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Exposure to chronic sustained hypoxia (SH), as experienced in high altitudes, elicits an increase in ventilation, named ventilatory acclimatization to hypoxia (VAH). We previously showed that rats exposed to short-term (24 h) SH exhibit enhanced abdominal expiratory motor activity at rest, accompanied by augmented baseline sympathetic vasoconstrictor activity. In the present study, we investigated whether the respiratory and sympathetic changes elicited by short-term SH are accompanied by carotid body chemoreceptor sensitization. Juvenile male Holtzman rats (60–80 g) were exposed to SH (10% O2 for 24 h) or normoxia (control) to examine basal and hypoxic-induced ventilatory parameters in unanesthetized conditions, as well as the sensory response of carotid body chemoreceptors in artificially perfused in situ preparations. Under resting conditions (normoxia/normocapnia), SH rats (n = 12) exhibited higher baseline respiratory frequency, tidal volume, and minute ventilation compared to controls (n = 11, P < 0.05). SH group also showed greater hypoxia ventilatory response than control group (P < 0.05). The in situ preparations of SH rats (n = 8) exhibited augmented baseline expiratory and sympathetic activities under normocapnia, with additional bursts in abdominal and thoracic sympathetic nerves during late expiratory phase that were not seen in controls (n = 8, P < 0.05). Interestingly, basal and potassium cyanide-induced afferent activity of carotid sinus nerve (CSN) was similar between SH and control rats. Our findings indicate that the maintenance of elevated resting ventilation, baseline sympathetic overactivity, and enhanced ventilatory responses to hypoxia in rats exposed to 24 h of SH are not dependent on increased basal and sensorial activity of carotid body chemoreceptors.

Study objectives Exposure to postnatal chronic intermittent hypoxia (pCIH), as experienced in sleep-disordered breathing, is a risk factor for developing cardiorespiratory diseases in adulthood. pCIH causes respiratory instability and motor dysfunction that persist until adult life. In this study, we investigated the impact of pCIH on the sympathetic control of arterial pressure in rats. Methods and Results Neonate male Holtzman rats (P0-1) were exposed to pCIH (6% O2 for 30 s, every 10 min, 8 h/day) during their first 10-15 days of life, while control animals were maintained under normoxia. In early adult life (P25-40), freely behaving pCIH animals (n=13) showed higher baseline arterial pressure levels linked to augmented sympathetic-mediated variability than control animals (n=12, P&lt;0.05). Using decerebrated in situ preparations, we found that juvenile pCIH rats exhibited a two-fold increase in thoracic sympathetic nerve activity (n=14) and elevated firing frequency of ventromedullary presympathetic neurons (n=7) compared to control rats (n=6-7, P&lt;0.05). This pCIH-induced sympathetic dysregulation was associated with increased HIF-1α (hypoxic inducible factor) mRNA expression in catecholaminergic pre-sympathetic neurons (n=5,P&lt;0.05). At older age (P90-99), pCIH rats displayed higher arterial pressure levels and larger depressor responses to ganglionic blockade (n=6-8, P&lt;0.05), confirming the sympathetic overactivity state. Conclusions pCIH facilitates the vasoconstrictor sympathetic drive by mechanisms associated with enhanced firing activity and HIF-1α expression in ventromedullary pre-sympathetic neurons. This excessive sympathetic activity persists until adulthood resulting in high blood pressure levels and variability, which contribute to developing cardiovascular diseases.

Purinergic receptors are present in the lateral parabrachial nucleus (LPBN), a pontine structure involved in the control of sodium intake. In the present study, we investigated the effects of α,β-methyleneadenosine 5'-triphosphate (α,β-methylene ATP, selective P2X purinergic agonist) alone or combined with pyridoxalphosphate-6-azophenyl-2',4'-disulfonic acid (PPADS, P2X purinergic antagonist) or suramin (non-selective P2 purinergic antagonist) injected into the LPBN on sodium depletion-induced 1.8% NaCl intake. Male Holtzman rats with stainless steel cannulas implanted into the LPBN were used. Sodium depletion was induced by treating rats with the diuretic furosemide (20mg/kg of body weight) followed by 24h of sodium-deficient diet. Bilateral injections of α,β-methylene ATP (2.0 and 4.0nmol/0.2μl) into the LPBN increased sodium depletion-induced 1.8% NaCl intake (25.3±0.8 and 26.5±0.9ml/120min, respectively, vs. saline: 15.2±1.3ml/120min). PPADS (4nmol/0.2μl) alone into the LPBN did not change 1.8% NaCl intake, however, pretreatment with PPADS into the LPBN abolished the effects of α,β-methylene ATP on 1.8% NaCl intake (16.9±0.9ml/120min). Suramin (2.0nmol/0.2μl) alone into the LPBN reduced sodium depletion-induced 1.8% NaCl intake (5.7±1.9ml/120min, vs. saline: 15.5±1.1ml/120min), without changing 2% sucrose intake or 24h water deprivation-induced water intake. The combination of suramin and α,β-methylene ATP into the LPBN produced no change of 1.8% NaCl intake (15.2±1.2ml/120min). The results suggest that purinergic P2 receptor activation in the LPBN facilitates NaCl intake, probably by restraining LPBN mechanisms that inhibit sodium intake.

