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Biomedical subjects

N H Secher

Publications and source records attributed to N H Secher.

At least 181 records · Page 10Linked to original sources
PubMed1992

Pituitary-adrenal responses to head-up tilt in humans: effect of H1- and H2-receptor blockade.

Effects of the histamine H1- or H2-receptor antagonists mepyramine (Mep) and cimetidine (Cim) on neuroendocrine and cardiovascular responses to 50 degrees head-up tilt were evaluated in seven human males. Central hypovolemia was characterized by two phases. The first is a normotensive phase with increases in heart rate (HR), total peripheral resistance (TPR), and decrease in cardiac output. Plasma adrenocorticotropic hormone, beta-endorphin, cortisol, catecholamines, and renin activity increased moderately. Normotension lasted 39 +/- 7 min during infusion of saline but was reduced by Mep [18 +/- 3 min, F(2,12) = 9.60, P less than 0.01] and was unaffected by Cim (44 +/- 4 min). The second is a hypotensive phase associated with presyncopal symptoms (hypovolemic shock) and decreases in HR and TPR and a further increase in pituitary-adrenal and sympathoadrenal activity. Decreases in mean arterial pressure and TPR were augmented by Mep, which inhibited release of norepinephrine. Cim inhibited epinephrine release without affecting the development of hypovolemic shock. It is concluded that histaminergic mechanisms are involved in activation of the sympathoadrenal system but not in the pituitary-adrenal axis during central hypovolemia in humans.

Adult↗
PubMed1992

Middle cerebral artery flow velocity and blood flow during exercise and muscle ischemia in humans.

Changes in middle cerebral artery flow velocity (Vmean), measured by transcranial Doppler ultrasound, were used to determine whether increases in mean arterial pressure (MAP) or brain activation enhance cerebral perfusion during exercise. We also evaluated the role of "central command," mechanoreceptors, and/or muscle "metaboreceptors" on cerebral perfusion. Ten healthy subjects performed two levels of dynamic exercise corresponding to a heart rate of 110 (range 89-134) and 148 (129-170) beats/min, respectively, and exhaustive one-legged static knee extension. Measurements were continued during 2-2.5 min of muscle ischemia. MAP increased similarly during static [114 (102-133) mmHg] and heavy dynamic exercise [121 (104-136) mmHg] and increased during muscle ischemia after dynamic exercise. During heavy dynamic exercise, Vmean increased 24% (10-47%; P less than 0.01) over approximately 3 min despite constant arterial carbon dioxide tension. In contrast, static exercise with a higher rate of perceived exertion [18 (13-20) vs. 15 (12-18) units; P less than 0.01] was associated with no significant change in Vmean. Muscle ischemia after exercise was not associated with an elevation in Vmean, and it did not provoke an increase in Vmean after static exercise. Changes in Vmean during exercise were similar to those recorded with the initial slope index of the 133Xe clearance method. The data show that middle cerebral artery mean flow velocity reflects changes in cerebral perfusion during exercise. Furthermore, they support the hypothesis that cerebral perfusion during exercise reflects an increase in brain activation that is independent of MAP, central command, and muscle metaboreceptors but is likely to depend on influence of mechanoreceptors.

Adult↗
PubMed1992

Regional cerebral artery mean flow velocity and blood flow during dynamic exercise in humans.

Transcranial Doppler ultrasound-determined middle (MCA) and anterior (ACA) cerebral artery mean flow velocities (Vmean) and pulsatility indexes (PI) were measured during "no-load" [21, 60, and 102 revolutions/min (rpm)] and loaded cycling (30, 60, and 149 W) at approximately 60 rpm. At rest Vmean MCA was 51 (36-55) cm/s (median and range; n = 10) and Vmean ACA was 41 (36-49) cm/s (n = 7; P < 0.05). With no load on the cycle Vmean MCA increased 4 (2-36), 10 (0-47), and 27% (4-58) (P < 0.05) at the three pedaling frequencies, respectively; arterial PCO2 (PaCO2) remained constant. During loaded cycling the increases were 19 (6-42), 25 (2-45), and 32% (12-67) (P < 0.01), respectively, with only a minimal change in PaCO2. No significant changes were observed in Vmean ACA. Changes in Vmean MCA were similar to those recorded by the initial slope index (ISI) of the 133Xe clearance method (n = 11), which in turn were smaller than increases recorded by the fast-compartment flow. PI ACA followed PI MCA during no-load as well as loaded exercise and increased with work rate, perhaps reflecting an increase in pulse pressure from 56 (48-63) mmHg at rest to 109 (88-123) mmHg at 149 W (P < 0.01). Data demonstrate a graded increase in regional cerebral perfusion during dynamic exercise corresponding to the MCA territory.

