A commonly accepted hypothesis is that a chronically high-sodium diet expands extracellular volume and finally reaches a steady state where sodium intake and output are balanced whereas extracellular volume is expanded. However, in a recent study where the main purpose was to investigate the role of natriuretic peptides under day-to-day sodium intake conditions (Heer M, Drummer C, Baisch F, and Gerzer R. Pflügers Arch 425: 390-394, 1993), our laboratory observed increases in plasma volume without any rise in extracellular volume. To scrutinize these results that were observed as a side effect, we performed a controlled, randomized study including 32 healthy male test subjects in a metabolic ward. The NaCl intake ranged from a low level of 50 meq NaCl/day to 200, 400, and 550 meq/day, respectively. Plasma volume dose dependently increased (P < 0.01), being elevated by 315 +/- 37 ml in the 550-meq-NaCl-intake group. However, in contrast to the increased plasma volume, comparable to study I, total body water did not increase. In parallel, body mass also did not increase. Mean corpuscular volume of erythrocytes, as an index for intracellular volume, was also unchanged. We conclude from the results of these two independently conducted studies that under the chosen study conditions, in contrast to present opinions, high sodium intake does not induce total body water storage but induces a relative fluid shift from the interstitial into the intravascular space.

Orthostatic intolerance is common when astronauts return to Earth: after brief spaceflight, up to two‐thirds are unable to remain standing for 10 min. Previous research suggests that susceptible individuals are unable to increase their systemic vascular resistance and plasma noradrenaline concentrations above pre‐flight upright levels. In this study, we tested the hypothesis that adaptation to the microgravity of space impairs sympathetic neural responses to upright posture on Earth. We studied six astronauts ∼72 and 23 days before and on landing day after the 16 day Neurolab space shuttle mission. We measured heart rate, arterial pressure and cardiac output, and calculated stroke volume and total peripheral resistance, during supine rest and 10 min of 60 deg upright tilt. Muscle sympathetic nerve activity was recorded in five subjects, as a direct measure of sympathetic nervous system responses. As in previous studies, mean (±s.e.m.) stroke volume was lower (46 ± 5 vs. 76 ± 3 ml, P= 0.017) and heart rate was higher (93 ± 1 vs. 74 ± 4 beats min−1, P= 0.002) during tilt after spaceflight than before spaceflight. Total peripheral resistance during tilt post flight was higher in some, but not all astronauts (1674 ± 256 vs. 1372 ± 62 dynes s cm−5, P= 0.32). No crew member exhibited orthostatic hypotension or presyncopal symptoms during the 10 min of postflight tilting. Muscle sympathetic nerve activity was higher post flight in all subjects, in supine (27 ± 4 vs. 17 ± 2 bursts min−1, P= 0.04) and tilted (46 ± 4 vs. 38 ± 3 bursts min−1, P= 0.01) positions. A strong (r2= 0.91–1.00) linear correlation between left ventricular stroke volume and muscle sympathetic nerve activity suggested that sympathetic responses were appropriate for the haemodynamic challenge of upright tilt and were unaffected by spaceflight. We conclude that after 16 days of spaceflight, muscle sympathetic nerve responses to upright tilt are normal.

The present study was performed with the aim of checking the suitability of EIT in imaging regional thoracic impedance variations during lung ventilation under predefined conditions and to compare EIT with established reference techniques. A new technique of functional EIT imaging designed to visualize physiologically relevant information from the sequentially registered series of thoracic distributions was introduced. Experiments were performed on five spontaneously breathing healthy subjects and on 12 anaesthetized supine pigs. 16 electrodes were placed around the thorax and consecutive transthoracic impedance distributions were measured at a rate of 1 Hz (Sheffield APT system mark I, IBEES, Sheffield, UK). Several voluntary breathing manoeuvres were performed in human subjects and the tracings of local impedance were compared with standard spirometry. In animal experiments EIT was applied during artificial ventilation at different ventilation rates and during stepwise passive emptying and filling of either one or both lungs while the respiratory muscles were relaxes. Further, selective blockade of lung regions resulting in regionally reduced ventilation was performed and the capability of EIT to follow and differentiate local ventilatory disturbances was checked by reference techniques (x-ray and staining methods). The experiments revealed an overall agreement between the spirometric and impedance data in all breathing patterns performed. A linear relationship between changes of the air content of the lungs and the regional thoracic impedance was shown (intraindividual correlation coefficient range, 0.986-0.999; n = 12 animals). The functional images of the impedance distribution across the thorax reproduced adequately the typical anatomical characteristics of the pig and the human thorax. The spatial resolution of EIT functional images was sufficient to differentiate lung areas corresponding to approximately 20 ml tissue volume. EIT with the additional evaluation procedure of functional imaging was shown to be a suitable and reliable method of imaging different ventilatory conditions with the potential to become a useful tool for monitoring respiratory function.

