Search

Postural stress requires immediate autonomic nervous action to maintain blood pressure. We determined time-domain cardiac baroreflex sensitivity (BRS) and time delay (tau) between systolic blood pressure and interbeat interval variations during stepwise changes in the angle of vertical body axis (alpha). The assumption was that with increasing postural stress, BRS becomes attenuated, accompanied by a shift in tau toward higher values. In 10 healthy young volunteers, alpha included 20 degrees head-down tilt (-20 degrees), supine (0 degree), 30 and 70 degrees head-up tilt (30 degrees, 70 degrees), and free standing (90 degrees). Noninvasive blood pressures were analyzed over 6-min periods before and after each change in alpha. The BRS was determined by frequency-domain analysis and with xBRS, a cross-correlation time-domain method. On average, between 28 (-20 degrees) to 45 (90 degrees) xBRS estimates per minute became available. Following a change in alpha, xBRS reached a different mean level in the first minute in 78% of the cases and in 93% after 6 min. With increasing alpha, BRS decreased: BRS = -10.1.sin(alpha) + 18.7 (r(2) = 0.99) with tight correlation between xBRS and cross-spectral gain (r(2) approximately 0.97). Delay tau shifted toward higher values. In conclusion, in healthy subjects the sensitivity of the cardiac baroreflex obtained from time domain decreases linearly with sin(alpha), and the start of baroreflex adaptation to a physiological perturbation like postural stress occurs rapidly. The decreases of BRS and reduction of short tau may be the result of reduced vagal activity with increasing alpha.

Internal jugular veins are the major cerebral venous outflow pathway in supine humans. In upright humans the positioning of these veins above heart level causes them to collapse. An alternative cerebral outflow pathway is the vertebral venous plexus. We set out to determine the effect of posture and central venous pressure (CVP) on the distribution of cerebral outflow over the internal jugular veins and the vertebral plexus, using a mathematical model. Input to the model was a data set of beat-to-beat cerebral blood flow velocity and CVP measurements in 10 healthy subjects, during baseline rest and a Valsalva manoeuvre in the supine and standing position. The model, consisting of 2 jugular veins, each a chain of 10 units containing nonlinear resistances and capacitors, and a vertebral plexus containing a resistance, showed blood flow mainly through the internal jugular veins in the supine position, but mainly through the vertebral plexus in the upright position. A Valsalva manoeuvre while standing completely re-opened the jugular veins. Results of ultrasound imaging of the right internal jugular vein cross-sectional area at the level of the laryngeal prominence in six healthy subjects, before and during a Valsalva manoeuvre in both body positions, correlate highly with model simulation of the jugular cross-sectional area (R(2) = 0.97). The results suggest that the cerebral venous flow distribution depends on posture and CVP: in supine humans the internal jugular veins are the primary pathway. The internal jugular veins are collapsed in the standing position and blood is shunted to an alternative venous pathway, but a marked increase in CVP while standing completely re-opens the jugular veins.

Objective: To test a new method (cross-correlation baroreflex sensitivity, xBRS) for the computation of time-domain baroreflex sensitivity on spontaneous blood pressure and heart interval variability using the EUROBAVAR data set., Methods: We applied xBRS to the 42 records in the EUROBAVAR data set, obtained from 21 patients in the lying and standing positions. One patient had a recent heart transplant and one was diabetic with evident cardiac autonomic neuropathy. xBRS computes the correlation between beat-to-beat systolic blood pressure and R-R interval, resampled at 1 Hz, in a sliding 10 s window, with delays of 0-5 s for interval. The delay with the greatest positive correlation is selected and, when significant at P = 0.01, slope and delay are recorded as one xBRS value. Each 1 s of the recording is the start of a new computation. Non-parametric tests are used., Results: With patients in the lying position, xBRS yielded a value of 12.4 ms/mmHg compared with the EUROBAVAR sequential 16.2 ms/mmHg, and for the standing positions the respective values were 6.2 and 6.7 ms/mmHg, giving lying to standing ratios of 1.96 and 2.10, respectively. xBRS yielded results for all files, with 20 values per minute on average at a lower within-patient variance. Best delays were 0, 1 and 2 s, and the delay increased by 102 ms when the patient was in the standing position. The xBRS method was successful in the patients with diabetes and the heart transplant., Conclusion: The xBRS method should be considered for experimental and clinical use, because it yielded values that correlated strongly with and were close to the EUROBAVAR averages, yielded more values per minute, had lower within-patient variance and measured baroreflex delay.

