Circulatory effects of carotid sinus stimulation and changes in blood volume distribution in hypertensive man

In 8 patients with moderate hypertension and 8 normotensive subjects an attempt was made to study the circulatory effects of high and low pressure baroreceptor stimulation. Intrathoracic low pressure receptors were stimulated by changes in blood volume distribution using lower body negative pressure (LBNP) and lower body positive pressure (LBPP). The carotid sinus was stimulated by sinusoidal neck suction. Blood pressure, central venous pressure, heart rate, cardiac output and forearm blood flow were recorded. During LBNP and LBPP changes in central blood volume, reflected in changes in central venous pressure, induced significantly greater changes in cardiac output and forearm blood flow in the hypertensive subjects. In both normotensive and hypertensive subjects mean arterial blood pressure was essentially unchanged during LBNP and a slight increase was found during LBPP. Heart rate and blood pressure response to stimulation of the carotid sinus decreased with increasing resting mean arterial pressure. The results suggest impairment of reflex adjustments, via arterial baroreceptors, possibly in particular to dynamic stimuli, rather than via intrathoracic “low pressure” baroreceptors in subjects with moderate hypertension.     

Influence of Age on Sensitivity and Effector Mechanisms of the Carotid Baroreflex

In 30 healthy subjects aged 20–48 years the hemodynamic response to carotid sinus stimulation (neck suction -40 mmHg) was studied. Heart rate, arterial pressure and cardiac output (dye dilution technique) were measured. In order to evaluate the effect of age on carotid sinus function the material was subdivided into two arbitrary subgroups, aged up to 30 years (n = 15) respectively 30 years and above (n = 15). Carotid sinus stimulation induced a significantly greater reduction in mean arterial pressure in the younger group compared to the older group. The heart rate reduction was, on the average, slightly greater in the younger group though the difference was not significant. In both groups a significant decrease in cardiac output contributed to the demonstrated reduction in mean arterial pressure. As the decrease in cardiac output was, on the average, slightly smaller in the younger group, the results indicate that the greater blood pressure response in the younger group was due to a greater reduction in peripheral vascular resistance. This is further supported by the finding of a significant correlation between changes in total peripheral vascular resistance, elicited by carotid sinus stimulation and age.     

Effect of Changes in Blood Volume Distribution on Circulatory Variables and Plasma Renin Activity in Man

In 8 healthy subjects the pressure around the lower body was changed to 40 mmHg above (LBPP) and below (LBNP) atmospheric, thereby altering the amount of blood pooled in the lower body. Heart rate, intraarterial blood pressure, central venous pressure, cardiac output (dye dilution technique) and forearm blood flow (venous occlusion plethysmography) were measured. Plasma renin activity was determined with a radioimmunological method. 6 subjects maintained a relative circulatory steady state during LBNP. LBNP caused significant decreases in central venous pressure (CVP), stroke volume and cardiac output (0) with an unchanged mean arterial pressure (MAP). Heart rate (HR) increased significantly. Calculated total peripheral vascular resistance (TPVR) and regional vascular resistance (RVR) in the forearm were significantly increased when measured 5–9 min after the onset of LBNP, whereas plasma renin activity (PRA) showed a definite increase only after 19 min of LBNP stimulation. No correlation was found between the changes in PRA and TPVR or RVR. Increasing the pressure around the lower body (LBPP) resulted in a slight but significant increase in MAP as well as a significant but transient increase in CVP. No significant changes were found in HR, Q or TPVR. In the forearm a decrease in RVR was demonstrated. PRA was not significantly changed. The results demonstrate that peripheral vascular resistance and PRA are both influenced by changes in blood volume distribution, possibly elicited via intrathoracic receptors sensitive to changes in central blood volume and/or CVP. The results also suggest that PRA does not play any significant part in the vasoconstriction during LBNP stimulation.     

Carotid baroreceptor reflexes in humans during orthostatic stress

Orthostatic stress, including standing, head-up tilting and lower body suction, results in increases in peripheral vascular resistance but little or no change in mean arterial pressure. This study was undertaken to determine whether the sensitivity of the carotid baroreceptor reflex was enhanced during conditions of decreased venous return. We studied eight healthy subjects and determined responses of pulse interval (ECG) and forearm vascular resistance (mean finger blood pressure divided by Doppler estimate of brachial artery blood velocity) to graded increases and decreases in carotid transmural pressure, effected by a neck suction/pressure device. Responses were determined with and without the application of lower body negative pressure (LBNP) at -40 mmHg. Stimulus-response curves were determined as the responses to graded neck pressure changes and the differential of this provided estimates of reflex sensitivity. Changes in carotid transmural pressure caused graded changes in R-R interval and vascular resistance. The cardiac responses were unaffected by LBNP. Vascular resistance responses, however, were significantly enhanced during LBNP and the peak gain of the reflex was increased from 1.2 +/- 0.3 (mean +/- S.E.M.) to 2.2 +/- 0.3 units (P < 0.05). The increased baroreflex gain may contribute to maintenance of blood pressure during orthostatic stress and limit the pressure decreases during prolonged periods of such stress.     

