Platelet activating factor as a proinflammatory mediator in acetic-induced colitis in the rat

Will, Peter C.; Thomas, T. K.; Iverson, Lindsay; Buckman, Dianne K.; Weis, William I.; Wilson, Chad; Srivastava, Anshu

doi:10.1007/bf01993272

Cited by 8 publications

(4 citation statements)

References 7 publications

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“…Of note, the concentration of BK in various inflamed tissues is in the range 50 n m to 0.1 μ m (Swift et al 1993; Hargreaves et al 1993) and that of PAF has been measured to be around 1.7 μ m (Will et al 1991; Appleyard & Hiller, 1995).…”

Section: Methodsmentioning

confidence: 99%

Nociceptive neuroendocrine negative feedback control of neurogenic inflammation activated by capsaicin in the rat paw: role of the adrenal medulla

Miao

Jänig

Levine

2000

The Journal of Physiology

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Bradykinin (BK)-induced synovial plasma extravasation (PE) in the rat knee joint is a neurogenic inflammatory response which is dependent on the sympathetic innervation of the synovia, but not on impulse activity in the sympathetic neurones (Miao et al. 1996a,b). Recently we have shown in the rat that this neurogenic inflammation is depressed in a frequency-dependent manner during activation of afferent C-fibres generated by electrical stimulation of the contralateral hindpaw at û 1-3 Hz. Hypophysectomy, blockade of corticosterone synthesis or removal of the adrenal glands 1. Recently we have found that inhibition of bradykinin-induced synovial plasma extravasation by transcutaneous electrical stimulation at strengths which excite unmyelinated afferent axons is mediated by the hypothalamo-pituitary-adrenal axis. 2. Here we tested whether stimulation of nociceptors in the rat paw by intradermally injected capsaicin inhibits bradykinin-induced synovial plasma extravasation and whether this inhibition is mediated by the hypothalamo-pituitary-adrenal or sympatho-adrenal axis. Furthermore, we tested whether inhibition of bradykinin-induced plasma extravasation generated by intraperitoneally injected capsaicin, which preferentially excites visceral afferents, is mediated by the hypothalamo-pituitary-adrenal or sympatho-adrenal axis. We used normal rats, subdiaphragmatically vagotomized rats, rats with denervated adrenal medullae and rats with acutely transected spinal cords at the segmental levels T1ÏTµ or T12ÏL1. 3. Injection of capsaicin into the plantar or palmar surface of the paws produced a depression of bradykinin-induced plasma extravasation. The inhibition elicited from the forepaw was larger than that from the hindpaw. 4. The inhibition of bradykinin-induced plasma extravasation elicited from both paws was potentiated by subdiaphragmatic vagotomy. 5. Denervation of the adrenal medullae abolished the inhibitory effect of intradermal capsaicin in vagus-intact and in vagotomized animals. 6. After spinalization at the segmental level T1ÏTµ, capsaicin injected into the forepaw did not depress bradykinin-induced plasma extravasation either in vagus-intact or in vagotomized animals. Capsaicin injected into the hindpaw in these spinalized animals produced a small depression. After spinalization at the segmental level T12ÏL1 no depression was produced by capsaicin injected into the hindpaw. 7. Depression of bradykinin-induced plasma extravasation generated by intraperitoneal injection of capsaicin in vagus-intact and in vagotomized animals was also abolished or attenuated after denervation of the adrenal medullae. This shows that this depression was also largely dependent on the activation of the sympatho-adrenal system. 8. We conclude that depression of bradykinin-induced plasma extravasation during stimulation of nociceptors by capsaicin is mediated predominantly by the sympathoadrenal pathway. This finding differs from the inhibitory mechanism of depression of bradykinin-induced plasma extravasation generated by...