In man assuming the upright position, end-tidal P(CO(2)) (P(ETCO(2))) decreases. With the rising interest in cerebral autoregulation during posture change, which is known to be affected by P(ETCO(2)), we sought to determine the factors leading to hypocapnia during standing up from the supine position. To study the contribution of an increase in tidal volume (V(T)) and breathing frequency, a decrease in stroke volume (SV), a ventilation-perfusion (V/Q) gradient and an increase in functional residual capacity (FRC) to hypocapnia in the standing position, we developed a mathematical model of the lung to follow breath-to-breath variations in P(ETCO(2)). A gravity-induced apical-to-basal V/Q gradient in the lung was modelled using nine lung segments. We tested the model using an eight-subject data set with measurements of V(T), pulmonary O(2) uptake and breath-to-breath lumped SV. On average, the P(ETCO(2)) decreased from 40 mmHg to 36 mmHg after 150 s standing. Results show that the model is able to track breath-to-breath P(ETCO(2)) variations (r(2)= 0.74, P P 0.05). Model parameter sensitivity analysis demonstrates that the decrease in P(ETCO(2)) during standing is due primarily to increased V(T), and transiently to decreased SV and increased FRC; a slight gravity-induced V/Q mismatch also contributes to the hypocapnia. The influence of cardiac output on hypocapnia in the standing position was verified in experiments on human subjects, where first breathing alone, and then breathing, FRC and V/Q were controlled.

Physiologists have always been challenged by the adjustments of the human body to hostile environments. The set of papers in this issue of The Journal of Physiology (Cox et al. 2002; Ertl et al. 2002; Levine et al. 2002) fits into the tradition of the study of human responses to extreme physical circumstances. The Neurolab project represents a huge undertaking that required major contributions from many different collaborators, and the coordination of efforts at different institutions. The studies succeeded because of the dedication and years of work of the astronauts involved. The manuscripts present the fundamental findings from the first direct recordings of sympathetic vasoconstrictor nerves and noradrenaline kinetics in humans during microgravity. Despite the difficulties of performing such measurements on the space shuttle and the small numbers of astronauts involved, unique data are set forth that represent a major advance in our understanding of the physiology of space flight.

We tested the reliability of noninvasive cardiac output (CO) measurement in different body positions by pulse contour analysis (CO(pc)) by using a transmission line model (K. H. Wesseling, B. De Wit, J. A. P. Weber, and N. T. Smith. Adv. Cardiol. Phys. 5, Suppl. II: 16-52, 1983). Acetylene rebreathing (CO(rebr)) was used as a reference method. Twelve subjects (age 21-34 yr) were studied: 1) six in whom CO(rebr) and CO(pc) were measured in the standing and 6 degrees head-down tilt (HDT) postures and 2) six in whom CO was measured in the 30 degrees HDT, supine, 30 degrees head up-tilt (HUT), and 70 degrees HUT postures on a tilt table. The CO(rebr)-to-CO(pc) ratio in (near) the supine position during rebreathing was used as the calibration factor for CO(pc) measurements. Calibrated CO(pc) (CO(cal sup)) consistently overestimated CO in the upright posture. The drop in CO with upright posture was underestimated by approximately 50%. CO(cal sup) and CO(rebr) values did not differ in the 30 degrees HDT position. Changes in the CO(rebr)-to-CO(pc) ratio are highly variable among subjects in response to a change in posture. Therefore, CO(pc) must be recalibrated for each subject in each posture.

We investigated the influence of ten days 6 degrees head-down tilt (HDT) on short-term cardiovascular control. To help differentiate between the effects of HDT-induced fluid redistribution and changed autonomic cardiovascular modulation under prolonged HDT, the effect of acute posture changes was investigated as well. Six healthy male volunteers were studied. Continuous finger blood pressure was measured non-invasively by means of Finapres. Heart rate (HR) was derived from the electrocardiogram. Responses to forced breathing (FRSA), Valsalva's manoeuvre (VM), Mental Stress (MS) and Sustained Handgrip (SHG) were measured. Changing posture from HDT to standing enhanced the BP and HR responses to VM, both during straining and after release. During prolonged HDT, responses to VM changed toward the pattern seen in the upright posture before HDT, suggesting a strong influence of fluid redistribution. Neither posture nor prolonged HDT influenced HR variation during FRSA and responses to MS and SHG. BP variation during FRSA was influenced by posture but not by prolonged HDT. Thus, cardiovascular reflex tests which reflect the parasympathetic (FRSA) or the sympathetic (MS and SHG) efferents to the heart were not influenced by posture or prolonged HDT. Only the responses to VM were affected by both posture and prolonged HDT. These results are probably due to a decrease in blood volume and stroke volume under prolonged HDT, an increase in venous distensibility and, to a lesser extent, to inadequate cardiovascular regulatory responses.

