Evidence map›Paper›PMID 35471232›Full record

ReviewArchives of toxicology2022

Mechanisms of opioid-induced respiratory depression.

Brian A Baldo, Michael A Rose

Registry-linked trialAbstract readReview
PubMed Publisher
In one paragraph

Review in Archives of toxicology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06225466 (Anesthesia With Neuromuscular Blockade and Reversal With Sugammadex Compared to Anesthesia Without Muscle Relaxation During Pediatric High-Risk Adenotonsillectomy), which is not on this map. Cited by 56 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 2 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT06225466 phase4completednot on this mapstarted 2024, after this paper: background citation

Anesthesia With Neuromuscular Blockade and Reversal With Sugammadex Compared to Anesthesia Without Muscle Relaxation During Pediatric High-Risk Adenotonsillectomy: A Randomized-Controlled Trial

TypeinterventionalSponsorUniversity of Texas Southwestern Medical CenterRan2024 to 2024Enrolled172ConditionsTonsillectomyArmsRocuronium, Sugammadex, Anesthesia without neuromuscular blockade
3 · Its place in the literature

Who cites it

56 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Trial
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  6. Article
  7. Article
  8. Review
  9. Carfentanil Depresses Inspiratory Motor Drive.Journal of substance abuse and alcoholism · 2026
    Article
  10. Article
  11. Outcompeting opioid-induced respiratory depression.Journal of thoracic disease · 2026
    Article
  12. Article
  13. Indole Alkaloids as Biased Opioid Receptor Modulators.Pharmaceuticals (Basel, Switzerland) · 2026
    Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Brian A BaldoKolling Institute of Medical Research, Royal North Shore Hospital of Sydney, 11 Bent Street, Lindfield, NSW, 2065, Australia. babaldo@iinet.net.au.ORCID 0000-0001-9401-4865
Michael A RoseUniversity of Sydney, Sydney, NSW, Australia.ORCID 0000-0002-7182-0474

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Opioid-induced respiratory depression (OIRD), the primary cause of opioid-induced death, is the neural depression of respiratory drive which, together with a decreased level of consciousness and obstructive sleep apnea, cause ventilatory insufficiency. Variability of responses to opioids and individual differences in physiological and neurological states (e.g., anesthesia, sleep-disordered breathing, concurrent drug administration) add to the risk. Multiple sites can independently exert a depressive effect on breathing, making it unclear which sites are necessary for the induction of OIRD. The generator of inspiratory rhythm is the preBötzinger complex (preBötC) in the ventrolateral medulla. Other important brainstem respiratory centres include the pontine Kölliker-Fuse and adjacent parabrachial nuclei (KF/PBN) in the dorsal lateral pons, and the dorsal respiratory group in the medulla. Deletion of μ opioid receptors from neurons showed that the preBötC and KF/PBN contribute to OIRD with the KF as a respiratory modulator and the preBötC as inspiratory rhythm generator. Glutamatergic neurons expressing NK-1R and somatostatin involved in the autonomic function of breathing, and modulatory signal pathways involving GIRK and KCNQ potassium channels, remain poorly understood. Reversal of OIRD has relied heavily on naloxone which also reverses analgesia but mismatches between the half-lives of naloxone and opioids can make it difficult to clinically safely avoid OIRD. Maternal opioid use, which is rising, increases apneas and destabilizes neonatal breathing but opioid effects on maternal and neonatal respiratory circuits in neonatal abstinence syndrome (NAS) are not well understood. Methadone, administered to alleviate symptoms of NAS in humans, desensitizes rats to RD.

Indexed as

Analgesics, OpioidRespiratory InsufficiencyAnimalsNaloxoneRatsReceptors, Opioid, muRespiratory CenterAnalgesics, OpioidNaloxoneReceptors, Opioid, muBrainstem centers and respirationKölliker-Fuse nucleus and opioid-induced respiratory depressionNeural mediation of opioid-induced respiratory depressionOpioid-induced respiratory depressionPathophysiology of opioid-induced respiratory depressionPre-Bötzinger complex and opioid-induced respiratory depression

Identifiers

What OpenQuestion holds

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Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.