Adult↗
PubMed1992

Leg vasoconstriction during dynamic exercise with reduced cardiac output.

We evaluated whether a reduction in cardiac output during dynamic exercise results in vasoconstriction of active skeletal muscle vasculature. Nine subjects performed four 8-min bouts of cycling exercise at 71 +/- 12 to 145 +/- 13 W (40-84% maximal oxygen uptake). Exercise was repeated after cardioselective (beta 1) adrenergic blockade (0.2 mg/kg metoprolol iv). Leg blood flow and cardiac output were determined with bolus injections of indocyanine green. Femoral arterial and venous pressures were monitored for measurement of heart rate, mean arterial pressure, and calculation of systemic and leg vascular conductance. Leg norepinephrine spillover was used as an index of regional sympathetic activity. During control, the highest heart rate and cardiac output were 171 +/- 3 beats/min and 18.9 +/- 0.9 l/min, respectively. beta 1-Blockade reduced these values to 147 +/- 6 beats/min and 15.3 +/- 0.9 l/min, respectively (P < 0.001). Mean arterial pressure was lower than control during light exercise with beta 1-blockade but did not differ from control with greater exercise intensities. At the highest work rate in the control condition, leg blood flow and vascular conductance were 5.4 +/- 0.3 l/min and 5.2 +/- 0.3 cl.min-1.mmHg-1, respectively, and were reduced during beta 1-blockade to 4.8 +/- 0.4 l/min (P < 0.01) and 4.6 +/- 0.4 cl.min-1.mmHg-1 (P < 0.05). During the same exercise condition leg norepinephrine spillover increased from a control value of 2.64 +/- 1.16 to 5.62 +/- 2.13 nM/min with beta 1-blockade (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Effects of axillary blockade on regional cerebral blood flow during dynamic hand contractions.

Regional cerebral blood flow (rCBF) was measured at orbitomeatal (OM) plane +5.0 and +9.0 cm in 10 subjects at rest and during dynamic hand contractions before and after axillary blockade. Handgrip strength was significantly reduced, and rating of perceived exertion increased after blockade. During hand contractions before blockade, contralateral hemispheric cerebral blood flow (CBF) at OM +9.0 increased from a resting value of 58 (49-75) to 63 (52-82) ml.100 g-1.min-1; contralateral motor sensory rCBF at OM +9 from 58 (50-77) to 71 (64-84); motor sensory rCBF at OM +5 from 67 (54-76) to 77 (64-87) and 70 (62-84) contralaterally and ipsilaterally, respectively; and supplementary motor area (SM) rCBF from 64 (53-69) to 75 (67-88) ml.100 g-1.min-1. During dynamic hand contractions after axillary blockade, CBF did not increase at OM +5 or in the SM. Furthermore, contralateral motor sensory rCBF at OM +9 increased much less. Axillary blockade had no effect on resting CBF, rCBF, or increases in the two during hand contractions of the opposite hand. Thus neural feedback from the contracting muscle is necessary for the increases in SM bilateral OM +5 motor sensory rCBF and the maximal increase in contralateral OM +9 motor sensory rCBF during dynamic hand contractions.

Adult↗
PubMed1992

Neural influence on cardiovascular and endocrine responses to static exercise in humans.

