Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Cardiovascular Deconditioning”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed2003

Proposed role of the paraventricular nucleus in cardiovascular deconditioning.

AIM: Cardiovascular deconditioning occurs in individuals exposed to prolonged spaceflight or bedrest and is associated with the development of orthostatic intolerance. Although the precise mechanisms remain to be fully elucidated, astronauts returning from space or bedrest patients returning to normal upright posture present with decreases in plasma volume and alterations in autonomic function. The hindlimb unloaded (HU) rat has been a useful model to study the effects of cardiovascular deconditioning as it mimics many of the changes that occur after spaceflight and bedrest. RESULTS: Experiments performed in HU rats suggest that cardiovascular deconditioning attenuates baroreflex mediated sympathoexcitation and enhances cardiopulmonary receptor mediated sympathoinhibition. These alterations appear to be due to changes in the central nervous system and may contribute to the pre disposition towards orthostatic intolerance associated with cardiovascular deconditioning. The paraventricular nucleus (PVN) of the hypothalamus is important in basal and reflex control of sympathetic outflow. Recent evidence suggests that nitric oxide (NO) is an important inhibitory neurotransmitter in the PVN and that alterations in nitroxidergic transmission in the PVN may be involved in elevated sympathetic tone in certain disease states. CONCLUSION: Based on evidence from other laboratories and published and preliminary data from our own laboratories, this review proposes a role for the PVN in cardiovascular deconditioning. In particular, we discuss the hypothesis that increased NO in the PVN contributes to the altered cardiovascular reflexes observed following deconditioning and how these reflexes may be related to the orthostatic intolerance observed after prolonged spaceflight or bedrest.

Animals↗
PubMed2004

Severe obesity associated with cardiovascular deconditioning, high prevalence of cardiovascular risk factors, diabetes mellitus/hyperinsulinemia, and respiratory compromise.

OBJECTIVE: To determine the extent and severity of obesity-related cardiorespiratory morbidity in children with body mass index (BMI) >or=40 kg/m(2). STUDY DESIGN: Cross-sectional analysis of a cohort comprised of 48 boys and girls aged 8 to 17 years with BMI >or=40 kg/m(2). Cardiorespiratory fitness (graded cycle exercise test), left ventricular (LV) mass (echocardiography), blood pressure, fasting lipid profile, fasting insulin, fasting glucose, HbA1c, and pulmonary function (spirometry and sleep studies) were measured. RESULTS: The cohort averaged 14.2 +/- 2 years of age with mean BMI of 45.5 kg/m(2). Only 2 patients had normal fitness; 37 of 48 had peak oxygen consumption <20 mL O(2)/minute. Hypertension was present in 10 of 48 patients. Mean lipid values were: triglycerides 103 +/- 48 mg/dL, HDL cholesterol 41 +/- 10 mg/dL, and LDL cholesterol 108 +/- 26 mg/dL. Type II diabetes mellitus was diagnosed in 6 patients. Mean fasting insulin was 31 +/- 19 microU/mL. Asthma treatment, small airways disease by pulmonary function testing, or both were present in 35 of 48 patients; upper airway obstruction was present in 7 patients. LV hypertrophy was present in 8 patients, with a mean LV mass of 43 +/- 11 g/m(2.7). CONCLUSIONS: Children and adolescents with BMI >or=40 kg/m(2) have substantial cardiorespiratory morbidity including severe physical deconditioning.

Adolescent↗
PubMed1998

Attenuated baroreflex control of sympathetic nerve activity after cardiovascular deconditioning in rats.

The effect of cardiovascular deconditioning on baroreflex control of the sympathetic nervous system was evaluated after 14 days of hindlimb unloading (HU) or the control condition. Rats were chronically instrumented with catheters and sympathetic nerve recording electrodes for measurement of mean arterial pressure (MAP) and heart rate (HR) and recording of lumbar (LSNA) or renal (RSNA) sympathetic nerve activity. Experiments were conducted 24 h after surgery, with the animals in a normal posture. Baroreflex function was assessed using a logistic function that related HR and LSNA or RSNA to MAP during infusion of phenylephrine and nitroprusside. Baroreflex influence on HR was not affected by HU. Maximum baroreflex-elicited LSNA was significantly reduced in HU rats (204 +/- 11.9 vs. 342 +/- 30.6% baseline LSNA), as was maximum reflex gain (-4.0 +/- 0.6 vs. -7.8 +/- 1.3 %LSNA/mmHg). Maximum baroreflex-elicited RSNA (259 +/- 10.8 vs. 453 +/- 28.0% baseline RSNA), minimum baroreflex-elicited RSNA (-2 +/- 2.8 vs. 13 +/- 4.5% baseline RSNA), and maximum gain (-5.8 +/- 0.5 vs. -13.6 +/- 3.1 %RSNA/mmHg) were significantly decreased in HU rats. Results demonstrate that baroreflex modulation of sympathetic nervous system activity is attenuated after cardiovascular deconditioning in rodents. Data suggest that alterations in the arterial baroreflex may contribute to orthostatic intolerance after a period of bedrest or spaceflight in humans.

