This research assessed the role of Hatha yoga in the modulation of vascular health. In study one, Hatha yoga practitioners were compared to sedentary controls to whom they were matched for age and body mass index. Practitioners of Hatha yoga were no different from sedentary individuals in terms of arterial stiffness or vascular endothelial function. Yoga practitioners possessed lower HbA1c (P < 0.05) levels and lower pulse pressure (P < 0.05) than their sedentary counterparts. Practitioners of Hatha yoga had lower body fat percentages, but this observed trend did not reach statistical significance (P = 0.052). In study two, a 12-week Hatha yoga intervention resulted in reductions in HbA1c levels (P < 0.05) and total cholesterol (P < 0.05) in previously sedentary adults. No changes were observed in carotid artery compliance or brachial artery flow-mediated dilation as a result of the intervention. In study three, obese and lean, apparently healthy adults completed an 8-week Bikram yoga intervention. Reductions in total- and LDL-cholesterol were observed in the lean subjects (P < 0.05), with no changes in lipid profiles in the obese group. The homeostasis model assessment of insulin resistance (HOMA-IR) decreased in the lean subjects, but this trend did not attain statistical significance (P = 0.06). Although an observed trend was shown at 60 minutes during the oral glucose tolerance test (P = 0.07), glucose tolerance remained unchanged in the obese subjects. Brachial artery flow-mediated improved by approximately 2% in the obese subjects, but this observed change did reach statistical significance (P = 0.10). Flexibility increased in both groups as a result of the Bikram yoga intervention. Therefore Hatha yoga improved lipid profiles and glycemic control in sedentary adults, but no effects on vascular health were demonstrated. / text

Orthostatic intolerance following exposure to simulated or actual microgravity is observed following spaceflight and extended periods of bed rest, and is not always associated with simultaneous hypotension. Differential adaptation of cephalic and caudal arterial vasculatures (as a result of removal of the normal hydrostatic gradient) is proposed as a potential mechanism underlying this phenomenon. A potential role for changes to the L-arginine/nitric oxide pathway in such adaptations has been suggested, predominantly from previous in vitro studies; using an established model of simulated microgravity (head-down tilt; HDT). This thesis investigates whether findings in isolated vessels are reflected by in vivo measurements of cephalic and caudal vascular function. Using carotid or iliac artery flow normalized to mean arterial pressure as an index of cerebral or hind limb vascular conductance, autoregulatory cerebral vasodilatation in response to lower body negative pressure was found to be impaired following HDT. In addition, α¬1-adrenoceptor agonist-mediated vasoconstriction was decreased in the cerebral vasculature and increased in the peripheral and hind limb vasculature. Administration of acetylcholine or the non-selective nitric oxide synthase (NOS) inhibitor Nω-nitro-L-arginine methyl ester (L-NAME) demonstrated a decreased contribution of NOS to cerebrovascular tone, but an increased contribution of NOS to peripheral vascular resistance and tone of the hind limb vasculature. Together with a lack of difference in the response to the selective inducible NOS (iNOS) inhibitor 1400W, these results suggest that differential adaptation of eNOS may account for the observed differences between control and HDT animals. Further investigation of the changes to the L-arginine/nitric oxide pathway suggest that these changes are not associated with changes in eNOS expression, but may be related to altered activity of eNOS. Furthermore, the bioavailability (as measured by pharmacokinetic half life) or the vascular effector mechanisms (as measured by the haemodynamic response to exogenously administered nitric oxide) responsible for the effects of nitric oxide were also shown to be unaffected by HDT. These findings suggest that differential adaptation of the L-arginine/nitric oxide pathway may contribute to the inability to raise total peripheral resistance and impaired cerebral autoregulation following HDT, thereby representing a mechanism of orthostatic intolerance following exposure to microgravity.

