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Related Concept Videos

Analgesia and Pain Management01:25

Analgesia and Pain Management

Pain is critical to various clinical pathologies, provoking an urgent need for effective management. Pain, whether acute or chronic, is a complex neurochemical process. Its alleviation depends on the type, with nonopioid analgesics effective for mild to moderate pain, such as musculoskeletal or inflammatory pain, while neuropathic pain responds best to anticonvulsants, tricyclic antidepressants, or serotonin/norepinephrine reuptake inhibitors. For severe acute or chronic pain, opioids may be...
Opioid Analgesics: Morphine and Other Natural Cogeners01:20

Opioid Analgesics: Morphine and Other Natural Cogeners

Opioids are a class of drugs that mimic endogenous opioid peptides and act on opioid receptors, and help in pain relief. These compounds are classified as natural, synthetic, or semi-synthetic. Natural opioids, like morphine, codeine, and thebaine, are derived from the opium poppy plant (Papaver somniferum or Papaver album) and are termed opiates. Synthetic opioids are artificial, while semi-synthetic opioids combine natural and synthetic compounds. Morphine, a prototypical opioid, possesses a...
Opioid Receptors: Overview01:22

Opioid Receptors: Overview

Opioid receptors, including the mu (μ, MOR), delta (δ, DOR), and kappa (κ, KOR) types, belong to the rhodopsin family of G protein-coupled receptors. These receptors are located throughout the central and peripheral nervous systems and in non-neuronal tissues such as macrophages and astrocytes. Opioid receptor ligands can be categorized into agonists or antagonists. Highly selective agonists include [d-Ala2, MePhe4, Gly(ol)5]-enkephalin or DAMGO for MOR, [D-Pen2, D-Pen5]-enkephalin or DPDPE for...
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Synthetic and semisynthetic opioids are pivotal in pain management and tackling opioid addiction. Semisynthetic opioids, including morphinans (morphine derivatives), oxycodone, oxymorphone, hydrocodone, and hydromorphone, have improved pharmacokinetic profiles compared to morphine. Additionally, heroin and 6-MAM (6-Monoacetylmorphine) show better CNS penetration than morphine due to heightened lipid solubility. Hydromorphone, a potent opioid, undergoes hepatic metabolism to form the active...
Desensitization and Tachyphylaxis01:20

Desensitization and Tachyphylaxis

Tachyphylaxis is described as a rapid decrease in response to a drug after repeated or continuous administration of the same drug dose. It is a phenomenon where the body becomes less responsive to a particular substance or intervention over time, requiring higher doses or stronger interventions to achieve the same effect. It results from adaptive changes in the body's receptors, signaling pathways, or physiological processes that occur in response to prolonged exposure to a stimulus.
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A Conditioned Place Preference Protocol for Measuring Incubation of Craving in Rats
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Morphine postconditioning attenuates ICAM-1 expression on endothelial cells.

Too Jae Min1, Joong-il Kim, Jae-Hwan Kim

  • 1Department of Anesthesiology and Pain Medicine, Korea University Ansan Hospital, Korea University College of Medicine, Ansan, Korea.

Journal of Korean Medical Science
|February 3, 2011
PubMed
Summary

Morphine post-conditioning reduces intercellular adhesion molecules-1 (ICAM-1) expression and neutrophil adhesion during reoxygenation injury. This protective effect involves kappa and delta opioid receptors and protein kinase C.

Keywords:
Cell CultureEndothelial CellsHumansMorphinePostconditioningReperfusion injuryUmblical Veins

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Area of Science:

  • Endothelial cell biology
  • Pharmacology
  • Reperfusion injury

Background:

  • Reperfusion injury involves increased intercellular adhesion molecules-1 (ICAM-1) expression.
  • Opioid receptors (ORs) play roles in cellular protection.
  • Morphine post-conditioning (MPostC) may offer protective effects against cellular injury.

Purpose of the Study:

  • To determine if MPostC attenuates ICAM-1 expression after reoxygenation injury.
  • To identify the specific opioid receptor subtypes involved in MPostC's protective effects.

Main Methods:

  • Human umbilical vein endothelial cells (HUVECs) underwent anoxia followed by reoxygenation.
  • MPostC was applied using varying morphine concentrations.
  • Opioid receptor subtype antagonists and a protein kinase C (PKC) inhibitor were used to investigate pathways.

Main Results:

  • MPostC significantly reduced ICAM-1 expression and neutrophil adhesion during reoxygenation.
  • The protective effects of MPostC were blocked by kappa-OR, delta-OR antagonists, and a PKC inhibitor.
  • The mu-OR antagonist did not affect MPostC's protective actions.

Conclusions:

  • MPostC attenuates ICAM-1 expression and neutrophil adhesion in endothelial cells during reoxygenation.
  • This effect is mediated through kappa and delta opioid receptors.
  • A protein kinase C-dependent pathway is involved in the protective mechanism of MPostC.