Animals↗
PubMed1996

Cardiovascular deconditioning through head-down tilt bed rest increases blood pressure variability and plasma renin activity.

BACKGROUND: The renin-angiotensin-aldosterone system may be of primary importance in the mechanism of bed rest cardiovascular deconditioning. HYPOTHESIS: This study was designed to test the hypothesis that bed rest cardiovascular deconditioning does not result simply from plasma volume loss, but is also at least partially attributable to a persistent disequilibrium of the neuroendocrine mediators of plasma volume homeostasis. We examined whether changes in the renin-angiotensin-aldosterone system occur in association with the cardiovascular deconditioning and hemodynamic instability induced by antiorthostatic 6 degrees head-down tilt bed rest. METHODS: Normal male volunteers (n = 10) were tested before, during, and after 14 d of head-down tilt with a high (150 mEq.d-1) salt intake, using head-down tilt as a model of cardiovascular deconditioning and lower body negative pressure (LBNP) as a model of orthostatic stress. RESULTS: Resting plasma renin activity was 2.22 +/- 0.85 ng.ml-1.h-1 (+/- SD) at baseline and increased to 4.14 +/- 1.21 ng.ml-1.h-1 at the end of head-down tilt (p < 0.05), but urine aldosterone, plasma aldosterone, and urine sodium did not change with head-down tilt. Although the plasma norepinephrine response to LBNP was accentuated, resting adrenergic tone did not change during head-down tilt. Cardiovascular deconditioning was associated with an increase in blood pressure variability during LBNP as assessed by both beat-to-beat standard deviation and spectral analysis. CONCLUSIONS: These data support a proposed link between blood pressure variability and the renin-angiotensin system in cardiovascular deconditioning.

Adult↗
PubMed2000

Are energy metabolism alterations involved in cardiovascular deconditioning after weightlessness? An hypothesis.

The physiopathogenesis of the cardiovascular deconditioning syndrome observed after actual and simulated microgravity is still under debate, despite numerous studies conducted on the role of blood volume, hormones involved in its regulation, sympathetic nervous system, baroreflexes and venous compliance. Orthostatic intolerance, a reduced exercise capacity and an increased heart rate at rest characterize this syndrome. Recent data suggest, first, the presence of a complex loop between the sympathetic nervous system, carbohydrate metabolism (insulin) and leptin hormone and, second, that this loop, an overall reflection of energy metabolism, participates in cardiovascular regulation. After a resume of studies conducted on fuel homeostasis during actual and simulated microgravity, the possible implications of energy metabolism in the development of the cardiovascular deconditioning syndrome will be discussed.

Adaptation, Physiological↗
PubMed2001

Regulation of sympathetic nervous system function after cardiovascular deconditioning.

