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Vestibulovegetative disorders on manned space flights are discussed. A study relating to the vestibular stimuli in respiration, diaphoresis cardiac rhythm and a broad complex of hemodynamic indices was conducted. Certain tests for astronaut candidates are discussed.
The effects of posture on time-based noninvasive measurements were determined utilizing the sequence supine-sitting-standing in a formal protocol in which observer biases were eliminated by blinding the measurement and calculation phases. Compared to the supine posture, the sitting and standing postures produced significant increases in heart rate, isovolumic contraction time, pre-ejection period and pre-ejection period/left-ventricular ejection time and significant decreases in ejection time and ejection time index. The response patterns are consistent with the hemodynamic correlates cited in the literature which show increased adrenergic activity and decreased venous return in the sitting and standing postures, the effect on venous return being dominant.
The early cardiovascular adaptation to zero gravity, simulated by head-down tilt at 5 deg, was studied in a series of 10 normal young men. The validity of the model was confirmed by comparing the results with data from Apollo and Skylab flights. Tilt produced a significant central fluid shift with a transient increase in central venous pressure, later followed by an increase in left ventricular size without changes in cardiac output, arterial pressure, or contractile state. The hemodynamic changes were transient with a nearly complete return to the control state within 6 h. The adaptation included a diuresis and a decrease in blood volume, associated with ADH, renin, and aldosterone inhibition.
In the horizontal position (supine and lateral), in the upright position (head up and head down) and during change of the cat body position in space, quantitative responses of regional blood volume and blood flow in the lungs (ml/100 cu cm) revealed presence of the gradient in the gravitation direction. Blood volume and blood flow of different lung portions changed qualitatively and quantitatively in different ways. These changes occurred only in the direction producing the equality of regional hydrostatical and hemodynamic loads in the lungs at either horizontal level.
A mathematical model of erythropoiesis control was used to simulate the effects of bedrest and zero-g on the circulating red cell mass. The model incorporates the best current understanding of the dynamics of red cell production and destruction and the associated feedback regulation. Specifically studied were the hemodynamic responses of a 28-day bedrest study devised to simulate Skylab experience. The results support the hypothesis that red cell loss during supine bedrest is a normal physiological feedback process in response to hemoconcentration enhanced tissue oxygenation and suppression of red cell production. Model simulation suggested the possibilities that this period was marked by some combination of increased oxygen-hemoglobin affinity, small reduction in mean red cell life span, ineffective erythropoiesis, or abnormal reticulocytosis.
This bibliography of citations to the international literature covers aspects of altitude acclimatization. Included are articles concerning high altitude environments, hypoxia, heart function and hemodynamic responses, physical exercise, human tolerances and reactions, physiological responses, and oxygen consumption. This updated bibliography contains 164 citations, 35 of which are new entries to the previous edition.
Three groups of athletes including long-distance runners, competitive and amateur weight lifters, and age- and sex-matched control subjects have been studied by hemodynamic and echocardiographic methods in order to determine the effect of the training programs on the cardiovascular response to static exercise. Blood pressure, heart rate, and double product data at rest and at fatigue suggest that competitive endurance (dynamic exercise) training alters the cardiovascular response to static exercise. In contrast to endurance exercise, weight lifting (static exercise) training does not alter the cardiovascular response to static exercise: weight lifters responded to static exercise in a manner very similar to that of the control subjects.
The mechanisms underlying the reductions in orthostatic tolerance associated with weightlessness are not well established. Contradictory results from measurements of leg volume changes suggest that altered venomotor tone and reduced blood flow may not be the only contributors to orthostatic intolerance. It is felt that a more accurate limb volume system which is insensitive to environmental factors will aid in better quantification of the hemodynamics of the leg. Of the varous limb volume techniques presently available, the ultrasonic limb volume system has proven to be the best choice. The system as described herein is free from environmental effects, safe, simple to operate and causes negligible radio frequency interference problems. The segmental ultrasonic ultrasonic plethysmograph is expected to provide a better measurement of limb volume change since it is based on cross-sectional area measurements.
