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Chen C.-Y.,Chang Gung Memorial Hospital | Chen C.-Y.,Transgenic and Molecular Immunogenetics Laboratory | Chen C.-Y.,Chang Gung University | Luo C.-F.,Chang Gung Memorial Hospital | And 6 more authors.
Acta Anaesthesiologica Taiwanica | Year: 2012

Background: A significant abrupt drop in heart rate is the most frequent complication during percutaneous microballoon compression of the trigeminal ganglion. It is suggested that co-Activation of the sympathetic and parasympathetic nervous systems plays an important role in this occurrence. We hypothesized that not only atropine, but also labetalol might be effective in preventing this cardiovascular reflex during percutaneous microballoon compression of the trigeminal ganglion. Methods: Patients who underwent percutaneous microballoon compression for trigeminal neuralgia between September 2007 and December 2009 were prospectively evaluated. The relationship between the hemodynamic changes and intraoperative use of atropine (0.01 mg/kg) or labetalol (0.05 mg/kg) was compared. One-way analysis of variance with Bartlett's and Tukey's post-tests was used, and a value of p < 0.05 was considered statistically significant. Results: In total, 119 patients who received percutaneous microballoon compression for trigeminal neuralgia were studied, of whom 38 received atropine before ganglion compression, 36 received labetalol, and 45 received normal saline as a control. Of the patients who received normal saline, 31.3% had moderate bradycardia (heart rate < 50 beats/min), 13.3% had severe bradycardia (heart rate < 40 beats/min), and 7% had arrhythmia. Of the patients who received atropine, 7.8% had moderate bradycardia, 7.8% had arrhythmia, and 5.3% had postcompression tachycardia by the end of ganglion compression. Of the patients who received labetalol, 16.7% had moderate bradycardia, 5.6% had severe bradycardia, and 2.8% had arrhythmia. Systemic blood pressure was markedly elevated straight after compression in all groups and tended to normalize 3 minutes afterwards. Conclusion: Both atropine and labetalol were able to lower the frequency of bradycardia. Neither of them could abolish episodes of bradycardia during the procedure. Patients receiving labetalol before microballoon compression were subject to a smaller change in hemodynamics. Our findings verified that the sympathetic and parasympathetic nervous systems may be involved in the complex interneuronal interaction of the trigeminocardiac reflex. Copyright © 2012, Taiwan Society of Anesthesiologists. Source


Liou J.-T.,Chang Gung Memorial Hospital | Liou J.-T.,Transgenic and Molecular Immunogenetics Laboratory | Liou J.-T.,Chang Gung University | Yuan H.-B.,Taipei Veterans General Hospital | And 7 more authors.
Pain | Year: 2012

Accumulated evidence suggests that the C-C motif chemokine ligand 5 (CCL5) modulates migration of inflammatory cells in several pathological conditions. This study tested the hypothesis that lack of CCL5 would modulate the recruitment of inflammatory cells to painful, inflamed sites and could attenuate pain in a murine chronic neuropathic pain model. Nociceptive sensitization, immune cell infiltration, multiple cytokine expression, and opioid peptide expression in damaged nerves were studied in wild-type (CCL5 +/+) and CCL5-deficient (CCL5 -/-) mice after partial sciatic nerve ligation (PSNL). Results indicated that CCL5 -/- mice had less behavioral hypersensitivity after PSNL. Macrophage infiltration and proinflammatory cytokines (tumor necrosis factor-α, interleukin [IL]-1β, IL-6, and interferon-γ) in damaged nerves following PSNL were significantly decreased in CCL5 -/- mice. Conversely, several antiinflammatory cytokine (IL-4 and IL-10) proteins were significantly increased in CCL5 -/- animals and the expression of enkephalin, β-endorphin, and dynorphin mRNA was significantly lower than in wild-type control mice. These results represent the first evidence that CCL5 is capable of regulating the pathway that controls hyperalgesia at the level of the peripheral injured site in a murine chronic neuropathic pain model. We demonstrated that lack of CCL5 modulated cell infiltration and the proinflammatory milieu within the injured nerve. Attenuated behavioral hypersensitivity in CCL5 -/- mice observed in the current study could be a result of decreased macrophage infiltration, mobilization, and functional ability at injured sites. Collectively, the present study results suggest that CCL5 receptor antagonists may ultimately provide a novel class of analgesics for therapeutic intervention in chronic neuropathic pain. © 2011 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved. Source


Liou J.-T.,Chang Gung Memorial Hospital | Liou J.-T.,Transgenic and Molecular Immunogenetics Laboratory | Liou J.-T.,Chang Gung University | Lui P.-W.,Puli Veterans Hospital | And 8 more authors.
Journal of Neuroimmunology | Year: 2011

