Laserterapia de baixa potência na modulação da temperatura tecidual e da hiperalgesia após lesão parcial do tendão do calcâneo em ratos

Abstract

Despite its reinforced structure, acute and chronic injuries Achilles tendon represent a complex clinical entity, occurring even during the execution of non-sports activities, at low intensities. The more therapeutic resources prove proven effective and advocated a mainstream treatment, structured in reducing pain and stimulate the mobility and discharge increasingly early weight, the better intervention strategies. With effects that reduce inflammation and stimulate tissue repair in low level laser therapy (LLLT) emerges as a promising clinical use, non-invasive, safe and effective for these injuries. The objective of this study was to evaluate the effects of LLLT on the modulation of tissue temperature and hyperalgesia and after partial injury of the Achilles tendon in rats, the experimental periods: 6 hours, 24 hours and 48 hours. The sample consisted of 45 rats, submitted evaluations: thermal, and hyperalgesia. After the evaluations were performed randomization of the mice into three groups, one being considered as a control and the other groups characterized by two doses of LLLT: 1.4 Joules and 2.1 Joules, soon realized after partial injury of the Achilles tendon, performed in all groups. Each group was composed of three sub-groups, corresponding to three experimental periods: 6 hours, 24 hours and 48 hours, characterized by the revaluation and subsequent eutanásia in order to evaluate the chemical inflammatory mediators (IL-6, TNF-α, IL-10) and activation of NKA-A receptor. Two-way ANOVA test with post hoc Bonferroni was applied between the experimental groups, for analysis. For evaluations by infrared thermography and hyperalgesia was used analysis of variance (ANOVA one-way) with post-hoc Tukey. Irradiation using LBP with 808 nm wavelength, doses J 1.4 and J 2.1, administered immediately after partial lesion of the Achilles tendon rats promotes the reduction of tissue temperature and inflammatory mediators at the site of injury, and 24 48 hours after injury. And yet, it reduces hyperalgesia and activation of pain receptors NK-A, increasing pressure stimulus threshold 6, 24 and 48 hours after application, regardless of the dose used.