892 research outputs found

    Aerospace medicine and biology: A continuing bibliography with indexes (supplement 349)

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    This bibliography lists 149 reports, articles and other documents introduced into the NASA Scientific and Technical Information System during April, 1991. Subject coverage includes: aerospace medicine and psychology, life support systems and controlled environments, safety equipment, exobiology and extraterrestrial life, and flight crew behavior and performance

    The effects of muscle mechanoreflex stimulation via passive muscle stretch on baroreflex function in humans

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    Human cardiovascular control during exercise is regulated by central command, muscle mechanoreflex stimulation and muscle metaboreflex activation. The muscle mechanoreflex can be stimulated by passive muscle stretch, which causes cardiovascular responses. However, the influence of passive stretch-induced muscle mechanoreflex stimulation on the baroreflex is unknown. Therefore, this thesis investigated the effects of muscle mechanoreflex stimulation via passive calf muscle stretch on baroreflex function in humans. Firstly, spontaneous baroreflex sensitivity decreases progressively during isometric exercise of increasing intensity. A concomitant rightward resetting of the baroreflex occurs, which shifts further rightward as exercise intensity increases. Secondly, muscle mechanoreflex stimulation by passive calf muscle stretch decreases spontaneous baroreflex sensitivity at rest, and during graded levels of local metabolite accumulation following isometric exercise of increasing intensity. Thirdly, muscle mechanoreflex stimulation by passive calf muscle stretch during concurrent local metabolite accumulation decreases the maximal gain of the function curve for carotid baroreflex control of heart rate, but not blood pressure. Overall, these findings suggest that muscle mechanoreflex stimulation via passive muscle stretch decreases baroreflex sensitivity via cardiac vagal inhibition, likely by modulating inputs at central integration sites. Also, metabolite sensitisation of stretch-sensitive muscle mechanoreceptive afferents is implied, which augments this cardiac vagal inhibition

    New perspectives on the melanocortins and their cardiovascular effects: Potential implications for the treatment of cardiovascular diseases with melanocortin analogues