Astronauts returning from space have reduced red blood cell masses, hypovolaemia and orthostatic intolerance, marked by greater cardio–acceleration during standing than before spaceflight, and in some, orthostatic hypotension and presyncope. Adaptation of the sympathetic nervous system occurring during spaceflight may be responsible for these postflight alterations. We tested the hypotheses that exposure to microgravity reduces sympathetic neural outflow and impairs sympathetic neural responses to orthostatic stress. We measured heart rate, photoplethysmographic finger arterial pressure, peroneal nerve muscle sympathetic activity and plasma noradrenaline spillover and clearance, in male astronauts before, during (flight day 12 or 13) and after the 16 day Neurolab space shuttle mission. Measurements were made during supine rest and orthostatic stress, as simulated on Earth and in space by 7 min periods of 15 and 30 mmHg lower body suction. Mean (±s.e.m.) heart rates before lower body suction were similar pre–flight and in flight. Heart rate responses to −30 mmHg were greater in flight (from 56 ± 4 to 72 ± 4 beats min−1) than pre–flight (from 56 ± 4 at rest to 62 ± 4 beats min−1, P < 0.05). Noradrenaline spillover and clearance were increased from pre–flight levels during baseline periods and during lower body suction, both in flight (n= 3) and on post–flight days 1 or 2 (n= 5, P < 0.05). In–flight baseline sympathetic nerve activity was increased above pre–flight levels (by 10–33 %) in the same three subjects in whom noradrenaline spillover and clearance were increased. The sympathetic response to 30 mmHg lower body suction was at pre–flight levels or higher in each subject (35 pre–flight vs. 40 bursts min−1 in flight). No astronaut experienced presyncope during lower body suction in space (or during upright tilt following the Neurolab mission). We conclude that in space, baseline sympathetic neural outflow is increased moderately and sympathetic responses to lower body suction are exaggerated. Therefore, notwithstanding hypovolaemia, astronauts respond normally to simulated orthostatic stress and are able to maintain their arterial pressures at normal levels.

Exposure to microgravity alters the distribution of body fluids and the degree of distension of cranial blood vessels, and these changes in turn may provoke structural remodelling and altered cerebral autoregulation. Impaired cerebral autoregulation has been documented following weightlessness simulated by head-down bed rest in humans, and is proposed as a mechanism responsible for postspaceflight orthostatic intolerance. In this study, we tested the hypothesis that spaceflight impairs cerebral autoregulation. We studied six astronauts ∼72 and 23 days before, after 1 and 2 weeks in space (n = 4), on landing day, and 1 day after the 16 day Neurolab space shuttle mission. Beat-by-beat changes of photoplethysmographic mean arterial pressure and transcranial Doppler middle cerebral artery blood flow velocity were measured during 5 min of spontaneous breathing, 30 mmHg lower body suction to simulate standing in space, and 10 min of 60 deg passive upright tilt on Earth. Dynamic cerebral autoregulation was quantified by analysis of the transfer function between spontaneous changes of mean arterial pressure and cerebral artery blood flow velocity, in the very low-(0.02-0.07 Hz), low-(0.07-0.20 Hz) and high-frequency (0.20-0.35 Hz) ranges. Resting middle cerebral artery blood flow velocity did not change significantly from preflight values during or after spaceflight. Reductions of cerebral blood flow velocity during lower body suction were significant before spaceflight (P < 0.05, repeated measures ANOVA), but not during or after spaceflight. Absolute and percentage reductions of mean (± S.E.M.) cerebral blood flow velocity after 10 min upright tilt were smaller after than before spaceflight (absolute, −4 ± 3 cm s −1 after versus −14 ± 3 cm s −1 before, P = 0.001; and percentage, −8.0 ± 4.8% after versus −24.8 ± 4.4% before, P < 0.05), consistent with improved rather than impaired cerebral blood flow regulation. Low-frequency gain decreased significantly (P < 0.05) by 26, 23 and 27% after 1 and 2 weeks in space and on landing day, respectively, compared with preflight values, which is also consistent with improved autoregulation. We conclude that human cerebral autoregulation is preserved, and possibly even improved, by short-duration spaceflight.