10 resultados para Dispositivo para Oclusão Septal

em Biblioteca Digital da Produção Intelectual da Universidade de São Paulo


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O tratamento da má oclusão de Classe II sem extrações dentárias vem ganhando popularidade na comunidade ortodôntica já há três décadas. Aparelhos funcionais fixos vêm sendo utilizados por profissionais, de maneira crescente, para promover compensações dentoalveolares e corrigir a má oclusão de Classe II. Os efeitos mais significativos são observados em pacientes com padrão de crescimento horizontal. Um caso clínico será relatado com o uso do aparelho fixo Twin Force Bite Corrector em uma paciente do sexo feminino, para a correção da Classe II. Esse dispositivo de ancoragem fixa dispensa o uso de aparelhos funcionais removíveis e não necessita da cooperação do paciente.

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There are fibers in the left ventricle (LV) (LV middle network) that in around one third of cases may be considered a true septal fascicle that arises from the common left bundle. Its presence and the evidence that there are 3 points of activation onset in the LV favor the quadrifascicular theory of the intravantricular activation of both ventricles. Since the 70s, different authors have suggested that the block of the left middle fibers (MS)/left septal fascicle may explain different electrocardiographic (ECG) patterns. The 2 hypothetically based criteria that are in some sense contradictory include: a) the lack of septal "q" wave due to first left and later posteriorly shifting of the horizontal plane loop and b) the presence of RS in lead V-2 (V-1-V-2) due to some anterior shifting of the horizontal plane vectorcardiogram loop. However, there are many evidence that the lack of septal q waves can be also explained by predivisional first-degree left bundle-branch block and that the RS pattern in the right precordial leads may be also explained by first-degree right bundle-branch block. The transient nature of these patterns favor the concept that some type of intraventricular conduction disturbance exists but a doubt remains about its location. Furthermore, the RS pattern could be explained by many different normal variants. To improve our understanding whether these patterns are due to MF/left septal fascicle block or other ventricular conduction disturbances (or both), it would be advisable: 1) To perform more histologic studies (heart transplant and necropsy) of the ventricular conduction system; 2) To repeat prior experimental studies using new methodology/technology to isolate the MF; and 3) To change the paradigm: do not try to demonstrate if the block of the fibers produces an ECG change but to study with new electroanatomical imaging techniques, if these ECG criteria previously described correlate or not with a delay of activation in the zone of the LV that receives the activation through these fibers or in other zones. (C) 2012 Elsevier Inc. All rights reserved.

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PURPOSE: Describe a modified technique to increase nostril cross-sectional area using rib and septal cartilage graft over alar nasal cartilages. METHODS: A modified surgical technique was used to obtain, carve and insert cartilage grafts over alar nasal cartilages. This study used standardized pictures and measured 90 cadaveric nostril cross-sectional area using Autocad (c); 30 were taken before any procedure and 60 were taken after grafts over lateral crura (30 using costal cartilage and 30 using septal cartilage). Statistical analysis were assessed using a model for repeated measures and ANOVA (Analysis of Variance) for the variable "area". RESULTS: There's statistical evidence that rib cartilage graft is more effective than septal cartilage graft. The mean area after the insertion of septal cartilage graft is smaller than the mean area under rib graft treatment (no confidence interval for mean difference contains the zero value and all P-values are below the significance level of 5%). CONCLUSIONS: The technique presented is applicable to increase nostril cross section area in cadavers. This modified technique revealed to enhance more nostril cross section area with costal cartilage graft over lateral crura rather than by septal graft.

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We have previously reported that noradrenaline (NA) microinjected into the lateral septal area (LSA) caused pressor and bradicardic responses that were mediated by vasopressin release into the circulation through the paraventricular nucleus of hypothalamus (PVN). Although PVN is the final structure involved in the cardiovascular responses caused by NA in the LSA, there is no evidence of direct connections between these areas, suggesting that some structures could be links in this pathway. In the present study, we verified the effect of reversible synaptic inactivation of the medial amygdaloid nucleus (MeA), bed nucleus of stria terminalis (BNST) or diagonal band of Broca (DBB) with Cobalt Chloride (CoCl2) on the cardiovascular response to NA microinjection into the LSA of unanesthetized rats. Male Wistar rats had guide cannulae implanted into the LSA and the MeA, BNST or DBB for drug administration, and a femoral catheter for blood pressure and heart rate recordings. Local microinjection of CoCl2 (1 mm in 100 nL) into the MeA significantly reduced the pressor and bradycardic responses caused by NA microinjection (21 nmol in 200 nL) into the LSA. In contrast, microinjection of CoCl2 into the BNST or DBB did not change the cardiovascular responses to NA into the LSA. The results indicate that synapses within the MeA, but not in BNST or DBB, are involved in the cardiovascular pathway activated by NA microinjection into the LSA.