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    The melanocortin peptides, including melanocyte-stimulating hormones, α-, ÎČ- and Îł-MSH, are derived from the precursor peptide proopiomelanocortin and mediate their biological actions via five different melanocortin receptors, named from MC1 to MC5. Melanocortins have been implicated in the central regulation of energy balance and cardiovascular functions, but their local effects, via yet unidentified sites of action, in the vasculature, and their therapeutic potential in major vascular pathologies remain unclear. Therefore, the main aim of this thesis was to characterise the role of melanocortins in circulatory regulation, and to investigate whether targeting of the melanocortin system by pharmacological means could translate into therapeutic benefits in the treatment of cardiovascular diseases such as hypertension. In experiments designed to elucidate the local effects of α-MSH on vascular tone, it was found that α-MSH improved blood vessel relaxation via a nitric oxide (NO)-dependent mechanism without directly contracting or relaxing blood vessels. Furthermore, α-MSH was shown to regulate the expression and function of endothelial NO synthase in cultured human endothelial cells via melanocortin 1 receptors. In keeping with the vascular protective role, pharmacological treatment of mice with α-MSH analogues displayed therapeutic efficacy in conditions associated with vascular dysfunction such as obesity. Furthermore, α-MSH analogues elicited marked diuretic and natriuretic responses, which together with their vascular effects, seemed to provide protection against sodium retention and blood pressure elevation in experimental models of hypertension. In conclusion, the present results identify novel effects for melanocortins in the local control of vascular function, pointing to the potential future use of melanocortin analogues in the treatment of cardiovascular pathologies.Melanokortiinien sydĂ€n- ja verisuonivaikutukset: Mahdollisuudet melanokortiinianalogien kĂ€ytölle sydĂ€n- ja verisuonisairauksien hoidossa. Melanokortiinit, joihin lukeutuvat α-, ÎČ- ja Îł-melanosyyttejĂ€ stimuloiva hormoni (MSH), ovat pÀÀasiassa aivoissa ilmenevĂ€n esiasteen pro-opiomelanokortiinin pilkkoutumisiessa syntyviĂ€, pienempiĂ€ peptidejĂ€, jotka vaikuttavat melanokortiinireseptoreiden vĂ€lityksellĂ€ elimistön fysiologisiin toimintoihin. Melanokortiinit osallistuvat merkittĂ€vĂ€lla tavalla elimistön energiatasapainon sekĂ€ sydĂ€men ja verenkiertoelimistön keskushermostoperĂ€iseen sÀÀtelyyn, mutta niiden paikalliset vaikutukset ja vaikutusmekanismit verenkierron sÀÀtelyssĂ€ ovat pitkĂ€lti tuntemattomia. LisĂ€ksi, melanokortiinien mahdollisista, terapeuttisista vaikutuksista sydĂ€n- ja verisuonisiarauksien hoidossa tiedetÀÀn hyvin vĂ€hĂ€n. TĂ€mĂ€n vĂ€itöskirjatutkimuksen keskeisimpĂ€nĂ€ tavoitteena oli tutkia melanokortiinien vaikutuksia verisuonten toiminnan sÀÀtelyssĂ€ sekĂ€ arvioida löydösten merkitystĂ€ uusien hoitomahdollisuuksien kannalta. Suonten toimintakykyĂ€ mittaavissa kokeissa havaitsimme, ettĂ€ α-MSH tehosti verisuonten sisĂ€pintaa verhoavan endoteelin kykyĂ€ laajentaa verisuonia ilman, ettĂ€ se itse suoraan vaikutti suonten supistumistilaan. TĂ€mĂ€ vaikutus oli yhteydessĂ€ verisuonten lisÀÀntyneeseen typpioksidin (NO) tuottoon ja herkkyyteen NO:n verisuonia laajentavalle vaikutukselle. ViljelemĂ€llĂ€ ihmisperĂ€isiĂ€ endoteelisoluja osoitimme melanokortiini 1 reseptoreiden vĂ€littĂ€vĂ€n α-MSH vaikutuksia NO:n tuotantoa sÀÀteleviin tekijöihin kuten endoteliaalisen NO syntaasin mÀÀrÀÀn ja aktiivisuuteen. NĂ€iden verisuonten toimintaa parantavien vaikutusten ansiosta, α-MSH-analogit paransivat verisuonten toimintaa kokeellisissa tautimalleissa, joihin liittyy erityisesti endoteelin toiminnan hĂ€iriö kuten lihavuuden yhteydessĂ€. LisĂ€ksi havaitsimme, ettĂ€ α-MSH:n synteettinen analogi lisÀÀ veden ja natriumin erittymistĂ€ elimistöstĂ€ sekĂ€ vaikuttaa terapeuttisesti kohonneen verenpaineen hoidossa hiirillĂ€. NĂ€mĂ€ löydökset laajentavat ymmĂ€rrystĂ€mme melanokortiinien vaikutuksista verenkierron sÀÀtelyssĂ€ tuoden samalla nĂ€yttöÀ uusista hoitomahdollisuuksista sydĂ€n- ja verisuonisairauksissa.Siirretty Doriast

    Autonomic Cardiovascular Control in Health and Disease

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    Influence of age on respiratory modulation of muscle sympathetic nerve activity, blood pressure and baroreflex function in humans

