Neurogenic Inflammation

Lynn, Bruce

doi:10.1159/000210778

Cited by 60 publications

(42 citation statements)

References 29 publications

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“…These results suggested that CGRP released from the peripheral nerve endings may stimulate the proangiogenic activities. Axon reflex is an event that was brought about by the passage of nerve impulses from sensory nerve endings to the effector organ along divisions of the nerve fibers without traversing a synapse (22). Axon reflex elicited by nociceptive stimulation may be closely related to the increased release of CGRP from nerve endings.…”

Section: Effects Of Continuous Infusion Of a Cgrp Antagonist On Tumormentioning

confidence: 99%

Neuronal system-dependent facilitation of tumor angiogenesis and tumor growth by calcitonin gene-related peptide

Toda

Suzuki²,

Hosono³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

116

110

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Section: Effects Of Continuous Infusion Of a Cgrp Antagonist On Tumormentioning

confidence: 99%

Neuronal system-dependent facilitation of tumor angiogenesis and tumor growth by calcitonin gene-related peptide

Toda

Suzuki²,

Hosono³

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

116

110

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“…9 This increased vascular permeability, accompanied by release of vasoactive mediators from mast cells, results in an inflammatory response (neurogenic edema). 10 The increased vascular permeability also results in extravasation of additional algogenic (pain producing) substances, such as histamine and serotonin. Histamine can also be released from mast cells during degranulation, a process promoted by substance P, kinins, interleukin-1 and nerve growth factor.…”

Section: Transductionmentioning

confidence: 99%

Preemptive analgesia I: physiological pathways and pharmacological modalities

Kelly

Ahmad

Brull

2001

Can J Anesth/J Can Anesth

259

181

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P Pu ur rp po os se e: : This two-part review summarizes the current knowledge of physiological mechanisms, pharmacological modalities and controversial issues surrounding preemptive analgesia.S So ou ur rc ce e: : Articles from 1966 to present were obtained from the MEDLINE databases. Search terms included: analgesia, preemptive; neurotransmitters; pain, postoperative; hyperalgesia; sensitization, central nervous system; pathways, nociception; anesthetic techniques; analgesics, agents.P Pr ri in nc ci ip pa al l f fi in nd di in ng gs s: : The physiological basis of preemptive analgesia is complex and involves modification of the pain pathways. The pharmacological modalities available may modify the physiological responses at various levels. Effective preemptive analgesic techniques require multi-modal interception of nociceptive input, increasing threshold for nociception, and blocking or decreasing nociceptor receptor activation. Although the literature is controversial regarding the effectiveness of preemptive analgesia, some general recommendations can be helpful in guiding clinical care. Regional anesthesia induced prior to surgical trauma and continued well into the postoperative period is effective in attenuating peripheral and central sensitization. Pharmacologic agents such as NSAIDs (non-steroidal anti-inflammatory drugs) opioids, and NMDA (Nmethyl-D-aspartate) -and alpha-2-receptor antagonists, especially when used in combination, act synergistically to decrease postoperative pain.C Co on nc cl lu us si io on n: : The variable patient characteristics and timing of preemptive analgesia in relation to surgical noxious input requires individualization of the technique(s) chosen. Multi-modal analgesic techniques appear most effective.Objectif : La présente revue, en deux parties, résume les connaissances actuelles sur les mécanismes physiologiques et les modalités pharmacologiques de lanalgésie préventive ainsi que sur les questions controversées qui lentourent.Sources : Des articles, de 1966 à aujourdhui, obtenus à partir des bases de données MEDLINE. Les termes de la recherche compren-

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“…Alternatively there may be some special feature in the anatomical organization of the microvasculature that is involved. It has also been suggested that spread of flare involves weak coupling between C fibre terminals (Lembeck, 1983;Lynn, 1988;Lynn & Cotsell, 1991). If the coupling involved organized synapses it might be directional and this could explain the asymmetry of the flare responses, however, at the moment, there is no evidence for such links between afferent terminals in skin.…”

Section: Discussionmentioning

confidence: 99%