Thesis--Uppsala. / Without thesis statement. Bibliography: p. [152]-162.

Thesis (Ph.D.) - University of St Andrews, May 2010.

Thesis (Ph.D.)--Montana State University--Bozeman, 2007. / Typescript. Chairperson, Graduate Committee: Michael J. Oudshoorn. Includes bibliographical references (leaves 155-163).

Additional appendix (5 p.) is pasted onto back end-paper. Bibliography: leaves 219-244. Investigates the complexity of the vagal reflexes arising from the upper gastrointestinal tract by recording single unit vagal afferents and efferents in the ferret. The potential involvement of various neurotransmitters in mediating and modulating gastrointestinal tract inputs is also explored.

Zugl.: Berlin, Humboldt-Univ., Diss., 2008

Introdução. Pacientes portadores de diabetes mellitus tipo 2 (DM2) podem apresentar fraqueza da musculatura inspiratória. O efeito do treinamento muscular inspiratório (TMI) nesses pacientes ainda é desconhecido. Objetivos. Avaliar os efeitos do TMI sobre a força muscular inspiratória, a função pulmonar, a capacidade funcional e a modulação autonômica em pacientes com DM2 com fraqueza da musculatura inspiratória. Métodos. A pressão inspiratória máxima (PImáx) foi avaliada em uma amostra de 148 pacientes com DM2 da qual 25 pacientes com PImáx < 70% do previsto foram randomizados para um programa de 8 semanas de TMI diário (n=12) ou TMI-placebo (n=13). A PImáx, a função pulmonar, o consumo máximo de oxigênio e a variabilidade da freqüência cardíaca foram avaliados antes e após o TMI. Resultados. Do total de pacientes avaliados, 29,05% (43 pacientes) apresentaram fraqueza muscular inspiratória. O TMI aumentou significativamente a PImáx (118%) e a resistência muscular inspiratória (320%), sem alterar a função pulmonar, a capacidade funcional e a modulação autonômica. Conclusões. O TMI, em pacientes com DM2 e fraqueza dos músculos inspiratórios, aumentou significativamente a PImáx sem modificar a função pulmonar, a capacidade funcional e a modulação autonômica. / Introduction. Subject with type 2 diabetes mellitus (DM2) can present weakness of the inspiratory muscle. The effect of the inspiratory muscle training (IMT) in these patients still is unknown. Objectives. To evaluate the effect of the IMT on the inspiratory muscle force, the pulmonary function, the functional capacity and the autonômica modulation in patients DM2 with weakness of the inspiratory muscle. Methods. The maximum inspiratory pressure (PImáx) was evaluated in a sample of 148 patients with DM2 of which 25 patients with PImáx < 70% of the foreseen one had been randomizeds for a program of 8 weeks of daily IMT (n=12) or IMT-placebo (n=13). The PImáx, the function pulmonary, the VO2 and the variability of the cardiac frequency had been evaluated before and after the IMT. Results. Of the total of evaluated patients, 29.05% (43 patients) had presented inspiratory muscle weakness. The IMT significantly increased the PImáx (118%) and the inspiratory muscle resistance (320%), without modifying the function pulmonary, the exercise capacity and the modulation autonomic. Conclusions. The IMT in patients with DM2 and weakness of the inspiratory muscles increased the PImáx without modifying the function pulmonary, the exercise capacity and the modulation autonomic significantly.