Humans subjected to prolonged periods of bed rest or microgravity undergo deconditioning of the cardiovascular system, characterized by resting tachycardia, reduced exercise capability, and a predisposition for orthostatic intolerance. These changes in cardiovascular function are likely due to a combination of factors, including changes in control of body fluid balance or cardiac alterations resulting in inadequate maintenance of stroke volume, altered arterial or venous vascular function, reduced activation of cardiovascular hormones, and diminished autonomic reflex function. There is evidence indicating a role for each of these mechanisms. Diminished reflex activation of the sympathetic nervous system and subsequent vasoconstriction appear to play an important role. Studies utilizing the hindlimb-unloaded (HU) rat, an animal model of deconditioning, evaluated the potential role of altered arterial baroreflex control of the sympathetic nervous system. These studies indicate that HU results in blunted baroreflex-mediated activation of both renal and lumbar sympathetic nerve activity in response to a hypotensive stimulus. HU rats are less able to maintain arterial pressure during hemorrhage, suggesting that diminished ability to increase sympathetic activity has functional consequences for the animal. Reflex control of vasopressin secretion appears to be enhanced following HU. Blunted baroreflex-mediated sympathoexcitation appears to involve altered central nervous system function. Baroreceptor afferent activity in response to changes in arterial pressure is unaltered in HU rats. However, increases in efferent sympathetic nerve activity for a given decrease in afferent input are blunted after HU. This altered central nervous system processing of baroreceptor inputs appears to involve an effect at the rostral ventrolateral medulla (RVLM). Specifically, it appears that tonic GABAA-mediated inhibition of the RVLM is enhanced after HU. Augmented inhibition apparently arises from sources other than the caudal ventrolateral medulla. If similar alterations in control of the sympathetic nervous system occur in humans in response to cardiovascular deconditioning, it is likely that they play an important role in the observed tendency for orthostatic intolerance. Combined with potential changes in vascular function, cardiac function, and hypovolemia, the predisposition for orthostatic intolerance following cardiovascular deconditioning would be markedly enhanced by blunted ability to reflexly activate the sympathetic nervous system.

Animals↗
PubMed2004

Effect of centrifuge-induced artificial gravity and ergometric exercise on cardiovascular deconditioning, myatrophy, and osteoporosis induced by a -6 degrees head-down bedrest.

We have reported that centrifuge-induced artificial gravity with ergometric exercise could reduce developing cardiovascular deconditioning in humans. In the present study, we examined this load could prevent the myatrophy and osteoporosis induced by head-down bedrest for 20 days. Subjects were ten healthy male volunteers with informed consent. They were requested to lie down at -6 degrees for 20 days, and evaluation for cardiovascular deconditioning, myatrophy, and osteoporosis. As the result, high G-load with low intensity exercise suppressed the orthostatic intolerance and increase in serum osteoporotic marker, whereas low G-load with high intensity ergometric exercise maintained the maximal oxygen intake, heart dimension, and prevented myatrophy. The combination of high/low G-load with low/high intensity exercise will determine the optimal protocol for prevention of cardiovascular deconditioning, myatrophy, and osteoporosis.

Adult↗
PubMed1993

Cardiovascular deconditioning effects of long-term simulated weightlessness in rats.

The aim of our serial work was to investigate the cardiovascular deconditioning effect of long-term simulated weightlessness and to elucidate its mechanisms. Our research goal was established in view of the following three reasons. Firstly, even after several decades of extensive research, there still exist significant gaps in our knowledge concerning microgravity induced cardiovascular effect. Secondly, to guarantee the health and safety of astronauts in the future prolonged missions, it is important to understand the cardiovascular adaptation to long-term weightlessness. Thirdly, the reported ultrastructural degenerative changes in myocardium of rats flown on the Cosmos 1887 biosatellite has raised concerns about the question whether long-term spaceflight may lead to myocardial degeneration. To achieve this, we considered an appropriate animal model to simulate cardiovascular and other effects of long-term microgravity was of first importance. By making some modifications to the Morey-Holton's model, a method of long-term tail-suspension with less stressful influence and no injurious effects on the tail skin was developed. Up to now, the longest period of suspension in our laboratory has been of 120-day long. In this paper, we will focus primarily on the findings from our recent works on the cardiovascular deconditioning effect of 90-/120-day tail-suspension and changes in baroreflex responsiveness and in contractility and ultrastructure of the heart in rats.

Animals↗
PubMed1999

[Effect of extremity cuffs as a countermeasure against the cardiovascular deconditioning during 21 d head-down bedrest].

OBJECTIVE: To affirm the protective effect of inflated cuffs. METHOD: The protective effect against the cardiovascular deconditioning of inflated cuffs on the upper parts of thighs and arms during the 1st through 10th days of 21 d bedrest has been reported previously. The effect of the cuffs during the rest of the 21 d bedrest were studied in this paper. Five subjects in cuffs group whose orthostatic tolerance were well maintained continued bed rest for 7 d without inflated cuffs. For the last 4 days of this period, inflated cuffs were again applied. Orthostatic tolerance of subjects in cuffs group with and without cuffs were measured. RESULT: Two of the five subjects suffered orthostatic intolerance on the 17th day. No sign of orthostatic intolerance were observed by the end of bedrest. CONCLUSION: (1) the cardiovascular deconditioning developed when inflated cuffs were not used, and (2) the use of inflated cuffs for 4 d improves the orthostatic tolerance.

