Opioid induced hyperalgesia in anesthetic settings

Lee, Hyeon Jeong; Yeomans, David C.

doi:10.4097/kjae.2014.67.5.299

Cited by 25 publications

(22 citation statements)

References 45 publications

(55 reference statements)

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“…The addition of [Sar 9 , Met(O 2 ) 11 ] to the substance P-conjugated to saporin makes the agent more stable and potent than when substance P alone is bound to saporin. The dose and pretreatment interval was based on the studies of Wiley et al (2007) and Choi et al (2012), who observed no loss of intrinsic lumbar dorsal horn neurons expressing the neurokinin 1 (NK1) receptor in deeper laminae and prominent loss of NK1 receptor in laminae I, and studies by others (Khasabov et al, 2002;Vierck et al, 2003;Wiley et al, 2007;Choi et al, 2012;Weisshaar and Winkelstein, 2014;Kras et al, 2015;Araldi et al, 2016aAraldi et al, , 2017bAraldi et al, , 2018.…”

Section: Intrathecal Administration Of Saporinsmentioning

confidence: 99%

Fentanyl Induces Rapid Onset Hyperalgesic Priming: Type I at Peripheral and Type II at Central Nociceptor Terminals

et al. 2018

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Systemic fentanyl induces hyperalgesic priming, long-lasting neuroplasticity in nociceptor function characterized by prolongation of inflammatory mediator hyperalgesia. To evaluate priming at both nociceptor terminals, we studied, in male Sprague Dawley rats, the effect of local administration of agents that reverse type I (protein translation) or type II [combination of Src and mitogen-activated protein kinase (MAPK)] priming. At the central terminal, priming induced by systemic, intradermal, or intrathecal fentanyl was reversed by the combination of Src and MAPK inhibitors, but at the peripheral terminal, it was reversed by the protein translation inhibitor. Mu-opioid receptor (MOR) antisense prevented fentanyl hyperalgesia and priming. To determine whether type I and II priming occur in the same population of neurons, we used isolectin B4-saporin or [Sar, Met(O)]-substance P-saporin to deplete nonpeptidergic or peptidergic nociceptors, respectively. Following intrathecal fentanyl, central terminal priming was prevented by both saporins, whereas that in peripheral terminal was not attenuated even by their combination. However, after intradermal fentanyl, priming in the peripheral terminal requires both peptidergic and nonpeptidergic nociceptors, whereas that in the central terminal is dependent only on peptidergic nociceptors. Pretreatment with dantrolene at either terminal prevented fentanyl-induced priming in both terminals, suggesting communication between central and peripheral terminals mediated by intracellular Ca signaling. application of fentanyl increased cytoplasmic Ca concentration in dorsal root ganglion neurons, which was prevented by pretreatment with dantrolene and naloxone. Therefore, acting at MOR in the nociceptor, fentanyl induces hyperalgesia and priming rapidly at both the central (type II) and peripheral (type I) terminal and this is mediated by Ca signaling. Fentanyl, acting at the μ-opioid receptor (MOR), induces hyperalgesia and hyperalgesic priming at both the central and peripheral terminal of nociceptors and this is mediated by endoplasmic reticulum Ca signaling. Priming in the central terminal is type II, whereas that in the peripheral terminal is type I. Our findings may provide useful information for the design of drugs with improved therapeutic profiles, selectively disrupting individual MOR signaling pathways, to maintain an adequate long-lasting control of pain.

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Section: Intrathecal Administration Of Saporinsmentioning

confidence: 99%

Fentanyl Induces Rapid Onset Hyperalgesic Priming: Type I at Peripheral and Type II at Central Nociceptor Terminals

et al. 2018

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“…Although the underlying mechanism of OIH is not yet completely understood[1, 3, 4, 10], previous reports from our groups have shown that CaMKIIα, which is highly expressed in the CeLC and superficial spinal dorsal horn, plays an important role in modulation of OIH[11, 12]. Either spinal or CeLC CaMKIIα inhibition can attenuate OIH [11, 12].…”

Section: Introductionmentioning

confidence: 99%

CaMKIIα may modulate fentanyl-induced hyperalgesia via a CeLC-PAG-RVM-spinal cord descending facilitative pain pathway in rats