Polycystic Ovary Syndrome (PCOS) is a complex endocrine disorder that increases a woman’s risk of developing cardiovascular disease and diabetes. Women with PCOS have extremely high rates of obesity, insulin resistance, cardiovascular morbidity and mortality. Obese women with PCOS also tend to have elevated sympathetic nerve activity and systemic markers of inflammation, which likely contribute to cardiometabolic risk and PCOS pathogenesis. While few medication or lifestyle intervention options for women with PCOS target elevated sympathetic nerve activity, inflammation, and insulin resistance, passive heat exposure shows promise as a novel intervention for improving cardiovascular and metabolic health in this population. Therefore, the purpose of this study was to examine changes in inflammation, cardiovascular, autonomic, and metabolic health in obese women with PCOS following a 30-session, 8-10 week chronic passive heat intervention (termed ‘heat therapy’). Eighteen obese women with PCOS (Age: 27±1y, BMI 41.3±1.1 kg·m2) were matched for age and body mass index (BMI), then divided into heat therapy (HT) or time control (CON). At the beginning (Pre), middle (Mid), and end (Post) of 8-10 weeks, subjects participated in study days to assess vascular, autonomic, and metabolic function, and additionally underwent a subcutaneous fat biopsy in Pre and Post. HT subjects took part in 30 one-hour hot tub sessions over 8-10 weeks (3-4 per week) in 40.5˚C water, while CON subjects completed all other testing but were not exposed to heat. No change in BMI was observed over the study in HT or CON; however; HT subjects exhibited dramatically improved vascular and metabolic function, as well as reduced sympathetic nerve activity and circulating inflammatory markers. In fat biopsies, insulin signaling was improved in HT subjects, while CON subjects remained stable over time. These findings show promise for HT as a treatment option for obese women with PCOS to improve cardiovascular and metabolic risk profiles. This dissertation includes previously published co-authored material.

Submitted by Livia Maria Silva Gomes (livia_sgomes@hotmail.com) on 2018-07-02T16:52:24Z No. of bitstreams: 1 Dissertacao_Defesa_Mestrado_ Livia_Gomes 02-07-2018.pdf: 1030259 bytes, checksum: 49dd1a96cea772d6ee1832593076c536 (MD5) / Approved for entry into archive by Telma Jaqueline Dias Silveira null (telmasbl@marilia.unesp.br) on 2018-07-02T19:22:11Z (GMT) No. of bitstreams: 1 gomes_lms_me_mar.pdf: 1030259 bytes, checksum: 49dd1a96cea772d6ee1832593076c536 (MD5) / Made available in DSpace on 2018-07-02T19:22:11Z (GMT). No. of bitstreams: 1 gomes_lms_me_mar.pdf: 1030259 bytes, checksum: 49dd1a96cea772d6ee1832593076c536 (MD5) Previous issue date: 2018-06-04 / Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) / Introdução: A busca por evidências para a reabilitação e o uso de técnicas terapêuticas aplicadas às disfagias orofaríngeas neurogênicas tornou-se fator determinante na elaboração dos programas de reabilitação. A manobra de deglutição de esforço tem sido frequentemente estudada, porém uma das questões ainda não esclarecidas em indivíduos com disfagia orofaríngea trata da sobrecarga cardíaca proveniente da execução de esforço. Objetivo: Comparar os efeitos da deglutição espontânea e da manobra de deglutição de esforço sobre a modulação da frequência cardíaca em indivíduos com disfagia orofaríngea neurogênica. Método: O estudo foi realizado em 23 indivíduos com disfagia orofaríngea neurogênica, 8 indivíduos pós Acidente Vascular Cerebral e 15 com Doença de Parkinson, ambos os sexos e idade entre 50 e 90 anos (média de idade de 67 anos). O protocolo constou de duas etapas onde foram analisados os índices lineares da variabilidade da frequência cardíaca durante 5 minutos em cada protocolo: 1) deglutição espontânea e; 2) deglutição de esforço monitorada por eletromiografia de superfície durante todo o protocolo com variação de 5,25% na ativação muscular durante a deglutição de esforço (p=0,009). Resultados: Não houve diferença estatisticamente significativa nos índices da variabilidade da frequência cardíaca durante o protocolo de deglutição de esforço comparado com a degutição espontânea do indivíduo da amostra estudada (RMSSD p= 0,3; LF (ms²) p= 0,3; SD1 p= 0,3). Conclusão: O esforço muscular executado durante a manobra de deglutição de esforço nos indivíduos com disfagia orofaríngea neurogênica dessa amostra não alterou a modulação autonômica cardíaca dos indivíduos. / Introduction: The search for evidence for rehabilitation and the use of therapeutic techniques applied to neurogenic oropharyngeal dysphagia has become a determining factor in the design of rehabilitation programs. The effort swallowing maneuver has been frequently studied, but one of the questions still not clarified in individuals with oropharyngeal dysphagia treats the cardiac overload from the execution of effort. Objective: To compare the effects of spontaneous deglutition and effort swallowing maneuver on heart rate modulation in individuals with neurogenic oropharyngeal dysphagia. Methods: The study was performed in 23 individuals with neurogenic oropharyngeal dysphagia, diagnosed with neurological diseases, aged between 50 and 90 years (mean age 67 years), in both sexes. We analyzed groups of individuals after stroke (N = 8) and with Parkinson's Disease (N = 15). The protocol consisted of two steps in which the linear indexes of the heart rate variability during 5 minutes in each protocol were analyzed: 1) spontaneous deglutition and; 2) effortful swallow, monitored by surface electromyography throughout the protocol with variation of 5.25% in muscle activation during effort swallowing (p = 0.009). Results: There was no statistically significant difference in the indices of heart rate variability during the effort swallowing protocol. Conclusion: The muscular effort performed during the maneuver of effort swallowing in individuals with neurogenic oropharyngeal dysphagia of this sample did not alter the autonomic cardiac modulation of the individuals. / FAPESP: 2016/04665-5