1. The magnitude and time course of circulatory adaptation to active standing were investigated in healthy premenarchic girls and boys (n = 24; 10-14 years old) by non-invasive measurement of heart rate and continuous finger blood pressure (Finapres). 2. Four subjects (two girls, two boys) showed presyncopal symptoms after 4-9 min of free standing. 3. In the 20 non-fainting subjects, changes in blood pressure and heart rate upon standing did not differ between girls (n = 10) and boys (n = 10). In the initial phase of standing (first 30 s) systolic and diastolic blood pressures dropped by 22 +/- 14 (mean +/- SD) and 16 +/- 7 mmHg, respectively, at 8 +/- 2 s. Blood pressure subsequently recovered and showed an overshoot in all subjects. The transient drop in blood pressure was accompanied by an increase in heart rate of 40 +/- 7 beats/min. These characteristic transient changes were not observed with passive head-up tilt. During the early steady-state phase (2 min), systolic blood pressure was similar to the supine value and diastolic blood pressure rose by 11 +/- 5 mmHg. Heart rate increased by 25 +/- 11 beats/min. In six of the subjects (three girls, three boys) the increase in heart rate exceeded 30 beats/min (postural tachycardia). Little further changes were observed during prolonged (10 min) standing.(ABSTRACT TRUNCATED AT 250 WORDS)

To assess if changes in the angle or speed of tilt could account for the differences between the initial (first 30 s) circulatory responses induced by active and passive changes in posture, as found in previous studies, we investigated the initial heart rate and blood pressure responses induced by stand up from supine and various head-up tilt manoeuvres in 12 healthy, male subjects. Comparison was made between 70 degrees head-up tilt in 3 s, 90 degrees head-up tilt also in 3 s and 70 degrees head-up tilt in 1.5 s, using an automatic pneumatic-driven tilt table with foot support. It was found that the initial heart rate and blood pressure responses induced by the three tilt manoeuvres were almost identical in time course and amplitude, but significantly different from those induced by stand up. The results of this study prove that regardless of the angle and speed of tilt, the initial circulatory responses induced by passive changes in posture are essentially different from the responses induced by active changes in posture.

The initial circulatory responses to an active change in posture (stand up from supine) were compared with the responses induced by a passive change in posture (head-up tilt) and a burst of muscular exercise on a bicycle ergometer (upright cycling) in order to differentiate between exercise- and orthostasis-induced effects. In eight subjects heart rate responses and in four subjects intra-arterial pressure transients were measured. In addition the effects of respiration on heart rate responses to the three manoeuvres were assessed. Both stand up and cycling induced almost superimposable and pronounced heart rate responses lasting for about 30 s. This contrasts with the more gradual increases following head-up tilt. Changing the respiratory phase during the performance of the manoeuvres exerted its effect on heart rate responses in the first 5 s only. Like stand up, cycling induced a transient blood pressure fall lasting for 30 s on average. As both manoeuvres were performed during inspiration the transients observed are not caused by involuntary Valsalva straining. In conclusion, the maximum and duration of the heart rate responses induced by stand up, cycling and head-up tilt are not influenced by respiratory activity. The initial fall in blood pressure following stand up is probably the result of the muscular effort of the manoeuvre and not due to the effects of orthostasis or Valsalva straining.

1. Continuous orthostatic responses of blood pressure and heart rate were measured in 40 healthy and active elderly subjects over 70 years of age in order to assess the time course and rapidity of orthostatic cardiovascular adaptation in old age. 2. During the first 30 s (initial phase) the effects of active standing and passive head-up tilt closely resembled those observed earlier in younger age groups. Standing up was accompanied by a drop (mean +/- SD) in systolic and diastolic blood pressures of 26 +/- 13 mmHg and 12 +/- 18 mmHg, respectively, at around 10 s, and a subsequent rise up to 11 +/- 17 mmHg and 8 +/- 6 mmHg above supine values at around 20 s. The drop in blood pressure upon standing was accompanied by a transient increase in heart rate with a maximum of 13 beats/min, followed by a gradual decrease to 7 beats/min above supine levels. These characteristic transient changes were absent upon a passive head-up tilt. 3. After 1-2 min of standing (early steady-state phase) diastolic blood pressure and heart rate increased significantly after active and passive postural changes. On average, for all subjects systolic blood pressure tended to increase from control during 5-10 min standing, reaching a significant difference at 10 min. During standing, the largest increases in systolic blood pressure were found in subjects with the lowest supine blood pressures. 4. In conclusion, for the investigation of orthostatic circulatory responses in elderly subjects the following factors have to be taken into account: active versus passive changes in posture, the timing of the blood pressure reading, and the level of supine blood pressure.