During the first four flights of the Space Shuttle, cardiovascular data were obtained on each crewmember as part of the operational medicine requirements for crew health and safety. From monitoring blood pressure and electrocardiographic data, it was possible to estimate the degree of deconditioning imposed by exposure to the microgravity environment. For this purpose, a quantitative cardiovascular index of deconditioning (CID) was derived to aid the clinician in his assessment. Isotonic saline was then investigated as a countermeasure against orthostatic intolerance and found to be effective in partially reversing the hemodynamic consequences. It was observed that the space flight environment of reentry might potentially be arrhythmogenic in at least one individual.
Klein et al. (1977) have questioned the concept of endurance training as an appropriate means of preparing for prolonged space flights. Their opinion was mainly based on reports of endurance athletes who had a decreased tolerance to orthostatic or gravitational stress induced by lower body negative pressure (LBNP), upright tilt, or whole body water immersion. The present investigation had the objective to determine if the hemodynamic response to LBNP is different between a high and average fit group of subjects. In addition, the discrete aspect of cardiovascular function which had been altered by chronic training was to be identified. On the basis of the results of experiments conducted with 14 young male volunteers, it is concluded that the reflex response to central hypovolemia is altered by endurance exercise training.
The cardiovascular system's adaptive changes during and after spaceflight are discussed. Cephalic fluid shifts are demonstrated by photographs along with calf girth and leg volume changes. Inflight measurements show an increase in average resting heart rate and systolic blood pressure, and a sympathetic-parasympathetic neural imbalance. Postflight findings include a small but reversible decrease in the left ventricular muscle mass. Since 1980, NASA's research has emphasized cardiovascular deconditioning and countermeasures: hemodynamic changes, endocrine and neurohumoral aspects, etiologic factors, and lower body negative pressure devices. Though human beings acclimate to the space environment, questions concerning the immediate and long-term aspects of spaceflight need to be answered for adequate planning of extended space missions.
The renin-angiotensin-aldosterone system may be implicated in hemodynamic alterations occurring in dysbaric disorders. This report concerns changes in plasma renin activity (PRA) induced by exposure of rabbits to a compression-decompression schedule that does not normally produce clinical manifestations of decompression sickness. The results revealed a significant increase in PRA in 19 of 23 animals following dysbaric exposure. Mean PRA rose from 1.18 ng ang I/ml hr (preexposure) to 2.40 ng ang I/ml hr (postexposure). The increase was particularly pronounced in female animals (217 percent). Asymptomatic intravascular gas bubbles (silent bubbles) were detected by gross or microscopic examination in the majority of the animals. Renin elaboration and secretion in asymptomatic dysbaric exposures may be mediated by bradykinin and/or prostaglandins released or activated in a chain reaction triggered by silent gas bubbles. This hypothesis is also applicable to increased PRA in altitude decompression. Alternatively elevation of PRA may result from decreased renal perfusion when dysbaric disorders are complicated by significant hypovolemia.
Hemodynamic responses and antidiuretic hormone (ADH) were measured during body position changes, designed to induce central blood volume shifts in ten cardiac and one heart-lung transplant recipients, to assess the contribution of cardiac volume receptors in the control of ADH release during the initial acute phase of exposure to weightlessness. Each subject underwent 15 min of a sitting-control period (C) followed by 30 min of 6 deg headdown tilt (T) and 30 min of resumed sitting (S). Venous blood samples and cardiac dimensions were taken at 0 and 15 min of C; 5, 15, and 30 min of T; and 5, 15, and 30 min of S. Blood samples were analyzed for hematocrit, plasma osmolality, plasma renin activity (PRA), and ADH. Heart rate and blood pressure were recorded every two min. Plasma osmolality was not altered by posture changes. Mean left ventricular end-diastolic volume increased (P less than 0.05) from 90 ml in C to 106 ml in T and returned to 87 ml in S. Plasma ADH was reduced by 20 percent (P less than 0.05) with T, and returned to control levels with S. These responses were similar in six normal cardiac-innervated control subjects. These data may suggest that cardiac volume receptors are not the primary mechanism for the control of ADH release during acute central volume shifts in man.