INTRODUÇÃO. A ingestão aguda de 500 ml de água pode elevar a pressão arterial de forma expressiva em indivíduos com disfunção autonômica, mas parece não afetar os níveis pressóricos de indivíduos jovens saudáveis. Na hipertensão arterial sistêmica podem ocorrer alterações na modulação autonômica e, em ratos hipertensos, há evidências de que a ingestão de água seja capaz de promover aumento da pressão arterial. Entretanto, em seres humanos hipertensos, os efeitos da ingestão aguda de água ainda não são conhecidos. OBJETIVOS. Avaliar os efeitos hemodinâmicos e autonômicos da ingestão aguda de água em indivíduos portadores de hipertensão arterial sistêmica, bem como investigar os mecanismos fisiológicos envolvidos na resposta pressora. MÉTODOS. Participaram do estudo 8 indivíduos portadores de hipertensão arterial sistêmica leve (idade = 42,5±7,8 anos; índice de massa corporal= 27,1±3,4 kg/cm2) e 10 indivíduos normotensos (idade = 37,3±7,5 anos; índice de massa corporal = 25,8±3,2 kg/cm2), os quais foram submetidos à ingestão de 500 ml de água após repouso na posição supina por 30 minutos. Foram avaliadas a pressão arterial (Finapress, Ohmeda), a freqüência cardíaca, o fluxo sangüíneo do antebraço, a resistência vascular do antebraço e a atividade nervosa simpática muscular no basal e aos 10, 20 e 30 minutos após a ingestão de água. Amostras sangüíneas venosas foram coletadas no basal e aos 10 e 30 minutos após a ingestão de água, para calcular as mudanças no volume plasmático. A variabilidade da pressão arterial sistólica e da freqüência cardíaca foi avaliada por análise espectral, utilizando-se a Transformação Rápida de Fourier. RESULTADOS. A ingestão de água resultou em significativo aumento máximo das pressões arteriais sistólica (Hipertensos = 19±7 mmHg; Normotensos = 17±7 mmHg, p = 0,001) e diastólica (Hipertensos = 14±4 mmHg; Normotensos = 14±5 mmHg, p = 0,001) nos indivíduos hipertensos e normotensos. Ambos os grupos também apresentaram significativa elevação máxima da resistência vascular no antebraço (Hipertensos = 19±11 unidades; Normotensos = 20±13 unidades, p = 0,001) e da atividade nervosa simpática muscular (Hipertensos = 8±2 disparos/min; Normotensos = 8±4 disparos/min, p = 0,001). RESULTADOS. Após a ingestão de água, houve redução da freqüência cardíaca (Hipertensos = - 5,6±2,1 bat/min; Normotensos = - 5,4±7,3 bat/min, p = 0,002), do fluxo sangüíneo no antebraço (Hipertensos = - 0,5±0,4 ml/min/100 ml tecidual; Normotensos = - 0,7±0,6 ml/min/100 ml tecidual, p = 0,001) e do volume plasmático (Hipertensos = - 0,8±0,8 %; Normotensos = - 1,0±0,9%, p = 0,002) nos indivíduos hipertensos e normotensos. A variabilidade da freqüência cardíaca e da pressão arterial sistólica não foi alterada pela ingestão de água. CONCLUSÃO. A ingestão aguda de água eleva similarmente as pressões arteriais sistólica e diastólica de indivíduos hipertensos leves e normotensos, provavelmente por aumento da resistência vascular periférica, secundário à ativação simpática. / Introduction. An acute water ingestion of 500 ml may significantly increase blood pressure in individuals with autonomic dysfunction. However, it doesn’t seem to influence the pressure levels of young, healthy subjects. When a systemic arterial hypertension is present, alterations can occur in the autonomic modulation mechanism, and there is scientific evidence that acute water drinking is responsible for increases in the arterial blood