1984
DOI: 10.1016/0014-2999(84)90653-8
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Leukotrienes reduce nociceptive responses to bradykinin

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Cited by 25 publications
(7 citation statements)
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“…The leukotriene C 4 concentration was not found to be increased by IL-1 injection. This lack of effect on LTC4 levels is of interest as previous studies using the same model have shown that the leukotrienes do not enhance the effects of acetylcholine but rather desensitize the nociceptors of the isolated rabbit ear to the painful stimuli of bradykinin [12]. It remains unclear which cells in the perfused rabbit ear are responsible for the IL-l-induced PGE 2 production.…”
Section: Discussionmentioning
confidence: 90%
“…The leukotriene C 4 concentration was not found to be increased by IL-1 injection. This lack of effect on LTC4 levels is of interest as previous studies using the same model have shown that the leukotrienes do not enhance the effects of acetylcholine but rather desensitize the nociceptors of the isolated rabbit ear to the painful stimuli of bradykinin [12]. It remains unclear which cells in the perfused rabbit ear are responsible for the IL-l-induced PGE 2 production.…”
Section: Discussionmentioning
confidence: 90%
“…Both prostaglandins and leukotrienes claimed to control inflammatory pain. 25,26 There is a simulative neuropeptide called substance P that acts as a transmitter within the nociception system, released by bradykinin. 21,27 It was believed to make use of chemical actions on circulatory and neural mechanisms.…”
Section: Pain Mediatorsmentioning
confidence: 99%
“…The behavioral end points employed include some that are described in somewhat vague terms and are difficult to quantify (e.g., "signs of discomfort", "gross, purposeful movement", "escape movement response", "vigorous attempt to remove the paw") and more specific, quantifiable responses ("lick/chew response", "ear flick"). All of the models summarized in Table 2 suffer in one respect or another (1974), Schweizer et al (1984), Schweizer and Brom (1985) Strictly, no, but intra-arterial injection of inflammatory mediators Wynn et al (1984), Bergman et al (1991Bergman et al ( , 1988, Hyatt et al (1989), Manzon (1989) (1) "Head lift" response; (2) "escape movement" response Voltage required to evoke behavioral responses Low from technical complexity (e.g., complicated surgery), low efficiency/throughput and low end point resolution (i.e., difficulty in reliably generating dose-effect functions for analgesics). Furthermore, the use of restraint in all of the models in which conscious rabbits are used introduces the potential confounding factors of stress-induced hypoalgesia or stress-induced hyperalgesia (Manning, 2004).…”
Section: Discussionmentioning
confidence: 99%