Adolescent↗
PubMed1995

Cardiovascular deconditioning occurs during a 7-day saturation dive at 31 ATA.

Cardiovascular deconditioning (CD) has been reported to occur within 24-48 h of exposure to 4, 11, or 31 ATA environment and following decompression to sea level pressure. The CD was indicated by orthostatic intolerance, exaggerated cardiovascular responses to a passive tilt, an elevated resting heart rate and a reduced stroke volume postdive. In this dive, one of the New Seatopia series, we used a non-syncope criterion, the cardiovascular index of deconditioning (CID; Bungo MW, Johnson PJ Jr. Aviat Space Environ Med 1983; 54:1001), to evaluate CD in 3 male subjects. The CID sums the changes in heart rate and blood pressure in response to orthostatic stress. An elevated CID indicates CD. We used a passive 70 degrees head up tilt as the orthostatic stress. The CID was measured before and after a bout of underwater exercise at predive, during the early, mid, and late exposure of the 7-d 31 ATA, and after the dive. The CID and circulatory responses to tilt were similar before and after the exercise. The CID increased (p < 0.05) from the predive value of 20 +/- 1.6 to 25 +/- 0.9 on the 2nd day, to 25 +/- 0.8 on the 4th day at 31 ATA, indicating the presence of CD at the early and mid periods of hyperbaric exposure. However, CID was indifferent (18 +/- 0.6) from the predive on the 7th day at 31 ATA. The increased CID corresponded to decreases in plasma volume during the early and mid periods of 31 ATA exposure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2003

Cardiovascular deconditioning in microgravity: some possible countermeasures.

Microgravity is an extreme environment inducing relevant adaptive changes in the human body, especially after prolonged periods of exposure. Since the early sixties, numerous studies on the effects of microgravity, during manned Space flights, have produced an increasing amount of information concerning its physiological effects, globally defined "deconditioning". Microgravity deconditioning of the cardiovascular system (CVD) is briefly reviewed. It consists of: (1) a decrease of circulating blood and interstitial fluid volumes, (2) a decrease of arterial blood diastolic pressure, (3) a decrease of ventricular stroke volume, (4) a decrease of the estimated left ventricular mass and (5) resetting of the carotid baroreceptors. The negative effects of microgravity deconditioning manifest themselves mostly upon the reentry to Earth. They consist mainly of: (1) dizziness, (2) increased heart rate and heart palpitations, (3) an inability to assume the standing position (orthostatic intolerance), (4) pre-syncopal feelings due to postural stress and (5) reduced exercise capacity. To avoid these drawbacks several countermeasures have been proposed; they will be briefly mentioned with emphasis on the "Twin Bikes System" (TBS). This consists of two coupled bicycles operated by astronauts and counter-rotating along the inner wall of a cylindrical Space module, thus generating a centrifugal force vector, mimicking gravity.

Algorithms↗
PubMed1996

Cardiovascular deconditioning and venous air embolism in simulated microgravity in the rat.

BACKGROUND: Astronauts conducting extravehicular activities undergo decompression to a lower ambient pressure, potentially resulting in gas bubble formation within the tissues and venous circulation. Additionally, exposure to microgravity produces fluid shifts within the body leading to cardiovascular deconditioning. A lower incidence of decompression illness in actual spaceflight compared with that in ground-based altitude chamber flights suggests that there is a possible interaction between microgravity exposure and decompression illness. HYPOTHESIS: The purpose of this study was to evaluate the cardiovascular and pulmonary effects of simulated hypobaric decompression stress using a tail suspension (head-down tilt) model of microgravity to produce the fluid shifts associated with weightlessness in conscious, chronically instrumented rats. METHODS: Venous bubble formation resulting from altitude decompression illness was simulated by a 3-h intravenous air infusion. Cardiovascular deconditioning was simulated by 96 h of head-down tilt. Heart rate, mean arterial blood pressure, central venous pressure, left ventricular wall thickening and cardiac output were continuously recorded. Lung studies were performed to evaluate edema formation and compliance measurement. Blood and pleural fluid were examined for changes in white cell counts and protein concentration. RESULTS: Our data demonstrated that in tail-suspended rats subjected to venous air infusions, there was a reduction in pulmonary edema formation and less of a decrease in cardiac output than occurred following venous air infusion alone. Mean arterial blood pressure and myocardial wall thickening fractions were unchanged with either tail-suspension or venous air infusion. Heart rate decreased in both conditions while systemic vascular resistance increased. CONCLUSIONS: These differences may be due in part to a change or redistribution of pulmonary blood flow or to a diminished cellular response to the microvascular insult of the venous air embolization.