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    New Findings What is the central question of this study? Does ageing influence the respiratory‐related bursting of muscle sympathetic nerve activity (MSNA) and the association between the rhythmic fluctuations in MSNA and blood pressure (Traube–Hering waves) that occur with respiration? What is the main finding and its importance? Despite the age‐related elevation in MSNA, the cyclical inhibition of MSNA during respiration is similar between young and older individuals. Furthermore, central respiratory–sympathetic coupling plays a role in the generation of Traube–Hering waves in both young and older humans. Healthy ageing and alterations in respiratory–sympathetic coupling have been independently linked with heightened sympathetic neural vasoconstrictor activity. We investigated how age influences the respiratory‐related modulation of muscle sympathetic nerve activity (MSNA) and the association between the rhythmic fluctuations in MSNA and blood pressure that occur with respiration (Traube–Hering waves; THW). Ten young (22 ± 2 years; mean ± SD) and 10 older healthy men (58 ± 6 years) were studied while resting supine and breathing spontaneously. MSNA, blood pressure and respiration were recorded simultaneously. Resting values were ascertained and respiratory cycle‐triggered averaging of MSNA and blood pressure measurements performed. The MSNA burst incidence was higher in older individuals [22.7 ± 9.2 versus 42.2 ± 13.7 bursts (100 heart beats)−1, P < 0.05], and was reduced to a similar extent in the inspiratory to postinspiratory period in young and older subjects (by ∌25% compared with mid‐ to late expiration). A similar attenuation of MSNA burst frequency (in bursts per minute), amplitude and total activity (burst frequency × mean burst amplitude) was also observed in the inspiratory to postinspiratory period in both groups. A significant positive correlation between respiratory‐related MSNA and the magnitude of Traube–Hering waves was observed in all young (100%) and most older subjects (80%). These data suggest that the strength of the cyclical inhibition of MSNA during respiration is similar between young and older individuals; thus, alterations in respiratory–sympathetic coupling appear not to contribute to the age‐related elevation in MSNA. Furthermore, central respiratory–sympathetic coupling plays a role in the generation of Traube–Hering waves in both healthy young and older humans

    Autonomic and Renal Alterations in the Offspring of Sleep-Restricted Mothers During Late Pregnancy

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    OBJECTIVES: Considering that changes in the maternal environment may result in changes in progeny, the aim of this study was to investigate the influence of sleep restriction during the last week of pregnancy on renal function and autonomic responses in male descendants at an adult age. METHODS: After confirmation of pregnancy, female Wistar rats were randomly assigned to either a control or a sleep restriction group. The sleep-restricted rats were subjected to sleep restriction using the multiple platforms method for over 20 hours per day between the 14th and 20th day of pregnancy. After delivery, the litters were limited to 6 offspring that were designated as offspring from control and offspring from sleep-restricted mothers. Indirect measurements of systolic blood pressure (BPi), renal plasma flow, glomerular filtration rate, glomerular area and number of glomeruli per field were evaluated at three months of age. Direct measurements of cardiovascular function (heart rate and mean arterial pressure), cardiac sympathetic tone, cardiac parasympathetic tone, and baroreflex sensitivity were evaluated at four months of age. RESULTS: The sleep-restricted offspring presented increases in BPi, glomerular filtration rate and glomerular area compared with the control offspring. The sleep-restricted offspring also showed higher basal heart rate, increased mean arterial pressure, increased sympathetic cardiac tone, decreased parasympathetic cardiac tone and reduced baroreflex sensitivity. CONCLUSIONS: Our data suggest that reductions in sleep during the last week of pregnancy lead to alterations in cardiovascular autonomic regulation and renal morpho-functional changes in offspring, triggering increases in blood pressure

    Placental function, body composition and cardiovascular autonomic function

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    Hypertension is an important modifiable risk factor for cardiovascular disease. An important recent advancement in hypertension research is an understanding that hypertension often may have a developmental origin. Birthweight is associated with hypertension across the lifespan and adult cardiovascular disease, such that those at both ends of the spectrum are at increased risk. Nonetheless, birthweight is a crude surrogate of fetal growth and it may be that quantification of body composition, may more accurately identify the “at risk” individual. A causative mechanism linking birthweight and cardiovascular risk is yet to be identified but may involve changes to the structure and function of organs including the placenta which may impair development and predispose individuals to later cardiovascular disease. The aims of this thesis were to investigate the associations between placental function, body composition and cardiovascular autonomic function. Studies outlines in this thesis indicate different mechanism control fat mass and fat free mass in the newborn and that placental weight partly mediates the association of maternal factors with newborn body composition. While low birthweight has previously been shown to be associated altered autonomic function in the infant our studies suggests that body fatness may provide information beyond that obtained from birthweight assessment alone. Previous studies have shown altered blood pressure control in those born preterm, our studies found altered cardiovascular outcomes even in the late preterm newborn. Assessment of body composition in children and adolescents at rest and in response to an exercise test suggests worsening of autonomic control due to adiposity and may develop over time during childhood and adolescence. Collectively, these results emphasise the implications of altered in-utero and early life exposures on cardiovascular outcomes

