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• W1750344559 abstract "Introduction Most pain-associated clinical symptoms are primarly caused by inflammation. As a cardinal sign of inflammation, pain actually has a protective role against further lesions (Kidd et al 2001). Thus, in normal conditions, inflammation isolates the damaged tissue and promotes tissue restoration, but this process may degenerate, being accused in many chronic diseases (Mungiu 2002). Tissue damage or the presence of irritants may trigger biochemical changes in peripheral sensory nerve endings, phenomenon called inflammatory process (Winter et al 1962). The release of proinflammatory mediators influences free sensory nerve endings and generates an enhanced action potential that is transmitted and results in the onset of pain. Persistent inflammation leads to increased excitability in sensory nerve fibers, amplifying response to nociceptive stimuli, phenomenon called hyperalgesia (Winter et al 1962; Kidd et al 2001). Pharmacological interventions in the treatment of inflammatory pain increasingly refer to the mechanisms by which proinflammatory mediators generate pain signals and initiate amplified transmission in neural circuits (Mungiu 2002). Lamotrigine (LTG) is an antiepileptic drug of the phenyltriazine class, chemically unrelated to existing antiepileptic drugs. LTG blocks voltage-dependent sodium channels and inhibits glutamate release (Nakamura-Craig & Follenfant 1995). Inhibition of voltage-dependent sodium channels leads to the stabilization of the presynaptic membrane and the decrease in the release of excitatory neurotransmitters in spinal dorsal horn neurons. Studies show that LTG produces voltage-dependent blocking of sustained repetitive neuronal discharges in neuronal cultures (Lees & Leach 1993) and inhibits the pathological release of glutamate and glutamate-generated action potentials (Messenheimer 1995). This mechanism supports the use of LTG to control nociception and epilepsy (Messenheimer 1995). Other studies have shown the effect of LTG in the fight against hyperalgesia and allodynia due to partial peripheral nerve injury( Arguelles et al 2002). The complex mechanism of action and the use in different conditions suggests the effect of LTG on voltage-dependent N-type and P-type calcium channels, as well as the inhibition of serotonin, dopamine, acetylcholine and norepinephrine reuptake (Lees & Leach 1993; Stefani et al 1996). The effect on the GABAergic system has also been demonstrated, consisting in Abstract. Objective: The purpose of this study is to assess the effects of lamotrigine (LTG) in experimental animal models of pain caused by inflammation. Materials and methods. The study was performed on 50 white male Wistar rats, weighing between 110 and 200 g, randomized into 5 groups: group 1 control injected with saline solution (0.5 ml/100 g) (C), group 2 – reference pain reliever, metamizole (50 mg/kg) (I), group 3 reference pain reliever, diclofenac (15 mg/kg) (D), group 4 LTG (50 mg/kg) (LTG50), group 5 LTG (20 mg/kg) (LTG20). The evolution of the inflammation was assessed by measuring the initial volume of the foot and, after induction of inflammation, by estimating the corresponding volume at different previously established times, using a plethysmometer Ugo Basile. The difference between the volume measured at different times and the baseline volume represented the volume of the induced edema and the hyperalgesic response latency produced by mechanical compression (analgesy-meter). The mechanical paw pressure test was applied basally after injection (0.5 ml/100g intraperitoneal injection). The average values, error and standard deviation were determined for each group and for each particular moment. Results: The measurement of the kaolin-injected paw volume did not show significant changes over the LTG-induced edema. Groups treated with LTG after inducing the inflammatory process reveal dose-dependent increased pain thresholds. LTG50 increased pain thresholds one hour after recording baseline values before the induction of the inflammatory process, both for the inflamed paw and for the opposite witness paw. The antihyperalgesic effect is noticeable, compared to the control group, after one hour for LTG50 (p=0.001) and after 1 and 2 hours for LTG20 (p=0.03). Compared to reference pain relievers employed in acute and inflammatory pain, metamizole and diclofenac, LTG did not significantly increase the pain threshold. Conclusions: LTG exhibits dose-dependent antihyperalgesic effects in acute inflammatory pain. In comparison with the control group, LTG displays noticeable antihyperalgesic effect in doses of 50 mg/kg and 20 mg/kg throughout the entire testing period, with similar effect to that of diclofenac during the first hour after administration." @default.
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• W1750344559 date "2014-01-01" @default.
• W1750344559 modified "2023-10-17" @default.
• W1750344559 title "Lamotrigine in an experimental animal model of inflammatory pain." @default.
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