Animals↗
PubMed1985

Visceral predictors of cardiovascular deconditioning in late middle-aged men.

A major task for space biologists is to try to delineate methods which can be used to predict the degree of cardiovascular deconditioning that given individuals might develop while in space. Toward that end, we have studied a number of different visceral and behavioral variables in a group of late middle-aged men (55-65 years) on day 1 and day 5 of a bedrest regimen. During each 8-h study period, data were collected every 15 min. Mean arterial blood pressure and plasma cortisol and norepinephrine concentrations were significantly higher on the day 5 than on the day 1 of bedrest; heart rate, core temperature, plasma epinephrine and subjective arousal were unchanged. Pair-wise correlations between each of these variables and the time to blackout on a +3-Gz test of acceleration tolerance administered on day 9 of bedrest (mean decrease in latencies from prebedrest was 52%) revealed a significant correlation for the mean arterial blood pressure variable. Thus, these data indicate that men in this age span with relatively low resting blood pressures are at greater risk for developing clinical signs relating to their cardiovascular deconditioning than other men with higher basal blood pressures.

Acceleration↗
PubMed1996

Central hypervolemia in the conscious rat: a model of cardiovascular deconditioning.

The aim of the present study as to investigate whether increased central hypervolemia induced by tail suspension (TS) in the rat is an appropriate model of cardiovascular deconditioning (CVD). First, the physiological relationship between central venous pressure (CVP) and extracellular fluid volume (ECFV) was studied. TS (20 degrees) increased CVP (5.8 +/- 0.7 vs. 2.8 +/- 0.8 mmHg; P < 0.01). After 24 h of TS, CVP had returned to control range while ECFV was reduced by 19%. CVP kinetics during 24 h of TS was not affected by either reduction (-20%) or augmentation (/35%) of the ECFV. The normalization of CVP is likely to be a consequence of ECFV reduction, which itself is reduced by increased urinary excretion of water and sodium. Second, recovery from TS was studied. Resumption of the horizontal position was shown to be associated with a significant increase of heart rate (HR) and a slight reduction of blood pressure (BP); there was an apparent delay between increased HR and reduced BP. This imbalance between HR and BP is compatible with CVD. A model of simulated orthostatism (SO) was developed to further investigate the responses of HR and BP. Interestingly, SO (90 degrees rotation) in the normal rat was associated with significant tachycardia and a slight increase of BP. This pattern remained stable for at least 3 h. In rats that were tail suspended for 48 h, episodes of hypotension and bradycardia (5 +/- 1 in 3 h) suggested a defect in adaptation to increased hydrostatic pressure. In conclusion, TS appears to be an appropriate model of CVD. Reduction process. Return to horizontal position in TS rats induced a tachycardia with minimal effects on BP; this pattern is close to that observed in humans assuming upright posture. SO in previously TS rats disclosed episodes of hypotension and bradycardia that deserve further investigation.

Animals↗
PubMed2003

[Effects of NO synthases inhibitor on cardiovascular deconditioning in rats after 7 d tail-suspension].

OBJECTIVE: To disclose the changes in pathophysiology of cardiovascular deconditioning (CVD) induced by tail-suspension (TS) and to explore the effects of NOS inhibitor on CVD in TS rats. METHOD: -30 degrees tail suspended rats were used as the model to simulate the physiological effects of microgravity. Wistar rats were randomly arranged into: control group (CON), 7 d TS group (TS 7 d) and TS 7 d + NOS inhibitor group (TS 7 d + L-NAME). Then, all the rats were subjected to +90 degrees head-up tilt to simulate the physiological effects of orthostatic stress (SO) after 7 d tail-suspension, only that the TS 7d + L-NAME rats were injected with 10(-6) M L-NAME (N-nitro-L-arginine methylester) through hypoglossal vein before tilting after 7 d TS. Carotid pressure and limb II ECG were measured with a PowerLab physiological system during 120 min tilt, and mean arterial pressure (MAP) and heart rate (HR) were analysized. RESULT: Only one transient episode of hypotension-bradycardia appeared during the tilt in CON rats, but seven episodes occurred in TS 7 d rats, while the TS 7 d + L-NAME rats has only a significant increase in MAP at 10 min. No differences were found between the other parameters in recumbent position and those during the tilt. CONCLUSION: The CVD in the rats induced by TS is relative to an increase of NO production. 10(-6) M L-NAME had an alleviating effects on the CVD, which might be due to the increase of peripheral resistance of blood vessels and the central sympathetic drive by the combination of L-NAME with NOS. The contribution of the perivascular nerves and pulmonary arteries to this effect remains to be further studied.

