Articles: hyperalgesia.
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Transient inflammation is known to alter visceral sensory function and frequently precede the onset of symptoms in a subgroup of patients with irritable bowel syndrome (IBS). Duration and severity of the initial inflammatory stimulus appear to be risk factors for the manifestation of symptoms. Therefore, we aimed to characterize dose-dependent effects of trinitrobenzenesulfonic acid (TNBS)/ethanol on: (1) colonic mucosa, (2) cytokine release and (3) visceral sensory function in a rat model. ⋯ In 0.2 ml TNBS/ethanol group, VMR was only enhanced after repeated visceral stimulation. Visceral hyperalgesia occurs after a transient colitis. However, even a mild acute but asymptomatic colitis can induce long-lasting visceral hyperalgesia in the presence of additional stimuli.
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Comparative Study
Differentiation between capsaicin-induced allodynia and hyperalgesia using a thermal operant assay.
Investigations of new analgesic treatments ideally are coupled with the use of compassionate methods for pain testing in animals. Recently, we described a novel operant thermal testing device that can be used to quantify orofacial pain. The objective of the current study was to differentiate thermal allodynia from hyperalgesia using this operant thermal assay. ⋯ The temporal profile for completing the task was also significantly altered following capsaicin treatment. These data demonstrate that using the operant orofacial assay in conjunction with capsaicin cream can provide a reproducible, sensitive, minimally invasive, and powerful approach for quantifying and studying enhanced thermal pain within the trigeminal system. This technique provides an alternative to reflex tests of orofacial sensitivity, and it presents a pivotal link for translating basic pain research into clinic trial strategies.
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Bothrops jararaca venom (Bjv) is known to induce local inflammation and severe pain. Since, mast cells are able to secrete mediators involved in algesic processes, in this study we examined the putative role of these cells in the hyperalgesia triggered by Bjv in the rat paw. We noted that treatment with mast cell stabilizer sodium cromoglicate as well as with histamine and 5-hydroxytriptamine receptor antagonists meclizine and methysergide, respectively, inhibited the Bjv-induced hyperalgesia. ⋯ Bjv-induced histamine secretion was clearly sensitive to treatment with sodium cromoglicate and sodium nedocromil. We further observed that metalloproteinase inhibitors 1,10-phenantroline and DM43 inhibited mast cell degranulation in vitro, under conditions where inhibitors of phospholipase A(2) as well as of serine- and cysteine-proteinases were inactive. Altogether, our findings indicate that mast cells seem to contribute to the hyperalgesia caused by Bjv in the rat paw, and also provide evidence that this response might be dependent on the ability of the Bjv to activate directly mast cells.
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Neuroscience letters · Jun 2006
Propentofylline attenuates vincristine-induced peripheral neuropathy in the rat.
The development of painful peripheral neuropathy is a dose-limiting side effect of numerous cancer chemotherapeutic agents. The present study utilized a rodent model of vincristine-induced neuropathy to determine whether a glial modulating agent, propentofylline, could attenuate vincristine-induced mechanical allodynia. Intravenous vincristine administered on days 1 through 5 and days 8 through 11 produced mechanical allodynia using 2 and 12 g von Frey filaments. ⋯ Daily intraperitoneal propentofylline at 10 mg/kg attenuated mechanical allodynia induced by vincristine administration. In addition, propentofylline was found to decrease spinal microglial and astrocytic activation on day 15. These data suggest that central glial cells may play an important role in the development of painful neuropathy following vincristine administration.
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The paradigm of early treatment of the migraine attack at mild pain intensity has become one alternative to circumventing the problem of compromised oral absorption of symptomatic drugs due to migraine-induced gastrointestinal dysmotility. Early treatment also has been proposed to be advantageous because most migraineurs could be less responsive to delayed treatment, owing to the development of central sensitization of the trigeminal pain transmission. Ranking the underlying principles, it seems that the improved response to an oral triptan formulation at mild migraine symptom intensity has more to do with less impaired gastrointestinal absorption in the early stage of the attack than decreasing the time and preventing chances for central sensitization and development of cutaneous allodynia. ⋯ Individually tailored use of the available triptan formulations will increase, without any doubt, the within-migraineur consistency of response. It also will reduce the overall proportion of migraine attacks or migraineurs not responding to triptan treatment. Notwithstanding, the recommendation of early treatment during the migraine attack when the pain is mild remains valid.