The cardiovascular response to 1 h of 60-deg head-down tilt was studied in 12 male subjects, ages 30-39 years, to simulate the early effects of weightlessness. Fluid shifts, hemodynamic variables, and indices of myocardial contractility were evaluated by utilizing electrocardiography, systolic time intervals, impedance cardiography, sphygmomanometry, and measurement of calf circumference. Most cardiovascular variables remained stable throughout the initial 30 min of the protocol, even though translocation of fluid from the legs to the thorax commenced immediately with the onset of head-down tilt. In contrast, minutes 30-60 were characterized by reduced stroke volume, cardiac output, mean stroke ejection rate, and Heather index concomitant with an elevation in mean arterial pressure. Intrathoracic fluid volume continued to increase, while leg volume continued to decrease. This latter physiological response suggests intrathoracic sequestration of fluid volume; blood was apparently redistributed to the pulmonary circulation rather than being retained in the great veins.
The method of Smith et al. (1985), which makes it possible to simultaneously measure the macrocirculation and microcirculation in an unanesthetized rat, was used to study the effect of acute hypokinesia on the rat microvascular system. The measurements yielded values of the length, diameter, and number of arteriolar and venular vessels; vascular patterns; branching ratios; and the amplitude and frequency of vasomotion. Early effects (30-60 min after the start of the head-down tilt) include a 10 percent increase in the diameter of arterioles, a slight increase of heart rate and mean arterial blood pressure, and an increase in the heart rate-pulse pressure product, with most of the changes returning to normal after 2-3 h. The baroreceptor reflex index was reduced by almost 50 percent for the first 2 h, but rebounded to almost 3 times the control value after 3 h. This indicates that, in spite of relatively small changes in gross hemodynamic parameters, the cardiovascular function is altered significantly during the acute phase of hypokinesia.
A large number of animal and human flight and ground-based studies were conducted to uncover the cardiovascular effects of weightlessness. Findings indicate changes in cardiovascular function during simulations and with spaceflight that lead to compromised function on reambulation and/or return to earth. This altered state termed cardiovascular deconditioning is most clearly manifest when in an erect body state. Hemodynamic parameters inidicate the presence of excessive tachnycardia, hypotension (leading to presyncope in one-third of the subjects), decreased heart volume, decreased plasma and circulating blood volumes and loss of skeletal muscle mass, particularly in the lower limbs. No clinically harmful effects were observed to date, but in-depth follow-ups were limited, as was available physiologic information. Available data concerning the causes for the observed changes indicate significant roles for mechanisms involved with body fluid-volume regulation, altered cardiac function, and the neurohumoral control of the control of the peripheral circulation. Satisfactory measures are not found. Return to preflight state was variable and only slightly dependent on flight duration. Future progress awaits availability of flight durations longer than several weeks.
The role of tolerance to orthostatic stress in the maintenance of high aerobic fitness in women was investigated by examining the responses of heart rate, stroke volume, cardiac output, Heather index of contractility, arterial pressure, peripheral resistance, change in calf circumference, and thoracic impedance of healthy female subjects to lower body negative pressure (LBNP) applied for 5 min at -50 mm Hg or until a subject became presyncopal. The testing protocol involved a stepwise reduction in pressure and consisted of two parts: an LBNP test in supine position followed by a treadmill test to peak aerobic capacity. Women were found to exhibit the same response pattern to LBNP as was previously reported by Convertino et al. (1984) for men. The results do not support the hypothesis that orthostatic tolerance in women is inversely related to aerobic fitness, as demonstrated by a finding that the peak aerobic capacity of subjects who became presyncopal did not differ from the peak of the tolerant subjects, and that hemodynamic responses to LBNPL were not a function of aerobic capacity.
Selected results of cardiocirculatory measurements in healthy volunteers who breathed 100 percent O2 continuously at 3.0 ATA for up to 3.5 hr, at 2.5 ATA for up to 6.0 hr, at 2.0 ATA for up to 11.9 hr, and at 1.5 ATA for up to 19.0 hr are reported. The results indicate that resting hemodynamic responses to prolonged hyperbaric oxygen breathing in man usually consist of small deviations from normal sea-level responses. Rapid onset of bradycardia occurred at all four oxygen pressures investigated. This effect was accompanied by a rate-dependent reduction in cardiac output and a degree of systematic vasoconstriction which were small in magnitude and appeared to be functionally unimportant.