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Peripheral arterial disease (PAD) defines atherosclerotic disease of the arteries to the legs. PAD begins early in life and remains asymptomatic over long periods. The ankle brachial index (ABI) is an important diagnostic test which can identify asymptomatic individuals and serve as a good marker of the underlying peripheral and systemic atherosclerosis. Recent advances in vascular biology proposed a role of inflammatory and haemostatic mechanisms in atherosclerotic disease. Although inflammatory and haemostatic markers have been associated with coronary atherosclerosis in large scale epidemiological studies their role in PAD development is not well established and for many markers unknown. Also, their relationship with the progression of early asymptomatic disease has not been studied before. The aim of this thesis was to examine 12 markers of inflammation and haemostasis in relation to peripheral atherosclerotic progression and incident PAD. The Edinburgh Artery Study was used for this analysis. This is a population based cohort study of 1,592 men and women recruited in 1987. ABI was measured at baseline and at two follow up examinations which were conducted after 5 and after 12 years. Also, subjects were followed up for cardiovascular events for 17 years. Conventional cardiovascular risk factors, C-reactive protein (CRP), interleukin-6 (IL-6), intercellular adhesion molecule 1 (ICAM-1), vascular adhesion molecule-1 (VCAM-1), E-selectin, fibrinogen, D-dimer, tissue plasminogen activator (t-PA), vonWillebrand factor (vWF), factor VII, fibrinopeptide A (FpA) and prothrombin fragments 1+2 (F1+2) were measured at baseline. Valid ABI measurements were available for 1,582 subjects at baseline, for 1,081 subjects at the 5 year follow up and for 816 subjects at the 12 year follow up. The population showed a progression in atherosclerotic disease assessed by the mean ABI decline over time. The mean change in ABI was -0.04 (0.18) after 5 years and -0.06 (0.19) after 12 years. From inflammatory markers, CRP (p <0.01), IL-6 (p <0.001) and ICAM-1 (p <0.01) were associated with atherosclerotic progression after 12 years, independently of baseline ABI and of conventional cardiovascular risk factors. Also, from haemostatic markers, fibrinogen (p =0.05) and D-dimer (p ≤ 0.05) were significantly associated with atherosclerotic progression independently of baseline ABI and cardiovascular risk factors. Moreover, subjects with higher levels of both D-dimer and IL-6 at baseline had the greatest ABI decline. Also, IL-6 showed the stronger independent effect on atherosclerotic progression and retained statistical significance after adjustments for all inflammatory markers and for fibrinogen and D-dimer. Approximately 26% of the baseline population developed at least one event of major CVD and 14% of the baseline population developed symptomatic PAD after 17 years of follow up. Inflammatory markers, CRP and IL-6 showed modest associations with PAD which lost statistical significance in the multivariable model. On the other hand, these markers were associated with incident major CVD with hazard ratios (95% CI) 1.6 (1.2, 2.3) and 1.8 (1.3, 2.6) respectively (top vs. bottom tertile) in the multivariable model. ICAM-1 showed weak associations with incident CVD, however, was significantly associated with PAD with hazard ratio (95% CI) 1.8 (1.2, 2.7) (top vs. bottom tertile) after adjustments for cardiovascular risk factors and CVD at baseline. Haemostatic markers, fibrinogen and D-dimer were associated with 2.2 (95% CI: 1.5, 3.2) and 1.7 (1.2, 2.6) increase in the risk of PAD development and 1.8 (1.3, 2.3) and 1.6 (1.2, 2.1) increase in the risk of CVD independently of cardiovascular risk factors and history of CVD at baseline, respectively. This analysis showed a major role of inflammatory markers, CRP, IL-6 and ICAM-1 in atherosclerotic development and progression. In addition, fibrinogen and D-dimer, but not other haemostatic factors, were associated with progressive and incident peripheral atherosclerosis. Since D-dimer and fibrinogen are acute phase reactants, these data support the hypothesis that inflammation is more related to atherosclerosis than is hypercoagulation. Most importantly, the majority of the reported associations were not explained by increased levels of cardiovascular risk factors or pre-existing clinical or subclinical arterial disease. Thus these markers are more likely to have a causal than a consequential role in atherosclerotic disease.

No description available.