At the onset of exercise, signals from the central nervous system result in immediate vagal withdrawal and resulting increases in heart rate and arterial blood pressure. From the second heart beat peripheral nerve (reflex) influence from exercising muscle can be detected. With continued exertion, especially with large muscle groups, this influence becomes increasingly important. Sympathetic nerve signals to resting muscle can be influenced by the central nervous system, but are dominated by influence from 'metaboreceptors' in exercising muscle, while sympathetic nerve signals to skin are more influenced by the central nervous system. Cardiovascular responses to static contractions increase with the percentage of maximum contraction intensity as well as with the muscle mass involved. Plasma catecholamines rise in proportion to increases in cardiovascular variables and are influenced by a central nervous mechanism early in the contraction. Furthermore, during static contractions the increase in plasma adrenaline (epinephrine) is larger relative to that of noradrenaline than during dynamic exercise. Both catecholamine responses and the responses of pituitary hormones depend on the active muscle mass, but are small compared to those established during dynamic exercise. Experiments designed to enhance central command, resulting in increased cardiovascular and endocrine responses compared to control experiments and experiments in which an attenuation of peripheral nerve influence resulted in reduced changes in these variables during exercise, contrast with the notion that the 2 neural control mechanisms are redundant. Rather, the 2 neural influences on the autonomic nervous system work in concert in eliciting the responses manifest during static exercise.

Cardiovascular Physiological Phenomena↗
PubMed1992

The effect of normoxic or hypobaric hypoxic endurance training on the hypoxic ventilatory response.

Cross-sectional studies in endurance athletes have demonstrated a diminished hypoxic ventilatory response (HVR) compared with mountaineers or sedentary controls. Conversely, short-term altitude acclimatization may increase the HVR. The longitudinal effect of training, either at sea level or altitude, on HVR has not been previously reported. We therefore studied 21 untrained men and women before and after 5 wk of cycle ergometer training at either sea level or 2,500 m. HVR was determined using the steady-state method (16). Minute ventilation (VE) was measured with a Tissot spirometer during the last minute of 5 min breathing room air, 8% and 12% O2, administered in random order. CO2 was added at the mouth in an effort to maintain end-tidal CO2 at baseline levels. Oxyhemoglobin saturation was measured directly from arterial blood with a hemoximeter (OSM 3). HVR was defined as the positive slope of the line relating VE to O2 saturation in l.min-1%-1. One group of subjects trained at sea level at 70% maximal oxygen uptake (VO2max; N = 7). A second group trained at 2,500 m in a hypobaric chamber, at the same relative exercise intensity (i.e., 70% altitude VO2max) or same absolute intensity (same power output) as group 1 (N = 14). Both groups trained on a bicycle ergometer for 45 min.d-1, 5 d.wk-1 for 5 wk.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Maximal oxygen uptake and work capacity after inspiratory muscle training: a controlled study.

The effect of inspiratory muscle training for 10 min twice a day for 27.5 days was evaluated in 20 human subjects, of whom 10 formed a training group and 10 a sham training group. The maximal oxygen uptake (VO2 max), maximal ventilation, breathing frequency during maximal exercise and the distance run in 12 min on a track were determined in addition to resting peak expiratory flow, forced vital capacity (FVC) and forced expiratory volume in 1 s (FEV1), with alveolar oxygen tension (pAO2) during maximal exercise being calculated. Inspiratory muscle training increased maximal inspiratory pressure from 93 (range 38-118) to 110 (65-165) mmHg in the training group (P less than 0.0005), but did not affect VO2 max, ventilation during maximal exercise, peak expiratory flow, FEV1 or FVC. However, breathing frequency during maximal exercise decreased slightly from 56 (44-87) to 53 (38-84) breaths min-1 (P less than 0.05) in the training group only; but the calculated pAO2 did not increase from the pre-training value of 126 (116-132) mmHg. The maximal distance run during 12 min increased similarly in the training and sham training groups by 8% (3-12%) and 6% (2-12%), respectively (P less than 0.01). The results of this study show that inspiratory muscle training resulting in a 32% (0-85%) increase in maximal inspiratory pressure does not change FEV1, FVC, peak expiratory flow, VO2 max or work capacity.

Adult↗
PubMed1991

Thoracic impedance as an index of body fluid balance during cardiac surgery.