Previous studies have demonstrated that inflammatory cells produce several mediators that can effectively counteract pain. This study was designed to test the hypothesis that exogenous administration of recombinant mouse granulocyte-colony-stimulating factor (rmG-CSF) to enhance the recruitment of inflammatory cells to painful inflamed sites could attenuate pain in a chronic neuropathic pain model in mice. Our results indicate that treatment with rmG-CSF increased several cytokines and opioid peptides content; however, it did not attenuate but exacerbate neuropathic pain. Our study highlights the potent pro-inflammatory potential of G-CSF and suggests they may be targets for therapeutic intervention in chronic neuropathic pain. © 2010 Elsevier B.V. Source


Day Y.-J.,Chang Gung Memorial Hospital | Day Y.-J.,Transgenic and Molecular Immunogenetics Laboratory | Day Y.-J.,Chang Gung University | Day Y.-J.,National Defense Medical Center | And 18 more authors.
Pain | Year: 2014

Interleukin-17 (IL-17) is involved in a wide range of inflammatory disorders and in recruitment of inflammatory cells to injury sites. A recent study of IL-17 knock-out mice revealed that IL-17 contributes to neuroinflammation and neuropathic pain after peripheral nerve injury. Surprisingly, little is known of micro-environment modulation by IL-17 in injured sites and in pathologically related neuroinflammation and chronic neuropathic pain. Therefore, we investigated nociceptive sensitization, immune cell infiltration, myeloperoxidase (MPO) activity, and expression of multiple cytokines and opioid peptides in damaged nerves of wild-type (IL-17 +/+) and IL-17 knock-out (IL-17-/-) mice after partial sciatic nerve ligation. Our results demonstrated that the IL-17-/- mice had less behavioral hypersensitivity after partial sciatic nerve ligation, and inflammatory cell infiltration and pro-inflammatory cytokine (tumor necrosis factor-α, IL-6, and interferon-γ) levels in damaged nerves were significantly decreased, with the levels of anti-inflammatory cytokines IL-10 and IL-13, and expressions of enkephalin, β-endorphin, and dynorphin were also decreased compared to those in wild-type control mice. In conclusion, we provided evidence that IL-17 modulates the micro-environment at the level of the peripheral injured nerve site and regulates progression of behavioral hypersensitivity in a murine chronic neuropathic pain model. The attenuated behavioral hypersensitivity in IL-17-/- mice could be a result of decreased inflammatory cell infiltration to the injured site, resulting in modulation of the pro- and anti-inflammatory cytokine milieu within the injured nerve. Therefore, IL-17 may be a critical component for neuropathic pain pathogenesis and a novel target for therapeutic intervention for this and other chronic pain states. ©2014 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved. Source


Liou J.-T.,Chang Gung Memorial Hospital | Liou J.-T.,Transgenic and Molecular Immunogenetics Laboratory | Liou J.-T.,Chang Gung University | Lee C.-M.,Chang Gung Memorial Hospital | And 15 more authors.
Pain | Year: 2013

Growing evidence suggests that leukocyte extravasation is initiated by the interaction of selectins with their ligands; as well as an essential role for P-selectin in the initial recruitment of inflammatory cells to sites of inflammation. In this study, P-selectin-deficient (P-sel-/-) mice were used to test the hypothesis that lack of P-selectin would attenuate the recruitment of inflammatory cells to the site of inflammation, thereby modulating pain in a murine chronic neuropathic pain model. Nociceptive sensitization and the microenvironment of the peripheral injury site were studied in wild-type (P-sel+/+) and P-selectin-deficient (P-sel-/-) mice after partial sciatic nerve ligation (PSNL). Variables measured included myeloperoxidase (MPO) activity, several inflammatory cell infiltration profiles, cytokines, and endogenous opioid peptide expression in damaged nerves. Results indicate that behavioral hypersensitivity, MPO activity, and infiltration of neutrophils and macrophages were attenuated in P-sel-/- mice after PSNL. Proinflammatory cytokines, tumor necrosis factor α, and interleukin (IL)-6, were reduced in damaged nerves following PSNL; however, several antiinflammatory cytokines - IL-1Ra, IL-4, and IL-10 - were significantly increased in P-sel-/- mice. In addition, endogenous opioid peptides mRNA was significantly lower in P-sel-/- mice compared with P-sel +/+ mice. The current results demonstrated that the absence of P-selectin in mice leads to an altered microenvironment that attenuated behavioral hypersensitivity. The specific role of P-selectin could have been a result of decreased neutrophils, as well as the accumulation of macrophages at the site of injury, which may subsequently modulate the inflammatory cytokine expression and impact behavioral hypersensitivity within the injured nerve. © 2013 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved. Source

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