pressure of laboratory rats with hypertension. However, in human subjects with hypertension, the effects of an acute water ingestion are not yet well known. Objectives. The current study aims to evaluate haemodynamics and autonomic response to acute water ingestion in human subjects that have systemic arterial hypertension, as well as to study the physiological mechanisms underlying in the pressure elevation phenomena. Method. The human subjects that participated were divided up into two study groups. The first group of eight subjects, had been diagnosed with stage I systemic hypertension (ages = 42.5±7.8 years; with a body mass index = 27.1±3.4 kg/cm2), and the second group consisted of 10 subjects that had normal pressure readings (ages = 37.3±7.5 years; with a body mass index equivalent to 25.8±3.2 kg/cm2). All participants had drunk 500ml of water, after resting for 30 minutes in the supine position. The following parameters were studied: arterial blood pressure (Finapress, Ohmeda), heart rate, forearm blood flow, forearm vascular resistance and basal muscle sympathetic nerve activity after 10, 20, and 30 minutes, immediately following the acute water ingestion. Venous blood samples were collected during the basal period of 10 and 30 minutes after water drinking, in order to calculate plasmatic volume changes. Systolic pressure and heart rate variability were evaluated by spectral analysis, utilizing the Fast Fourier Transform. Results. There was a significant maximum increase in systolic and diastolic arterial pressure, in both, hypertensive and normotensive human subjects, as a direct consequence of acute water ingestion. Systolic pressure increase was of 19±7 mmHg, in hypertensive subjects; while the same pressure increase was of 17±7 mmHg, for normotensive subjects, (p = 0.001). Similarly, the diastolic pressure increase in hypertensive subjects had an equivalent to 14±4 mmHg, and in normotensive subjects showed an increase equivalent to 14±5 mmHg, (p = 0.001). Similarly, the diastolic pressure increase in hypertensive subjects had an equivalent to 14±4 mmHg, and in normotensive subjects showed an increase equivalent to 14±5 mmHg, (p = 0.001). Also, both groups presented a significant maximum increase in forearm vascular resistance (Hypertensive = 19±11 units; normotensive = 20±13 units, p = 0.001) and in muscle sympathetic nerve activity (Hypertensive = 8±2 bursts/min, normotensive = 8±4 bursts/min, p = 0.001). After acute water ingestion, both, hypertensive and normotensive human subjects showed a decreased heart rate, forearm blood flow, and plasmatic volume. The heart rate decrease in hypertensive subjects was equal to - 5.6±2.1 beats/min; and for normotensive subjects was = - 5.4±7.3 beats/min, (p = 0.002), the forearm blood flow decrease in hypertensive subjects was = - 0.5±0.4 ml/min/100 ml tissue, and in normotensive subjects was = - 0.7±0.6 ml/min/100 ml tissue, (p = 0.001), and the plasmatic volume drop in hypertensive subjects was = - 0.8±0.8 %; and for normotensive subjects was = - 1.0±0.9%, (p = 0.002). Heart rate and systolic arterial pressure variability were not altered by acute water ingestion. CONCLUSION. An acute water ingestion equally increases systolic and diastolic arterial pressure in human subjects with stage I hypertension, as well as those normotensive ones, probably by increasing peripheral vascular resistance, which is secondary to sympathetic activity.