Animals↗
PubMed1990

Cardiovascular deconditioning during weightlessness simulation and the use of lower body negative pressure as a countermeasure to orthostatic intolerance.

The cardiovascular function is one of the main disturbed by weightlessness: it is particularly affected by the astronaut's return to Earth, where symptoms linked to the cardiovascular deconditioning syndrom appear in the following forms: (1) orthostatic intolerance with its risk of syncope: (2) higher submaximal oxygen consumption for an equivalent work load. Lower Body Negative Pressure (LBNP) is intended to stimulate the venous system of the lower limbs; however, the specific effects of periodical LBNP sessions on the orthostatic intolerance have never been studied. With this objective in mind, 5 volunteers took part in two recent antiorthostatic bedrest experiments for 30 days. In the first experiment 3 subjects were submitted to several sessions of LBNP experiment per day and 2 others were controls; in the second experiment the LBNP group of the 1st one became controls and vice-versa. Two orthostatic investigations were performed: (1) 5 days before the bedrest; (2) at the end of the 30 day bedrest period. The results showed: (1) when the subjects were control, a high orthostatic intolerance post bedrest with 3 syncopes and one presyncopal state during the first minutes of the tilt test; (2) when the subjects were submitted to LBNP sessions, no orthostatic intolerance.

Adult↗
PubMed1998

Mechanisms of the cardiovascular deconditioning induced by tail suspension in the rat.

The aim of the present work was to obtain insights into the pathophysiology of cardiovascular deconditioning (CVD) induced by tail suspension (TS) in the rat: during TS, when central venous pressure (CVP) has been normalized (E. Martel, P. Champéroux, P. Lacolley, S. Richard, M. Safar, and J. L. Cuche. J. Appl. Physiol. 80: 1390-1396, 1996), and during simulated orthostatism (SO), when transient episodes of hypotension and bradycardia are disclosed, bradycardia with SO represents a response that seems peculiar to the rat compared with humans. According to basic physiology, a reduced activity of the sympathetic system induced by increased CVP was suspected but was not supported by data obtained through spectral analysis of blood pressure (BP) and heart rate (HR) variability or measurements of plasma catecholamine concentration during TS. Nonetheless, indirect evidence was obtained. During SO, plasma catecholamine concentration was lower in TS rats than in controls, suggesting a reduced synthesis of catecholamines, itself secondary to reduced activity of the sympathetic system. Furthermore, after 48 h of TS, the number of binding sites and affinity of alpha-receptors in rat aorta were increased, compatible with a reduced level of neurotransmitter in the synaptic cleft. A second series of experiments was carried out to study hypotension and bradycardia in TS rats during SO. Hypersensitivity of serotonergic mechanisms was suspected. Two 5-HT3 receptor antagonists (ondansetron and MDL-72222) blocked hypotension and restored tachycardia, basic features of orthostatic adaptation of the circulatory system. Response to the 5-HT3 receptor agonist was measured through dose-response curves of BP and HR after injection of 2-methylserotonin. After low doses, hypotension (10 micrograms/kg) and bradycardia (3 and 10 micrograms/kg) were significantly greater in 48-h TS rats than in controls. Thus CVD in the rat induced by TS appears to implicate at least two mechanisms: reduced activity of the sympathetic system and hypersensitivity of serotonergic mechanisms.

Animals↗
PubMed1998

Effect of acute saline infusion on the cardiovascular deconditioning after 20-days head-down tilt bedrest.

Recent study showed that dehydration induced by prolonged exercise significantly impaired orthostatic tolerance with tachycardia and hypotension, and subsequent rehydration restored it. As physiological changes during exposure to actual or simulated microgravity can be viewed as dehydration process, we hypothesized that rehydration after prolonged bedrest may be a promising candidate to countermeasure not only fluid volume loss but also autonomic nervous deconditioning. Therefore, the purpose of present study was to determine the effect of acute rehydration by saline infusion on orthostatic cardiovascular deconditioning after bedrest.

Bed Rest↗