Periods of apnoea, commonly observed in prematures and newborns, are an important risk factor for the development of cardiorespiratory diseases in adulthood. In the present study, we evaluated changes in pulmonary ventilation and respiratory motor pattern in juvenile and adult rats exposed to postnatal chronic intermittent hypoxia (pCIH). Newborn male Holtzman rats (P1) were submitted to pCIH (6% O 2 for 30 s, every 9 min, 8 h a day (09.30-17.30 h)) during their first 10 days of life, while control animals were maintained under normoxic conditions (20.8% O 2). Thereafter, animals of both groups were maintained under normoxia until the experiments. Unanaesthetized juvenile pCIH rats (n = 27) exhibited elevated tidal volume and respiratory irregularities (P < 0.05) compared to control rats (n = 7). Decerebrate, arterially perfused in situ preparations of juvenile pCIH rats (n = 11) displayed augmented phrenic nerve (PN) burst amplitude and reduced central vagus nerve activity in comparison to controls (n = 10). At adulthood, pCIH rats (n = 5) showed enhanced tidal volume (P < 0.05) and increased respiratory variability compared to the control group (n = 5). The pCIH-induced changes in ventilation and respiratory motor outputs were prevented by treatment with the DNA methyltransferase inhibitor decitabine (1 mg kg −1 , I.P.) during the exposure to pCIH. Our data demonstrate that pCIH in rats impacts, in a persistent way, control of the respiratory pattern, increasing PN activity to the diaphragm and reducing the vagal-related activity to laryngeal muscles, which, respectively, may contribute to improve resting pulmonary ventilation and predispose to collapse of the upper airways during quiet breathing.

Os déficits de equilíbrio postural podem levar a limitações nas atividades de vida diária, reduzindo a autonomia e aumentando o risco de quedas dos indivíduos. A fisioterapia dispõe de uma variedade de recursos que podem ser utilizados para a reabilitação do equilíbrio postural, e a realidade virtual é um dos recursos que vem sendo utilizado com este objetivo, pois através de repetição, feedback e motivação, pode proporcionar ao usuário maior controle do equilíbrio postural. Objetivo: Revisar a literatura existente sobre os efeitos das intervenções com jogos de realidade virtual na reabilitação de déficits de equilíbrio postural. Método: Foi realizada uma revisão de literatura utilizando Descritores em Ciências da Saúde (DECs), com análise de publicações impressas em livros do acervo da Biblioteca Júlio Bordignon da Faculdade de Educação e Meio Ambiente – FAEMA, e consulta de trabalhos indexados e publicados nas bases de dados LILACS, SCIELO, PubMed e Google Acadêmico. Considerações Finais: Os estudos analisados apontam que a intervenção terapêutica com o uso da realidade virtual como uma ferramenta tecnológica para a reabilitação do equilíbrio postural mostrou ser de grande importância e poderia auxiliar as terapias tradicionais, no entanto, mais estudos serão necessários para entender qual é o mecanismo pelo qual a realidade virtual atua melhorando o equilíbrio postural. ABSTRACT: Postural balance deficits can lead to limitations in activities of daily living, reducing autonomy and increasing the risk of falls of individuals. Physiotherapy has a variety of resources that can be used for the rehabilitation of postural balance, and virtual reality is one of the resources that has been used with this objective, because through repetition, feedback and motivation can provide the user greater control of the postural balance. Aim: To review the existing literature on the effects of interventions with virtual reality games in the rehabilitation of postural balance deficits. Method: A review of the literature was performed with Descritores em Ciências da Saúde (DECs) an analysis of publications printed on books from the Júlio Bordignon Library of the Faculdade de Educação e Meio Ambiente - FAEMA, and confer of papers indexed and published in the databases LILACS, SCIELO, PubMed and Google Scholar. Conclusions:  The studies analyzed indicate that therapeutic intervention with the use of virtual reality as a technological tool for the rehabilitation of postural balance has been shown to be of great importance and could help traditional therapies; however, further studies will be necessary to understand the mechanism by which virtual reality works by improving postural balance.

One critical problem of sheet formed products is its dimensional accuracy. This is related to springback (elastic recovery), after forming load releasing. It may happen in any forming process; however, it is easier noted and quantified in bending process. Needless to say that this problem is undesirable since it affects assemblies, mainly at aeronautics industry [1]. Although, literature provides some models for predicting springback in conventional bending, this is not the case for non conventional bending using polyurethanic die and that's why the process has been treated on trial and error basis at shop, implying in product discharge. So, this work intends to present a theoretical model for predicting springback. Model validation has been done by experimental results. Predicted values are in a good agreement with these latter. KEYWORDS:Springback, sheet metal formed by bending process, non conventional bending process.

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