Orthostatic intolerance following exposure to simulated or actual microgravity is observed following spaceflight and extended periods of bed rest, and is not always associated with simultaneous hypotension. Differential adaptation of cephalic and caudal arterial vasculatures (as a result of removal of the normal hydrostatic gradient) is proposed as a potential mechanism underlying this phenomenon. A potential role for changes to the L-arginine/nitric oxide pathway in such adaptations has been suggested, predominantly from previous in vitro studies; using an established model of simulated microgravity (head-down tilt; HDT). This thesis investigates whether findings in isolated vessels are reflected by in vivo measurements of cephalic and caudal vascular function. Using carotid or iliac artery flow normalized to mean arterial pressure as an index of cerebral or hind limb vascular conductance, autoregulatory cerebral vasodilatation in response to lower body negative pressure was found to be impaired following HDT. In addition, α¬1-adrenoceptor agonist-mediated vasoconstriction was decreased in the cerebral vasculature and increased in the peripheral and hind limb vasculature. Administration of acetylcholine or the non-selective nitric oxide synthase (NOS) inhibitor Nω-nitro-L-arginine methyl ester (L-NAME) demonstrated a decreased contribution of NOS to cerebrovascular tone, but an increased contribution of NOS to peripheral vascular resistance and tone of the hind limb vasculature. Together with a lack of difference in the response to the selective inducible NOS (iNOS) inhibitor 1400W, these results suggest that differential adaptation of eNOS may account for the observed differences between control and HDT animals. Further investigation of the changes to the L-arginine/nitric oxide pathway suggest that these changes are not associated with changes in eNOS expression, but may be related to altered activity of eNOS. Furthermore, the bioavailability (as measured by pharmacokinetic half life) or the vascular effector mechanisms (as measured by the haemodynamic response to exogenously administered nitric oxide) responsible for the effects of nitric oxide were also shown to be unaffected by HDT. These findings suggest that differential adaptation of the L-arginine/nitric oxide pathway may contribute to the inability to raise total peripheral resistance and impaired cerebral autoregulation following HDT, thereby representing a mechanism of orthostatic intolerance following exposure to microgravity.

Made available in DSpace on 2014-06-11T19:28:35Z (GMT). No. of bitstreams: 0 Previous issue date: 2003-10Bitstream added on 2014-06-13T20:37:41Z : No. of bitstreams: 1 cunha_mgs_me_guara.pdf: 2546988 bytes, checksum: 7f90dfedf806a463275bbea800769557 (MD5) / O presente trabalho consiste no estudo do comportamento do fluxo sangüíneo na artéria braquial, através de sinais captados por um microfone acoplado no estetoscópio e utilizado para transformar o sinal acústico (sonoro) em elétrico, e enviá-lo para o computador. O estudo foi realizado oferecendo-se diferentes pressões no esfigmomanômetro, o qual foi adaptado com dois manômetros. Um dos manômetros, graduado em mmHg, não foi modificado, possui o selo do INMETRO e atuou como referência, ao outro foi inserido um extensômetro, que transformou o sinal de pressão em sinal elétrico, utilizando uma ponte amplificada, enviando-o para uma placa de aquisição de dados no computador. Foi traçada uma curva de calibração do sinal elétrico (em mV) com relação ao manômetro graduado em mmHg. Foi proposto um protocolo para aquisição destes sinais a serem analisados, baseado em protocolos de aferição de pressão arterial. O comportamento do fluxo sangüíneo foi comparado às diferentes pressões exercidas pelo esfigmomanômetro. Ao analisar estes dados, foram propostos limites de normalidades da intensidade do sinal do fluxo sangüíneo em diferentes freqüências nas cinco fases da escala de Koroktov. O trabalho mostrou também os limites de normalidade da pressão arterial, utilizando-se o sinal adquirido pela extensometria. Finalmente, foi oferecido mais um auxílio no diagnóstico de patologias do sistema cardiovascular. / The present work consists to study the features of blood flow in to the brachial artery through signals detected by a microphone coupled together a stethoscope. This apparatus changes the acoustics in eletric signal and, then, sends to the computer. This study was implemented exhibiting different pressures in the sphygnomanometer, where two manometers, graded in mmHg, were coulpled. One that has the INMETRO certificate of gauging instruments was not modificate and, then, it was used as the standard. In the other, an extensometer was coupled together, which through an amplifier bridge, pressure signals are transformed in electric signals and sent to a data adapter unit connected to the computer. A gauging curve for the eletric signals versus pressure signals was ploted. It was proposed a protocol to adquire these data signals, based on the protocol of brachial pressure measurement. The features of blood flow were compared at different sphygnomanometer pressures. In the analysis process of the data, normality boundaries of intensity were proposed to the blood flow signal at different frequencies in the five phases of the Koroktov scale. The work also showed the normality boundaries of brachial pressure using the data signals adquired by the extensometry process. Finally, it was provided an one more aid in to diagnose pathologies in the cardiovascular system.

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