Navegando por Assunto "Tenotomia"

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Acesso aberto (Open Access)
Inibição nitrérgica local favorece o processo de regeneração do tendão de aquiles em ratos submetidos à tenotomia
(Universidade Federal do Pará, 2011-05-27) MORAES, Suellen Alessandra Soares de; SILVA, Anderson Manoel Herculano Oliveira da; http://lattes.cnpq.br/8407177208423247
The tendon injuries prevalence has been increased usually by repetitive movements in the occupational and recreational activities of society. The main features this injury involve healing dysfunction and loss of extracellular matrix. At this tissue, the extracellular matrix is basically made of type I collagen and the loss of this protein associated with problems in the remodeling have been considered the major responsible for the symptomatic and functional effects of injury. Additionally the literature reports the nitric oxide synthase expression was up-regulated throughout the repair process. At this context the propose of this work is investigated the nitrergic local inhibition in tissue and functional recovery after tendon injury. We used a experimental model of Achilles tendon rupture for establish pathophysiological changes similar to chronic tendinopathy. The animals were divided into experimental groups control, injury+vehicle (saline, 0,9%), injury+L- Nω-nitro-L-arginine methyl ester (L-NAME, 5mM) and injury+sodium nitroprusside (SNP, 3mM), which were followed until the 21º day, when were killed to collect samples. In order to access nitric oxide production Griess nitrite assay was used. Functional recovery was calculated by Achilles Functional Index (AFI) in 0, 7, 14 and 21 days. Tendons were also processed for histomorphological and autofluorescence analysis. The body weight gain was also evaluated. We characterized the effect of drugs about tissue without stronger systemic influences by maintenance of body weight and plasmatic levels of nitrite. The L-NAME led to significant decrease in the cellular density, vessel formation between collagen network, accelerated the tissue organization and restored early the functional pattern at 21 days after injury. On the other hand, the treatment with SNP and vehicle remained the tissue disorganization and low functional performance. Taken together our results suggest a positive effect of local suppression of NOS after rupture for tissue remodeling, contributing to tendon regeneration.
Acesso aberto (Open Access)
Local inhibition of nitrergic activity in tenotomized rats accelerates muscle regeneration by increasing fiber area and decreasing central core lesions
(Universidade Federal do Pará, 2017-02) SEABRA, Aline Damasceno; MORAES, Suellen Alessandra Soares de; BATISTA, Evander de Jesus Oliveira; GARCIA, Tarcyane Barata; SOUZA, Martha Costa de; OLIVEIRA, Karen Renata Matos; SILVA, Anderson Manoel Herculano Oliveira da
Muscular atrophy is a progressive degeneration characterized by muscular proteolysis, loss of mass and decrease in fiber area. Tendon rupture induces muscular atrophy due to an intrinsic functional connection. Local inhibition of nitric oxide synthase (NOS) by No-nitro-L-arginine methyl ester (L-NAME) accelerates tendon histological recovery and induces functional improvement. Here we evaluate the effects of such local nitrergic inhibition on the pattern of soleus muscle regeneration after tenotomy. Adult male Wistar rats (240 to 280 g) were divided into four experimental groups: control (n=4), tenotomized (n=6), vehicle (n=6), and L-NAME (n=6). Muscular atrophy was induced by calcaneal tendon rupture in rats. Changes in muscle wet weight and total protein levels were determined by the Bradford method, and muscle fiber area and central core lesion (CCL) occurrence were evaluated by histochemical assays. Compared to tenotomized (69.3±22%) and vehicle groups (68.1%±17%), L-NAME treatment induced an increase in total protein level (108.3±21%) after 21 days post-injury. A reduction in fiber areas was observed in tenotomized (56.3±1.3%) and vehicle groups (53.9±3.9%). However, L-NAME treatment caused an increase in this parameter (69.3±1.6%). Such events were preceded by a remarkable reduction in the number of fibers with CCL in L-NAME-treated animals (12±2%), but not in tenotomized (21±2.5%) and vehicle groups (19.6±2.8%). Altogether, our data reveal that inhibition of tendon NOS contributed to the attenuation of atrophy and acceleration of muscle regeneration.
Acesso aberto (Open Access)
Regeneração tendínea em modelo murino: estudo da plasticidade central e investigação do efeito da modulação nitrérgica na plasticidade periférica
(Universidade Federal do Pará, 2015-08-10) MORAES, Suellen Alessandra Soares de; SILVA, Anderson Manoel Herculano Oliveira da; http://lattes.cnpq.br/8407177208423247
Tendon injuries cause strong impact on people due to pain and functional limitation resulting therefrom. After injury, the tissue starts to present a network of nerves. Furthermore, there is evidence for the occurrence of central plasticity after injury. Among the molecular factors involved in injury repair, nitric oxide (NO) is implicated in tissue remodeling, but its effects are not yet well understood. The purpose of this study is to ascertain the existence of central plasticity and the influence of NO in peripheral plasticity, functional limitation and tendon regeneration in murine model. To study the effects of NO in peripheral plasticity, we used control animals (CTRL, without injury) or animals treated with saline (SAL, 0.9% NaCl), L-nitro-arginine-methyl-ester (L-NAME, NO-synthesis inhibitor) and sodium nitroprusside (SNP, NO donor) every other day until the 21st day post injury (DPI). To evaluate central plasticity (L5 segment), an injury was performed alone and the spinal cord collected at 2 or 21 DPI. We analyzed the integrity and tissue organization in tendon samples by H&E, transmission electron microscopy and immunofluorescence, which was also used to evaluate peripheral plasticity. To assess tendon functional recovery, we determined the Achilles functional index, the joint angle and the open field. In spinal cord studies, we investigated glial reactivity and neuron involvement after injury by co-localizations with the cell activation indicator c-Fos. The findings of this research show that NO inhibition promotes tissue organization in association to an increase in collagen synthesis, secretion and deposition. Besides, L-NAME local administration seems to favor cell differentiation to tenocyte-like morphological types and improve the organization of nerve branches in between the collagen mesh in correlation with functional recovery at 21 DPI. On the other hand, increased levels of NO by SNP promoted worsening in almost all parameters analyzed. Our data also show tendon injury triggers a central plasticity process with an increase in glial reactivity at 2 DPI and ipsilateral cell activation at 2 and 21 DPI. Afterall, our findings point out occurrence of central plasticity after tendon injury and favoring of tissue repair and peripheral plasticity through nitrergic blockage, unraveling fundamental aspects of tissue recovery that may represent new targets for a therapeutical approach in tendon injuries.