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We have previously reported that stimulation of alpha-1 adrenoceptors by noradrenaline (NA) injected into the lateral septal area (LSA) of anaesthetized rats causes pressor and bradycardic responses that are mediated by acute vasopressin release into the circulation through activation of the paraventricular nucleus (PVN). Although the PVN is the final structure of this pathway, the LSA has no direct connections with the PVN, suggesting that other structures may connect these areas. To address this issue, the present study employed c-Fos immunohistochemistry to investigate changes caused by NA microinjection into the LSA in neuronal activation in brain structures related to systemic vasopressin release. NA microinjected in the LSA caused pressor and bradycardic responses, which were blocked by intraseptal administration of alpha-1 adrenoceptor antagonist (WB4101, 10 nmol/200 nL) or systemic V-1 receptor antagonist (dTyr(CH2)5(Me)AVP, 50 mu g/kg). NA also increased c-Fos immunoreactivity in the prelimbic cortex (PL), infralimbic cortex (IL), dorsomedial periaqueductal gray (dmPAG), bed nucleus of the stria terminalis (BNST), PVN, and medial amygdala (MeA). No differences in the diagonal band of Broca, cingulate cortex, and dorsolateral periaqueductal gray (dlPAG) were found. Systemic administration of the vasopressin receptor antagonist dTyr AVP (CH2)5(Me) did not change the increase in c-Fos expression induced by intra-septal NA. This latter effect, however, was prevented by local injection of the alpha-1 adrenoceptor antagonist WB4101. These results suggest that areas such as the PL, IL, dmPAG, BNST, MeA, and PVN could be part of a circuit responsible for vasopressin release after activation of alpha-1 adrenoceptors in the LSA.

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The lateral septal area (LSA) is a limbic structure involved in autonomic, neuroendocrine and behavioural responses. An inhibitory influence of the LSA on baroreflex activity has been reported; however, the local neurotransmitter involved in this modulation is still unclear. In the present study, we verified the involvement of local LSA adrenoceptors in modulating cardiac baroreflex activity in unanaesthetized rats. Bilateral microinjection of the selective a1-adrenoceptor antagonist WB4101 (10 nmol in a volume of 100 nl) into the LSA decreased baroreflex bradycardia evoked by blood pressure increases, but had no effect on reflex tachycardia evoked by blood pressure decreases. Nevertheless, bilateral administration of the selective a2-adrenoceptor antagonist RX821002 (10 nmol in 100 nl) increased baroreflex tachycardia without affecting reflex bradycardia. Treatment of the LSA with a cocktail containing WB4101 and RX821002 decreased baroreflex bradycardia and increased reflex tachycardia. The non-selective beta-adrenoceptor antagonist propranolol (10 nmol in 100 nl) did not affect either reflex bradycardia or tachycardia. Microinjection of noradrenaline into the LSA increased reflex bradycardia and decreased the baroreflex tachycardic response, an opposite effect compared with those observed after double blockade of a1- and a2-adrenoceptors, and this effect of noradrenaline was blocked by local LSA pretreatment with the cocktail containing WB4101 and RX821002. The present results provide advances in our understanding of the baroreflex neural circuitry. Taken together, data suggest that local LSA a1- and a2-adrenoceptors modulate baroreflex control of heart rate differently. Data indicate that LSA a1-adrenoceptors exert a facilitatory modulation on baroreflex bradycardia, whereas local a2-adrenoceptors exert an inhibitory modulation on reflex tachycardia.

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OBJETIVO: Caracterizar o controle motor dos músculos masseter e temporal e a morfologia do músculo masseter em atividades da função mastigatória em indivíduos com oclusão normal; verificar a compatibilidade entre os exames de eletromiografia de superfície (EMGs) e ultrassonografia (USG). MÉTODOS: Participaram 22 indivíduos adultos, de ambos os gêneros, sem alterações no sistema miofuncional orofacial. Os procedimentos adotados para avaliação dos participantes foram: EMGs dos músculos masseteres (MM) e temporais (MT); e USG dos MM, na realização de três tarefas - repouso muscular, apertamento dentário com algodão, apertamento dentário sem algodão. RESULTADOS: Para análise estatística dos dados foram utilizados os testes de Kolmogorv-Smirnov, teste-T pareado e Correlação de Spearman, com nível de significância de 5%. Na EMGs observou-se diferença entre a ativação de MM e MT no apertamento dentário com e sem algodão, sendo MT mais ativo que MM em ambas as tarefas. Não foram observadas diferenças entre as hemifaces, tanto na EMGs quanto na USG. Observou-se também correlação positiva entre os exames na condição de apertamento dentário sem algodão esquerdo e na condição de apertamento dentário esquerdo com algodão, e tendência à significância no apertamento dentário direito sem algodão. CONCLUSÃO: A associação da EMGs e USG na investigação da funcionalidade muscular traz importantes informações sobre fisiologia da musculatura esquelética. Os resultados do presente estudo indicam haver correlação entre a EMGs e a USG, ou seja, o aumento da atividade elétrica e o aumento correspondente da espessura do músculo.