Thoracic impedance at 2.5 (TI2.5) and 100 kHz (TI100), central venous pressure (CVP), and body fluid balance were recorded together with rectal temperature and arterial haematocrit in 15 consecutive patients subjected to coronary artery bypass grafting. I.v. fluid and blood were administered in an excess of 3.18 (1.38-9.35) 1 during the operation. TI2.5 decreased from 51.7 (39.2-66.4) to 34.9 (21.1-45.7) ohm (P = 0.001), while TI100 decreased from 41.9 (31.4-55.0) to 30.3 (18.3-40.8) ohm (P = 0.002). CVP, 6 (3-11) mmHg [0.8 (0.4-1.5) kPa], was the same before and after surgery. Temperature decreased during cardiopulmonary bypass from 35.4 (34.1-36.6) to 26.7 (22.9-31.0) degrees C and haematocrit from 39 (34-46)% to a lowest value of 27 (23-32)% (P = 0.0001). A close linear correlation between TI and body fluid balance was observed (TI2.5: r = -0.96, TI100: r = -0.95, P = 0.0001). Corrections of TI for temperature and/or haematocrit improved the correlation between TI and fluid balance to 0.99 (TI2.5) and 0.98 (TI100). The data indicate that changes in thoracic impedance can be used to monitor body fluid balance during cardiac surgery.

Aged↗
PubMed1991

Blood volume distribution during head-up tilt induced central hypovolaemia in man.

We evaluated regional electrical impedance (Z degree) at 2.5 and 100 kHz to separate intra- and extracellular fluid changes and correlated Z degree over the thorax (TI) to relative changes in the central blood volume (CBV) induced by head-up tilt. In nine experiments head-up tilt resulted in normotensive central hypovolaemia associated with a 3.7 +/- 0.4 Ohm (mean +/- SE) increase in TI100 kHz after 60 min. In 24 experiments pre-syncopal symptoms were induced after 43 +/- 2 min, when TI100 kHz had increased 4.2 +/- 0.2 Ohm. Head-up tilt instantly decreased the activity of technetium labelled erythrocytes (99Tcm) over the thorax by 24 +/- 2%, and increased 99Tcm over the thigh by 68 +/- 10% (P less than 0.01, n = 8) with no further changes during the sustained tilt. Haematocrite increased during head-up tilt from 43.1 +/- 0.3 to 47.9 +/- 0.6% (P less than 0.01, n = 8). Accordingly, the increase in TI (6.3 +/- 0.6 vs. 4.5 +/- 0.4 Ohm, n = 6) and the decrease in Z degree through one leg (7.2 +/- 1.2 vs. 2.8 +/- 0.5 Ohm, n = 6) at 2.5 kHz was more pronounced than at 100 kHz. Also the changes in TI were correlated to CBV as calculated from 99Tcm and haematocrite (r = 0.90, P less than 0.01). The results suggest that: (1) Hypovolaemic shock is associated with a faster increase of TI than normotensive head-up tilt. (2) Head-up tilt is characterized by an initial decrease in CBV followed by a further decrease in plasma volume, which eventually leads to hypovolaemic shock. (3) Blood volume changes during head-up tilt are reflected in regional Z degree.

Adult↗
PubMed1991

Effect of training on central factors in fatigue following two- and one-leg static exercise in man.

Leg strength and fatigue developed during 150 repeated two- and one-leg isometric maximal voluntary contractions were determined before and after a 5-week one- (n = 6) or two- (n = 7) leg training programme including a control group of five subjects. Two- and one-leg training increased two- and one-leg strength by 59 (range 8-107) and 36% (-1-69) respectively (P less than 0.01) with no significant difference between the two groups. Two-leg training decreased (P less than 0.05) fatigue only during two-leg maximal voluntary contractions (from 20 [11-26] to 13% [6-27]); and one-leg training fatigue only during one-leg maximal voluntary contractions (from 20 [15-23] to 11% [9-24]) despite the fact that both legs were trained. Surface electromyographic activity decreased during both repeated two- and one-leg maximal voluntary contractions (P less than 0.01) but a reduction in electromyographic decay was seen (P less than 0.05) during two-leg maximal voluntary contractions after two-leg training. Training increased fast-twitch b fibre size (P less than 0.01), and glycogen depletion was seen in fast-twitch (a and b) fibres, but the relative fast-twitch b area did not increase significantly. No training effects were seen in the control group. The results show that an approximately 47% increase in muscle strength may take place without a significant change in the relative percentage of muscle fibre types or in the average muscle fibre size. Furthermore, the specificity of the training response to fatigue developed during repeated two- and one-leg maximal voluntary contractions suggests a change in the nervous influence on the motor units.

Adult↗
PubMed1991

Calcitonin gene-related peptide (CGRP) and leg vascular resistance during head-up tilt induced hypovolaemic shock in man.

