Effect of fedotozine on the cardiovascular pain reflex induced by distension of the irritated colon in the anesthetized rat

Langlois, A.; Diop, Laurent; Rivière, Pierre; Pascaud, X.; Junien, Jean‐Louis

doi:10.1016/0014-2999(94)90780-3

Cited by 51 publications

(22 citation statements)

References 28 publications

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“…Indeed, after TNBS-induced rectocolitis, colonic and abdominal responses were observed at a lower diameter of distension than in control animals (Morteau et al, 1994). In our hands, intracolonic administration of acetic acid induced the sensitization of nociceptive visceral afferents, which in turn produced colonic hypersensitivity (Langlois et al, 1994). However, the time course and the chronicity of the development of these hyperalgesia and allodynia are poorly understood.…”

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confidence: 53%

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Pregabalin (CI-1008) Inhibits the Trinitrobenzene Sulfonic Acid-Induced Chronic Colonic Allodynia in the Rat

Diop¹,

Raymond²,

Fargeau³

et al. 2002

J Pharmacol Exp Ther

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In human, digestive disorders are often associated with visceral pain. In these pathologies, visceral pain threshold is decreased indicating a visceral hypersensitivity. Pregabalin [CI-1008; S-(ϩ)-3-isobutylgaba] presents antihyperalgesic actions in inflammatory somatic pain models. This study was designed to evaluate 1) the effect of injection of TNBS into the colon on visceral pain threshold, and 2) the antihyperalgesic effect of pregabalin on TNBS-induced chronic colonic allodynia. A significant decrease in the colonic pain threshold was observed in trinitrobenzene sulfonic acid (TNBS)-treated animals (17.8 Ϯ 1.27 versus 43.4 Ϯ 1.98 mm Hg). Pregabalin (30 -200 mg/kg s.c.) and morphine (0.1-1 mg/kg s.c.) showed a dose-related inhibition of TNBS-induced colonic allodynia. Pregabalin did not inhibit the colonic inflammatory effect of TNBS. In normal conditions (control animals), morphine (0.3 mg/kg s.c.) significantly increased the colonic pain threshold, whereas pregabalin (200 mg/kg s.c.) did not modify the colonic pain threshold. Pregabalin suppressed the TNBS-induced colonic allodynia but did not modify the colonic threshold in normal conditions. The ability of pregabalin to block the chronic colonic allodynia indicates that it is effective in abnormal colonic hypersensitivity, suggesting a possible effect in chronic pain in irritable bowel syndrome.

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confidence: 53%

“…Indeed, TNBS-induced rectocolitis produces a colonic allodynia (Morteau et al, 1994). In our laboratory, we have demonstrated that colonic hypersensitivity can also be induced by intracolonic instillation of acetic acid (Langlois et al, 1994). This effect was observed during 1 day.…”

Section: Pregabalin and Visceral Pain 1019mentioning

confidence: 80%

Pregabalin (CI-1008) Inhibits the Trinitrobenzene Sulfonic Acid-Induced Chronic Colonic Allodynia in the Rat

Diop¹,

Raymond²,

Fargeau³

et al. 2002

J Pharmacol Exp Ther

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“…It has been shown in experimental studies that chemical stimuli/irritation of the viscera leads to an alteration of normal reflexes (7,60,80,90) and an increased sensitization of the afferent innervations of these visceral structures (17,39,93). This leads to excitation of spinal neurons accompanied by a change in their receptive field properties (33,34).…”

Section: Spinal Nmda Receptors and Colonic Inflammationmentioning

confidence: 99%

NMDA Receptors and Colitis: Basic Science and Clinical Implications

Zhou

Verne

2008

rev analg

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During the last decade, research focusing primarily on alterations in the peripheral and central nervous system has improved our understanding of the pathophysiological mechanisms of chronic visceral pain. These studies have demonstrated significant physiological changes following injury to the viscera in the firing patterns of both primary afferent neurons that transmit nociceptive information from the viscera and in central neurons that process the nociceptive information. A number of receptors, neurotransmitters, cytokines, and second messenger systems in these neurons have been implicated in the enhancement of visceral nociception. N-methyl-d-aspartic acid (NMDA) receptors play an important role in chronic visceral pain and hypersensitivity that is present in the setting of colonic inflammation. NMDA receptors are found in the peripheral nervous system as well as the central terminal of primary afferent neurons and have been shown to play an important role in regulating the release of nociceptive neurotransmitters. Recent work has demonstrated the presence of NMDA receptors in the enteric nervous system. In this article, we will discuss more recent evidence of the role of NMDA receptors in visceral pain associated with colitis.

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“…38 Evidence from several experimental studies in animals indicates that fedotozine influences visceral sensitivity. [39][40][41] The efficacy of fedotozine against noxious visceral stimuli has been confirmed in an elegant manner in rats. 42 Intraperitoneal administration of acetic acid induces the expression of Fos, which is a marker of neuronal activation.…”

Section: Opiatesmentioning

confidence: 96%