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Editorial
. 2009 Dec;111(6):1175-6.
doi: 10.1097/ALN.0b013e3181bdfa2e.

Opiates, sleep, and pain: the adenosinergic link

Jason T Moore, Max B Kelz
Editorial

Opiates, sleep, and pain: the adenosinergic link

Jason T Moore et al. Anesthesiology. 2009 Dec.
No abstract available

PubMed Disclaimer

Conflict of interest statement

Conflict of Interest: The authors are not supported by, nor maintain any financial interest in, any commercial activity that may be associated with the topic of this article.

Figures

Figure 1
Figure 1
Schematic cartoon depicting the interactions among pain, opiates, and sleep along with the proposed role of adenosine. (1) The experience of pain is known to impair sleep. (2) Recently it has become clear that sleep disruption can directly exacerbate pain. (3) The use of opiates to alleviate pain leads to desired analgesia as well as (4) undesired side effects on nuclei capable of modulating arousal such as the substantia innominata of the basal forebrain (BF), the pontine reticular formation (PRF), the ventrolateral preoptic nucleus (VLPO), and other sites. (5) It is unknown whether opiates modulate endogenous adenosine levels in sleep-active loci such as the VLPO or in other wake-active loci. (6) As reported in the current issue, in the BF and the PRF, such effects are likely mediated by a focal decrease in endogenous adenosine. Although not shown, it is worth noting that systemic infusions of adenosine elicit analgesia as evidenced by reduced opioid requirements in animal models as well as in double-blinded clinical studies. However, the fraction of adenosine’s analgesic properties that arises from its somnogenic effects awaits evaluation. Conversely, caffeine, which antagonizes the actions of adenosine, is the world’s most widely used psychostimulant. One might rightly question whether caffeine use and ensuing sleep disruption leads to opioid dose escalation and hyperalgesia.
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