Calcitonin gene-related peptide is a potent vasodilator and its distribution in perivascular nerves suggests a role in the regulation of vascular tone. We evaluated leg vascular resistance together with total peripheral resistance and the arterial plasma concentrations of calcitonin gene-related peptide and catecholamines during 50 degrees head-up tilt induced hypotension in 7 males. During tilt mean arterial pressure, heart rate, total peripheral resistance, leg vascular resistance and plasma noradrenaline increased, while cardiac output and leg blood flow decreased. After 45 +/- 9 min (mean +/- SE) presyncopal symptoms appeared together with decreases in mean arterial pressure (81 +/- 6 to 56 +/- 9 mmHg), heart rate (97 +/- 6 to 73 +/- 8 beats min-1), leg vascular resistance (158 +/- 9 to 109 +/- 8 mmHg min l-1) and total peripheral resistance (17 +/- 3 to 10 +/- 2 mmHg min l-1) (P less than 0.01). Plasma calcitonin gene-related peptide increased from 32 +/- 3 to 35 +/- 3 pmol l-1 (P less than 0.01) and adrenaline from 1.1 +/- 0.2 to 1.7 +/- 0.3 nmol l-1 (P less than 0.01), while noradrenaline did not change. The results indicate that presyncopal symptoms induced by head-up tilt are associated with regional as well as total decreases in vascular resistance accompanied by moderate increases in arterial plasma concentrations of calcitonin gene-related peptide and adrenaline.

Adult↗
PubMed1991

Hormonal, metabolic, and cardiovascular responses to static exercise in humans: influence of epidural anesthesia.

To determine the role of reflex neural mechanisms for hormonal, metabolic, heart rate (HR), and blood pressure (MABP) changes during static exercise, seven health young males performed 10-min periods of two-legged static knee extension both during control and during epidural anesthesia. Comparisons were made at identical absolute (29 Nm) and relative [15% maximal voluntary contraction (MVC)] force. Afferent nerve blockade was verified by hypesthesia below T10-T12 and attenuated postexercise ischemic pressor response. Leg strength was reduced to 67 +/- 5% of control. At same relative force, increases in MABP and HR occurred more rapidly without than with epidural anesthesia (P less than 0.05). This difference was diminished during identical absolute force. Changes in plasma concentrations of catecholamines followed the pattern of HR and MABP responses, with differences between epidural and control experiments being most pronounced early in the work period. Plasma beta-endorphin was elevated only after control exercise. No response at 15% MVC was found for growth hormone, adrenocorticotropic hormone, insulin, glucagon, cortisol, glycerol, free fatty acids, or glucose (P greater than 0.05). In conclusion, during static exercise with large muscle groups and moderate relative force, modest changes in plasma hormones and metabolites take place. Furthermore, afferent nervous feedback from contracting muscles is important in regulation of blood pressure, heart rate, and catecholamine responses during static exercise in humans.

Adult↗
PubMed1991

Effect of axillary blockade on regional cerebral blood flow during static handgrip.

Regional cerebral blood flow (rCBF) was determined at rest and during static handgrip before and after regional blockade with lidocaine. A fast rotating single photon emission computer tomograph system with 133Xe inhalation was used at orbitomeatal plane (OM) +2.5 and +6.5 cm in eight subjects. Median handgrip force during the control study was 41 (range 24-68) N, which represented 10% of the initial maximal voluntary contraction (MVC) and was 24 (18-36) N after axillary blockade (P less than 0.05), which represented 21% of the new MVC. During static handgrip, the rating of perceived exertion was 14 (10-16) exertion units before and 18 (15-20) after blockade (P less than 0.05). Hemispheric mean CBF did not change during handgrip. However, premotor rCBF increased from 55 (44-63) to 60 (50-69) ml.100 g-1.min-1 (P less than 0.05) and motor sensory rCBF from 57 (46-65) to 63 (55-71) ml.100 g-1.min-1 (P less than 0.05) to both the ipsilateral and contralateral sides during handgrip before, but not after, axillary blockade. There was no change in rCBF to other regions of the brain. Regional anesthesia with lidocaine did not alter resting rCBF. However, despite a greater sense of effort during static handgrip, there was no increase in rCBF after partial sensory and motor blockade. Thus bilateral activation occurs in the premotor and motor sensory cortex during static handgrip, and this activation requires neural feedback from the contracting muscles.

