Investigation of cardiorespiratory effects of the selective 5‐HT4 agonist BIMU‐8 in etorphine‐immobilised goats (<i>Capra aegagrus hircus</i>) in a randomized, blinded and controlled trial

Tod, Nadine; Stalder, Gabrielle; Rauch, Hanna; Boehmdorfer, Stefan; Haw, Anna; Gerritsmann, Hanno; Painer, Johanna; Meyer, Leith C. R.

doi:10.1002/vetr.76

Cited by 2 publications

(2 citation statements)

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“…In two recent studies, the effect of the 5HT4a receptor agonist BIMU8 was tested on etorphine- and sufentanil-induced respiratory depression. 26,44 In etorphine-immobilized goats, BIMU8 reduced etorphine toxicity with a reversal of the drop in respiratory rate and normalization of blood gasses. 44 In the animals, blood pressure dropped after infusion of BIMU8, and some goats developed muscle rigidity or muscle spasms.…”

Section: Serotonin Receptor Agonistsmentioning

confidence: 99%

“…26,44 In etorphine-immobilized goats, BIMU8 reduced etorphine toxicity with a reversal of the drop in respiratory rate and normalization of blood gasses. 44 In the animals, blood pressure dropped after infusion of BIMU8, and some goats developed muscle rigidity or muscle spasms. In conscious rats, however, BIMU8 failed to counter sufentanil-induced respiratory depression, although this may be dose-related.…”

Section: Serotonin Receptor Agonistsmentioning

confidence: 99%

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Advances in Reversal Strategies of Opioid-induced Respiratory Toxicity

et al. 2021

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Opioids may produce life-threatening respiratory depression and death from their actions at the opioid receptors within the brainstem respiratory neuronal network. Since there is an increasing number of conditions where the administration of the opioid receptor antagonist naloxone is inadequate or undesired, there is an increased interest in the development of novel reversal and prevention strategies aimed at providing efficacy close to that of the opioid receptor antagonist naloxone but with fewer of its drawbacks such as its short duration of action and lesser ability to reverse high-affinity opioids, such as carfentanil, or drug combinations. To give an overview of this highly relevant topic, the authors systematically discuss predominantly experimental pharmacotherapies, published in the last 5 yr, aimed at reversal of opioid-induced respiratory depression as alternatives to naloxone. The respiratory stimulants are discussed based on their characteristics and mechanism of action: nonopioid controlled substances (e.g., amphetamine, cannabinoids, ketamine), hormones (thyrotropin releasing hormone, oxytocin), nicotinic acetylcholine receptor agonists, ampakines, serotonin receptor agonists, antioxidants, miscellaneous peptides, potassium channel blockers acting at the carotid bodies (doxapram, ENA001), sequestration techniques (scrubber molecules, immunopharmacotherapy), and opioids (partial agonists/antagonists). The authors argue that none of these often still experimental therapies are sufficiently tested with respect to efficacy and safety, and many of the agents presented have a lesser efficacy at deeper levels of respiratory depression, i.e., inability to overcome apnea, or have ample side effects. The authors suggest development of reversal strategies that combine respiratory stimulants with naloxone. Furthermore, they encourage collaborations between research groups to expedite development of viable reversal strategies of potent synthetic opioid-induced respiratory depression.

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Section: Serotonin Receptor Agonistsmentioning

confidence: 99%