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Section: Methodsmentioning

confidence: 99%

Nociceptive neuroendocrine negative feedback control of neurogenic inflammation activated by capsaicin in the rat paw: role of the adrenal medulla

Miao

Jänig

Levine

2000

The Journal of Physiology

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“…. PAF has also been implicated in the pathogenesis of disorders of the lower intestine, including neonatal necrotizing enterocolitis (106) and IBD (119)(120)(121)(122)(123). PAF is produced in increased amounts in the mucosa of humans (119) and animals (l2D-122) with colitis, as well as in the stool of IBD patients (123).…”

Section: Pafmentioning

confidence: 99%

Inflammatory Mediators in Gastrointestinal Defense and Injury

Wallace

2001

Exp Biol Med (Maywood)

108

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Inflammation of the mucosal layer of the gastrointestinal (GI) tract Is not only a feature almost always associated with ulceration of those tissues, but it also plays an Important role In both the production and healing of the lesions. The mediators that coordinate inflammatory responses also have the capability to alter the resistance of the mucosa to Injury Induced by noxious substances, while others render the mucosa more susceptible to injury. In this article, we provide a review of the inflammatory mediators that modulate GI mucosal defense. Among the mediators discussed are nitric oxide, the eicosanoids (prostaglandins, leukotrienes, and thromboxanes), neuropeptldes, cytokines, and proteinases. Many of these mediators are considered potential therapeutic targets for the treatment of ulcerative diseases of the digestive tract.

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“…These doses of BK and PAF have previously been demonstrated to be ED 50 values on their respective dose‐response curves (Green et al , 1993a). Of note, the concentration of BK in various inflamed tissues is in the range of 50 nM to 0.1 μM (Swift et al , 1993; Hargreaves et al , 1993 and Hargreaves, personal communication) while that of PAF is approximately 1.7 μm (Will et al , 1991; Appleyard & Hillier, 1995). A similar concentration of BK has been used as a component of so‐called ‘inflammatory soup’(e.g., Steen et al , 1995).…”

Section: Methodsmentioning

confidence: 99%

Contribution of adrenal hormones to nicotine‐induced inhibition of synovial plasma extravasation in the rat

Miao

Benowitz

Heller

et al. 1997

British J Pharmacology

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1 In this study, we examined the mechanism(s) by which s.c. nicotine inhibits synovial plasma extravasation. We found that nicotine dose-dependently inhibited bradykinin (BK)-and platelet activating factor (PAF)-induced plasma extravasation. 2 The eect of nicotine on both BK-and PAF-induced plasma extravasation was attenuated by adrenal medullectomy. ICI-118,551 (a selective b 2 -adrenoceptor blocker) (30 mg ml 71, intra-articularly) signi®cantly attenuated the inhibitory action of high-dose (1 mg kg 71 ) nicotine on BK-induced plasma extravasation without aecting the inhibition by low-(0.01 mg kg 71 ) dose nicotine or that on PAFinduced plasma extravasation by nicotine at any dose. This suggested that b 2 -adrenoceptors mediate the inhibitory actions of high-dose, but not low-dose, nicotine. We also found that systemic naloxone (an opioid receptor antagonist) (two hourly injections of 1 mg kg 71 , i.p.) attenuated the inhibitory action produced by all doses of nicotine on BK-or PAF-induced plasma extravasation, suggesting the contribution of endogenous opioids. 3 RU-38,486 (a glucocorticoid receptor antagonist) (30 mg kg 71 , s.c.) and metyrapone (a glucocorticoid synthesis inhibitor) (two hourly injections of 100 mg kg 71 , i.p.) both attenuated the action of high-dose nicotine without aecting that of low-dose nicotine. 4 Spinal mecamylamine (a nicotinic receptor antagonist) (0.025 mg kg 71, intrathecally, i.t.) attenuated the action of high-dose, but not low-dose, nicotine, suggesting that part of the action of high-dose nicotine is mediated by spinal nicotinic receptors. 5 Combined treatment with ICI-118,551, naloxone and RU-38,486 attenuated the action of low-dose nicotine by an amount similar to that produced by naloxone alone but produced signi®cantly greater attenuation of the eect of high-dose nicotine when compared to the action of any of the three antagonists alone.

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Platelet activating factor as a proinflammatory mediator in acetic-induced colitis in the rat

Cited by 8 publications

References 7 publications

Nociceptive neuroendocrine negative feedback control of neurogenic inflammation activated by capsaicin in the rat paw: role of the adrenal medulla

Nociceptive neuroendocrine negative feedback control of neurogenic inflammation activated by capsaicin in the rat paw: role of the adrenal medulla

Inflammatory Mediators in Gastrointestinal Defense and Injury

Contribution of adrenal hormones to nicotine‐induced inhibition of synovial plasma extravasation in the rat

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