Adult↗
PubMed1991

Neural control of the forearm cutaneous vasoconstrictor response to dynamic exercise.

This study was designed to evaluate the relative importance of intended effort ("central command") and of the absolute intensity of dynamic exercise to the cutaneous vasoconstrictor response to the onset of exercise in humans. Skin blood flow (laser-Doppler flowmetry) was measured from the forearm in six healthy individuals during 3-min periods of high- and low-intensity exercise with and without partial neuromuscular blockade. Cutaneous vascular conductance (CVC) was calculated from the ratio of skin blood flow to mean arterial pressure and expressed as a percent change from rest. A rating of perceived exertion (RPE) was expressed as a subjective measure of intended effort. Under control conditions, CVC decreased by 22% (median; range 7-42%, P less than 0.05) during high-intensity exercise [218 (186-268) W; RPE 16 (14-19) exertion units]. In contrast, during control low-intensity exercise [106 (88-128) W; RPE 10 (9-14) exertion units], during low-level exercise with curare [77 (54-98) W; RPE 13 (11-16) exertion units], and during maximal exercise with curare [106 (88-124) W; RPE 19 (18-20) exertion units], CVC did not change significantly. These results suggest that factors related to the activity of the exercising muscle and its metabolism rather than intended effort determine the cutaneous vasoconstrictor response to the initiation of intense dynamic exercise in humans.

Adult↗
PubMed1991

Muscle mass effect on arterial desaturation after maximal exercise.

We measured arterial oxygen saturation before and immediately after randomly allocated 6 min of "all-out" maximal arm cranking, treadmill running, and ergometer rowing in 10 men and women with a median maximal oxygen uptake of 4.47 (range 3.22-5.34) 1.min-1. Arterial saturation for oxygen was unaltered after arm cranking, but decreased 1.7 (-2.5-6.0) % (P less than 0.05) after running, and 2.2 (1.0-8.7) % (P less than 0.01) after rowing. Arterial saturation was inversely related to capillary blood lactate, which reached 11.8 (7.4-14.0), 12.6 (8.9-18 2), and 14.3 (12.0-19.3) mmol.l-1 (P less than 0.01), respectively, and arterial bicarbonate fell to 15.0 (13.0-23.6), 12.4 (7.2-20.4), and 10.8 (0.0-12.5) mmol.l-1 (P less than 0.01). Thus, pH decreased to 7.25 (7.22-7.40), 7.17 (6.95-7.35), and 7.09 (6.84-7.19) (P less than 0.01). When measured immediately post-exercise, arterial oxygen tension was unchanged or elevated from rest, eliminating the possibility that the arterial desaturation was caused by a pulmonary diffusion limitation. The results of this investigation show that arterial desaturation associated with maximal exercise takes place in proportion to the involved muscle mass, as do deviations in blood lactate, bicarbonate, and hydrogen concentrations.

Adult↗
PubMed1990

Non-invasive blood pressure monitoring during head-up tilt using the Penaz principle.

Continuous blood pressure measurement by a non-invasive means is of clinical utility in many situations where changes in cardiovascular hemodynamics and blood volume distribution are likely to occur. We have compared blood pressure measurements using the Penaz principle (Finapres, Ohmeda) to an intra-arterial catheter system during head-up tilt (reverse Trendelenburg's position) which models central hypovolemia. Twelve healthy volunteers were raised to a 60 degree head-up tilt position for 60 min or until presyncope occurred. Seven subjects developed presyncopal symptoms at a mean time of 38 +/- 6 min with blood pressure measured by the Penaz principle falling from 140 +/- 8/72 +/- 4 to 82 +/- 10/54 +/- 6 mmHg (18.7 +/- 1.1/9.6 +/- 0.5 to 10.9 +/- 1.3/7.2 +/- 0.8 kPa) (P less than 0.01), at which point they were returned to a horizontal position with an immediate rise in blood pressure. During the maximal drop in blood pressure, heart rate decreased from 82 +/- 7 to 45 +/- 5 (P less than 0.01). Overall, the non-invasive system had a correlation coefficient of 0.98 as compared to the intra-arterial method and ECG for blood pressure and heart rate in all 12 subjects during rest, tilt, and recovery. We conclude that the Penaz principle apparatus is a useful monitor of symptomatic hypotension during central hypovolemia.

Adult↗