Yin

Chen

et al. 2017

PLoS ONE

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Each of the lateral capsular division of central nucleus of amygdala(CeLC), periaqueductal gray (PAG), rostral ventromedial medulla(RVM) and spinal cord has been proved to contribute to the development of opioid-induced hyperalgesia(OIH). Especially, Ca2+/calmodulin-dependent protein kinase IIα (CaMKIIα) in CeLC and spinal cord seems to play a key role in OIH modulation. However, the pain pathway through which CaMKIIα modulates OIH is not clear. The pathway from CeLC to spinal cord for this modulation was explored in the present study. Mechanical and thermal hyperalgesia were tested by von Frey test or Hargreaves test, respectively. CaMKIIα activity (phospho-CaMKIIα, p-CaMKIIα) was evaluated by western blot analysis. CaMKIIα antagonist (KN93) was micro-infused into CeLC, spinal cord or PAG, respectively, to evaluate its effect on behavioral hyperalgesia and p-CaMKIIα expression in CeLC, PAG, RVM and spinal cord. Then the underlying synaptic mechanism was explored by recording miniature excitatory postsynaptic currents (mEPSCs) on PAG slices using whole-cell voltage-clamp methods. Results showed that inhibition of CeLC, PAG or spinal CaMKIIα activity respectively by KN93, reversed both mechanical and thermal hyperalgesia. Microinjection of KN93 into CeLC decreased p-CaMKIIα expression in CeLC, PAG, RVM and spinal cord; while intrathecal KN93 can only block spinal but not CeLC CaMKIIα activity. KN93 injected into PAG just decreased p-CaMKIIα expression in PAG, RVM and spinal cord, but not in the CeLC. Similarly, whole-cell voltage-clamp recording found the frequency and amplitude of mEPSCs in PAG cells were decreased by KN93 added in PAG slice or micro-infused into CeLC in vivo. These results together with previous findings suggest that CaMKIIα may modulate OIH via a CeLC-PAG-RVM-spinal cord descending facilitative pain pathway.

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“…OIH is related to high opioid dosage, long duration of opioid use, and abrupt discontinuation of opioids after surgery. Therefore, many mechanism- based combinations of other adjuvant drugs have been used to attenuate sensitization of the central pronociceptive process and reduce the unpleasant hyperalgesic response [ 1 ].…”

Section: Introductionmentioning

confidence: 99%

Effect of intraoperative infusion of ketamine on remifentanil-induced hyperalgesia

Choi

Lee

Park

et al. 2015

Korean J Anesthesiol

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BackgroundOpioid induced hyperalgesia (OIH) is related with high opioid dosage, a long duration of opioid administration, and abrupt discontinuation of infused opioids in anesthetic settings. Ketamine is known to attenuate OIH efficiently, but methods of administration and methods to quantify and assess a decrease in OIH vary. We demonstrated the existence of remifentanil-induced hyperalgesia and investigated the ability of ketamine to attenuate OIH.MethodsSeventy-five patients undergoing laparoscopic gynecologic surgery under remifentanil-based anesthesia were assigned to one of the following groups: (1) group RL (remifentanil 0.05 µg/kg/min), (2) group RH (remifentanil 0.3 µg/kg/min), or (3) group KRH (remifentanil 0.3 µg/kg/min + ketamine 0.5 mg/kg bolus with 5 µg/kg/min infusion intraoperatively). Desflurane was administered for maintenance of anesthesia to target bispectral index scores (40-60) and hemodynamic parameters (heart rate and blood pressure < ± 20% of baseline values). All parameters related to OIH and its attenuation induced by ketamine were investigated.ResultsThere was no significant difference among the three groups related to demographic and anesthetic parameters except the end-tidal concentration of desflurane. Additional analgesic consumption, numerical rating scale scores at 6 and 24 h, and cumulative fentanyl dose were significantly higher in group RH than in the other two groups. The value difference of the Touch-Test sensory evaluation was significantly higher negative in group RH than in the other two groups.ConclusionsRemifentanil-induced hyperalgesia is significantly attenuated by intraoperative bolus and infusion of ketamine. Ketamine also decreased tactile sensitization, as measured by Touch-Test sensory evaluation.

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Opioid induced hyperalgesia in anesthetic settings

Cited by 25 publications

References 45 publications

Fentanyl Induces Rapid Onset Hyperalgesic Priming: Type I at Peripheral and Type II at Central Nociceptor Terminals

Fentanyl Induces Rapid Onset Hyperalgesic Priming: Type I at Peripheral and Type II at Central Nociceptor Terminals

CaMKIIα may modulate fentanyl-induced hyperalgesia via a CeLC-PAG-RVM-spinal cord descending facilitative pain pathway in rats

Effect of intraoperative infusion of ketamine on remifentanil-induced hyperalgesia

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