Blood Pressure and Heart Rate Regulating Capacity of the Carotid Sinus during Changes in Blood Volume Distribution in Man

The influence of changes in blood volume distribution on the carotid baroreflex was studied in 18 subjects. Blood volume distribution was changed by varying the pressure around the lower body above and below ambient, thereby varying the amount of blood pooled in this region and exerting a secondary influence on the central blood volume. The carotid arterial stretch receptors were stimulated by varying the pressure in an air-tight box enclosing the neck. To obtain a standardized carotid sinus stimulus (SCS) the pressure in the box was varied sinusoidally between -10 and ? 40 mmHg with a fixed frequency of 0.03 Hz. The effects on heart rate and blood pressure were assessed by harmonic analysis performed off-line on a digital computer. During lower body negative pressure of –40 mmHg (LBNP - 40), i.e. during a procedure known to reduce the central blood volume, SCS induced an augmented effect on the blood pressure regulating capacity but not on the heart rate response. Expressing the blood pressure regulating capacity as peak-to-peak changes in systolic arterial pressure, the response during LBNP 40 mmHg was almost twice the control value. The opposite stimulus–lower body positive pressure–influenced the SCS-induced effects only slightly but on the average a minor reduction in both blood pressure and heart rate regulating capacity was found compared with the control condition, though the difference did not reach significant levels. The results support the hypothesis that changes in blood volume distribution modify the function of the carotid baroreflex, possibly via intrathoracic receptors sensitive to changes in central blood volume and/or central venous pressure.     

Lower Body Negative Pressure and Effects of Autonomic Heart Blockade on Cardiovascular Responses

Heart rate, arterial pressure and cardiac output were recorded in eight healthy male volunteers during exposure to 80 mmHg of lower body negative pressure (LBNP) in the supine position before and after beta-adrenergic and combined beta-adrenergic and parasympathetic blockade of the heart as induced by the i.v. administration of propranolol 0.25 mg/kg b.wt. and atropine 0.04 mg/kg b.wt. After propranolol, heart rate response to LBNP averaged 48 % of that observed without blockade indicating that LBNP-induced cardioacceleration is of both sympathetic and parasympathetic origin. Tolerance to LBNP was reduced by beta-adrenergic blockade, since the decrease in mean arterial pressure during LBNP was exaggerated by such blockade. Although the addition of atropine markedly elevated mean arterial pressure and cardiac output in the control situation, tolerance to LBNP was not enhanced by this drug as judged from the arterial pressure response. Post-LBNP overshoot in mean arterial pressure was strikingly augmented by combined cardiac effector blockade and was in part due to a lingering elevation of total peripheral resistance, cardiac output remaining decreased for more than 110 s after release of LBNP.     

Lower body negative pressure and effects of autonomic heart blockade on cardiovascular responses.

Heart rate, arterial pressure and cardiac output were recorded in eight healthy male volunteers during exposure to 80 mmHg of lower body negative pressure (LBNP) in the supine position before and after beta-adrenergic and combined beta-adrenergic and parasympathetic blockade of the heart as induced by the i.v. administration of propranolol 0.25 mg/kg b.wt. and atropine 0.04 mg/kg b.wt. After propranolol, heart rate response to LBNP averaged 48% of that observed without blockade indicating that LBNP-induced cardioacceleration is of both sympathetic and parasympathetic origin. Tolerance to LBNP was reduced by beta-adrenergic blockade, since the decrease in mean arterial pressure during LBNP was exaggerated by such blockade. Although the addition of atropine markedly elevated mean arterial pressure and cardiac output in the control situation, tolerance to LBNP was not enhanced by this drug as judged from the arterial pressure response. Post-LBNP overshoot in mean arterial pressure was strikingly augmented by combined cardiac effector blockade and was in part due to a lingering elevation of total peripheral resistance, cardiac output remaining decreased for more than 110 s after release of LBNP.     

The effects of lower body negative pressure on baroreceptor responses in humans

In healthy human subjects the immediate responses of pulse interval and the steady-state responses of arterial blood pressure and cardiac output to changes in carotid sinus transmural pressure were determined before and during the application of a subatmospheric pressure to the lower part of the body. Increases in carotid sinus transmural pressure, effected by applications of subatmospheric pressure to the neck (neck suction) resulted in prolongation of pulse interval and decrease in blood pressure; opposite responses were obtained to application of a positive pressure (neck pressure). Application of lower body negative pressure resulted in a decrease in pulse interval (heart rate increase) but little change in blood pressure. During lower body negative pressure, the responses of pulse interval to neck pressure were reduced but those to neck suction were unaffected; the responses of blood pressure to neck suction were enhanced but those to neck pressure were unaffected. From experiments in which cardiac output was also determined, it was seen that lower body negative pressure reduced cardiac output, increased calculated total body vascular resistance and augmented the resistance response to neck suction although not to neck pressure. These results are compatible with the view that application of lower body negative pressure does not change the sensitivity of the baroreceptor reflex and that the changes in the responses are due to non-linearities of the stimulus-response curves.     