    Short-Term Fasting and Autonomic Control

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    Obesity is a chronic metabolic disorder associated with increased risk of cardiovascular disease. Evidence suggests that chronic intermittent fasting improves cardiometabolic health and reduces arterial blood pressure. However, the mechanisms underlying the reductions in blood pressure and improved cardiovascular health observed from chronic fasting studies remain unclear. The autonomic nervous system has a central role in the regulation of blood pressure and is essential for cardiovascular homeostasis. We conducted a study to investigate how acute fasting influences autonomic control of blood pressure at rest and during stress. Twenty-five young, healthy, normal weight, normotensive participants were tested twice, once in the fed state (3 hours postprandial) and again in the fasted state (24 hours postprandial). Aim 1 of the study was to determine the influence of an acute fast on hemodynamics, peripheral neural activity, and cardiovascular control at rest. To fulfill this aim we measured 24-hour ambulatory blood pressure for both conditions leading up to an autonomic function test. During the autonomic function test, we controlled breathing at 0.25 Hz and measured blood pressure, heart rate, muscle sympathetic nerve activity, and forearm blood flow for 10 minutes. Fasting reduced overall ambulatory blood pressure and heart rate compared to the fed condition. From the autonomic test we measured enhanced vagal modulation of the heart through 1) increased R-R interval and heart rate variability measured via spectral analysis; 2) Increased spontaneous (rest) and dynamic (Valsalva Maneuver) cardiovagal baroreflex sensitivity indicating enhanced reflexive vagal activation. Fasting did not alter peripheral sympathetic activity or blood pressure during the autonomic test. However, forearm vascular resistance and stroke volume were increased during the fasting condition. Aim 2 investigated if fasting influenced cardiovascular and neural reactivity to a mental stressor (5 min mental arithmetic). Fasting did not augment neural or cardiovascular reactivity to a mental stress challenge. Aim 3 investigated if fasting reduced orthostatic tolerance to intense lower body negative pressure (LBNP). LBNP was applied in a stepwise manner until participants became presyncopal. Fasting reduced the duration of negative pressure participants could tolerate before presyncope occurred. The reduced tolerance to central hypovolemia seems to have been caused by an impaired ability to increase peripheral resistance as measured from the forearm. This dissertation provides novel insight into how systemic energy balance influences autonomic regulation of blood pressure. Specifically, that fasting reduces 24-hour ambulatory blood pressure, increases vagal modulation of the heart, and enhances cardiovagal baroreflex sensitivity

    Investigation of the baroreflex of the rat : steady state and dynamic features

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    The baroreflex is one of the most important feedback systems in the body to maintain blood pressure variation within the homeostatic range. In this dissertation, the important features of the carotid and aortic baroreflexes have been extensively investigated on ventilated, central nervous system intact, neuromuscular blocked (NMB) rats using different control system and signal processing tools. Studies have demonstrated that sinoaortic denervation (SAD) caused substantial increases in the blood pressure variability. Comparing the pre- and post-SAD blood pressure spectra, there was a significant increase of power in the very low frequency region (0.00195 -0.2 Hz), and a significant decrease of power in the low frequency region (0.2 - 0.6 Hz) after SAD. The dominant power change after SAD was in the very low frequency region of the blood pressure spectra. The carotid and aortic baroreflexes were accessed by volumetric manipulation of the carotid sinus and electrical manipulation of the aortic depressor nerve (ADN) using step and sinusoidal stimulations. Myelinated ADN-A fibers and myelinated + unmyelinated ADN-A+C fibers were accessed separately in the experiments. Results showed that the baroreflex functions as a \u27low-pass\u27 filter, with -3dB cutoff frequency at approximately \u3c0. I Hz. The major working area of the baroreflex system is in the VLF region of the blood pressure spectra. The estimated system transportation lag was 1.07s, which would cause the baroreflex system to oscillate at frequencies around 0.4 Hz. Analyses demonstrated that it is not likely that the baroreflex is activated only occasionally, such as in response to postural shifts, but operates continuously to bring the blood pressure into balance. It is theoretically and experimentally demonstrated that the absolute gain of the open-loop baroreflex system can be predicted by the ratio of the pre-and post- blood pressure amplitude spectra
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