Objetivos/Hipótese: A Piridostigmina bloqueia a acetilcolinesterase, promove estimulação colinérgica e aumenta a variabilidade da freqüência cardíaca (VFC) em indivíduos saudáveis e com insuficiência cardíaca. Os efeitos sobre a modulação autonômica no diabetes mellitus tipo 2 (DM2) são desconhecidos. Nós testamos a hipótese de que a administração de piridostigmina aumenta a VFC em pacientes com DM2 e neuropatia autonômica cardiovascular (NAC). Métodos: Estudamos 34 pacientes com DM2 e NAC com idade entre 30 e 70 anos. Dezessete receberam 30 mg de piridostigmina via oral, de 8/8h por 24h (PI) e 17 receberam placebo (PL). A VFC foi avaliada pela média (RRMed) e desvio padrão dos intervalos RR (SDNN), pela raiz quadrada da média das diferenças sucessivas entre intervalos RR (RMSSD) e pelos índices do Mapa de Retorno Tridimensional P1, P2, P3 e MN. Resultados: Não houve diferenças significativas entre os grupos PI e PL quanto às características clínicas basais e à VFC sob efeito de piridostigmina e PL (RRMed - 748 ± 99 vs 733 ± 111ms; SDNN - 107 ± 26 vs 108 ± 36ms; RRMSD - 20,7 ± 12,7 vs 20,3 ± 10ms; P1 - 63 ± 11 vs 69 ± 14; P2 - 66 ±13 vs 63 ± 15; P3 - 86 ± 34 vs 80 ± 24 e MN - 392 ± 241 vs 369 ± 185). Conclusão: A piridostigmina não modifica a VFC em pacientes com DM2 e NAC. / Aims/Hypothesis: Pyridostigmine blocks acetylcholinesterase, promotes cholinergic stimulation and increases heart rate variability (HRV) in healthy individuals and with cardiac heart failure. The effects on the autonomic modulation in diabetes mellitus type 2 (DM2) are unknown. We have tested the hypothesis that the administration of pyridostigmine increases HRV in DM2 and CAN patients (CAN). Methods: We have studied 34 DM2 and CAN patients aged between 30 and 70 years old. Seventeen received 30mg of pyridostigmine via oral administration, every 8 hours during 24 hours (PY) and 17 received placebo (PL). HRV was assessed by the mean of all normal R-R intervals RR (mean RR) and the standard deviation of all normal R-R intervals (SDNN), by the root-mean-square of successive differences (RMSSD) and by the three-dimensional return map indices P1, P2, P3 and MN. Results: There were no significant differences between the PY and PL groups as to the baseline clinical characteristics and to HRV under the effect of pyridostigmine and PL (mean RR - 748 ± 99 vs 733 ± 111ms; SDNN - 107 ± 26 vs 108 ± 36ms; RRMSD - 20,7 ± 12,7 vs 20,3 ± 10ms; P1 - 63 ± 11 vs 69 ± 14; P2 - 66 ±13 vs 63 ± 15; P3 - 86 ± 34 vs 80 ± 24 e MN - 392 ± 241 vs 369 ± 185). Conclusion: Pyridostigmine does not modify HRV in DM2 and CAN patients.