2014
DOI: 10.1016/j.ejphar.2013.08.007
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Pharmacological strategy for overcoming opioid-induced ventilatory disturbances

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Cited by 12 publications
(11 citation statements)
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“…It also reverses opioid suppression of hypoglossal motor neuron activity, suggesting it may improve airway patency (i.e., decreases "snoring"). 3,5,6 …”
Section: Breathing Stimulants Old and Newmentioning
confidence: 99%
“…It also reverses opioid suppression of hypoglossal motor neuron activity, suggesting it may improve airway patency (i.e., decreases "snoring"). 3,5,6 …”
Section: Breathing Stimulants Old and Newmentioning
confidence: 99%
“…We have previously described the possibility of non-opioids for treatment of opioid-induced ventilatory disturbances [19], where cholinesterase inhibitors, 5-HT 1A agonists and drugs that increase the cAMP content are important candidates that act in the central respiratory-related areas. On the other hand, agents such as doxapram, GAL-021 and almitrine that block potassium channels in the carotid bodies are also useful approaches for offsetting opioid-induced respiratory depression without loss of analgesia [10,45].…”
Section: Discussionmentioning
confidence: 99%
“…Opioids slowed breathing frequency and reduced its depth, and also dampen ventilatory responses to hypercapnia and hypoxia principally through activation of μ opioid receptors [11,19,29,36]. Naloxone, an antagonist of μ opioid receptors, naloxone effectively and rapidly reverses ventilatory depression induced by opioids, however it attenuates opioid analgesia concomitantly [7].…”
Section: Introductionmentioning
confidence: 96%
“…As peripheral and central chemoreceptors are stimulated by the decreasing pH of their environment during hypercapnia, stress-related mechanisms trigger the release of opioids (Fukuda, et al 2006, Gamble & Milne 1990, Grönroos & Pertovaara 1994. Exogenous, as well as endogenous, opioids are linked to the depression of ventilatory rates, a lessened "need to breathe", and other sedative effects which may further support the tie between anesthesia and hypercapnia (Kimura & Haji 2014, Pattinson, et al 2007, Zhang, et al 2007. In vitro studies of the analgesic properties of CO2 showed that under conditions of severe acidosis (pH ~6.7), rat spinal cords exhibited nociceptive responses that were similar to spinal cords treated with the analgesic dexmedetomidine (Otsuguro, et al 2007).…”
Section: Induction Of Anesthesia and Analgesiamentioning
confidence: 99%
“…Exposure to CO2 depresses the reactivity of both respiratory and nonrespiratory neurons (Lipski, 1986). During hypercapnia, stress-induced opioids are released (Gamble and Milne, 1990, Grönroos and Pertovaara, 1994, Fukuda et al, 2006, and these opioids are linked with the depression of ventilatory response, a lessened "need to breath" and other sedative effects that induce anesthesia and analgesia (Pattinson et al, 2007, Zhang et al, 2007, Kimura and Haji, 2014. Severely hypercapnic (pH ~6.7) rat spinal cords were shown to exhibit the same amount of nociception as spinal cords treated with the analgesic dexmedetomidine and guinea pigs exhibited deep anesthesia for 50 seconds after being exposed to 80% CO2 for 30 seconds (Kohler et al, 1999, Otsuguro et al, 2007.…”
Section: Introductionmentioning
confidence: 99%