purpose of the Study:

  • To investigate the direct effects of morphine on pulmonary vasculature.
  • To identify the mechanisms responsible for morphine-induced pulmonary vascular changes.

Main Methods:

  • Isolated, perfused canine and feline left lower lobe (LLL) preparations were used.
  • Morphine sulfate was administered via the pulmonary artery.
  • Pulmonary vascular resistance (PVR) was measured using the arterial and venous occlusion technique.
  • The roles of alpha-adrenergic receptors, histamine H1 receptors, and opiate receptors were assessed using specific antagonists and naloxone.

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Main Results:

  • Morphine administration (0.6 mg/kg) increased PVR by approximately 100% in both species.
  • The increase in PVR was attributed to pulmonary venoconstriction.
  • The effect of morphine was not influenced by alpha-adrenergic antagonists.
  • Chlorpheniramine reversed the morphine-induced PVR increase.
  • Pretreatment with naloxone blocked the effect of morphine on PVR, while post-treatment did not.

Conclusions:

  • Rapid administration of morphine induces pulmonary venoconstriction.
  • This venoconstriction is mediated by histamine release from the lung.
  • Histamine release is a key mechanism underlying the association between acute pulmonary edema and narcotic abuse.