Cardiovascular responses to changes in carotid sinus transmural pressure in man.

To study the relative importance of cardiac and peripheral effector mechanisms in the carotid sinus baro-reflex in man cardiovascular responses to equal changes of the carotid sinus transmural pressure (Ptm) in either direction of the normal were recorded and compared in eight physically well-trained young male volunteers. In both the supine and the 70 degrees head-up position, a decrease in Ptm produced a more potent reflex response of the systemic arterial pressure than did a similar increase in Ptm. Whereas the arterial pressure response to increased Ptm was due solely to a reduction in vascular resistance, a significant increase in cardiac output contributed to the more potent pressor response to a decrease in Ptm and thus to the predominantly antihypotensive properties that characterize the carotid sinus baroreceptor control system in man. However, since combined beta-adrenergic and parasympathetic blockade abolished the effect of reduced Ptm on cardiac output without greatly impairing the blood pressure response, it is concluded that adjustments in cardiac output are not of critical importance in the buffering function of the carotid sinus baroreceptors. Autonomic cardiac blockade exaggerated the fall in cardiac output on head-up tilt, the arterial pressure remaining unaffected due to a compensatory increase in systemic vascular resistance.     

Regulation of arterial blood pressure in humans during isometric muscle contraction and lower body negative pressure

Previous studies have shown that the blood pressure response to isometric handgrip remains unchanged during reductions in preload induced by lower body negative pressure (LBNP). The purpose of the present study was to assess the beat-by-beat haemodynamic mechanisms allowing for precise control of mean arterial pressure (MAP). We have followed the cardiovascular variables involved in the regulation of MAP during isometric handgrip with and without additional application of LBNP during defined periods of the ongoing contraction. Sixteen subjects participated. Mean arterial blood pressure (MAP), heart rate (HR), stroke volume (SV), cardiac output (CO), blood flow velocity in the brachial artery, acral skin blood flow, as well as total (TPR) and local (LPR) peripheral resistance were continuously recorded/calculated before, during and after 2 min of handgrip both with and without concomitant LBNP. The main finding was that MAP increased at the same rate and to the same absolute level whether or not LBNP was applied. A uniform increase in MAP was observed even though the cardiovascular variables evolved differently in the periods with and without LBNP. At the onset of LBNP at –20 mmHg, there was a transient drop in MAP and a transient increase in HR, but within seconds, MAP was regulated back to the slope caused by the isometric handgrip proper. CO and SV, which were declining gradually, showed an additional marked but gradual reduction upon LBNP application. At the same time, both LPR and TPR increased markedly and continuously. In summary, the increase in MAP during isometric handgrip remained essentially unchanged by LBNP-induced alterations in preload. The increase in MAP was caused by a marked increase in peripheral resistance. This supports the concept of a central set point, continuously regulated upwards as long as the isometric handgrip persists. Furthermore, it reveals a considerable flexibility in the cardiovascular control mechanisms used to achieve the desired arterial pressure.     

Effects of diazepam on the carotid sinus baroreflex control of circulation in rabbits

To examine the effects of diazepam on the carotid sinus baroreflex control of circulation, bilateral carotid occlusion was performed on 14 conscious rabbits with aortic denervation. The responses of mean arterial pressure, heart rate, cardiac output and total peripheral resistance were obtained. The haemodynamic responses to carotid occlusion were evaluated at cumulative doses of 0.5 and 1.0 mg kg-1 of diazepam. The administration of diazepam decreased cardiac output and increased total peripheral resistance significantly, but did not affect the arterial pressure and heart rate. The response of total peripheral resistance to carotid occlusion was significantly increased from 0.118 +/- 0.018 (mean +/- SE) to 0.154 +/- 0.026 mmHg min ml-1 at 1.0 mg kg-1 of diazepam. The heart rate response was attenuated significantly from 41 +/- 5 to 24 +/- 4 beats min-1 at 1.0 mg kg-1 of diazepam. Diazepam did not alter the response of arterial pressure to carotid occlusion. We suggest that the dissociated effects of diazepam on the reflex control of circulation reflect the dissociated influences of diazepam on the central sympathetic and vagal-mediated pathways.     

Noise-enhanced heart rate and sympathetic nerve responses to oscillatory lower body negative pressure in humans

By injecting noise into the carotid sinus baroreceptors, we previously showed that heart rate (HR) responses to weak oscillatory tilt were enhanced via a mechanism known as "stochastic resonance." It remains unclear, however, whether the same responses would be observed when using oscillatory lower body negative pressure (LBNP), which would unload the cardiopulmonary baroreceptors with physically negligible effects on the arterial system. Also, the vasomotor sympathetic activity directly controlling peripheral resistance against hypotensive stimuli was not observed. We therefore investigated the effects of weak (0 to approximately -10 mmHg) oscillatory (0.03 Hz) LBNP on HR and muscle sympathetic nerve activity (MSNA) while adding incremental noise to the carotid sinus baroreceptors via a pneumatic neck chamber. The signal-to-noise ratio of HR, cardiac interbeat interval, and total MSNA were all significantly improved by increasing noise intensity, while there was no significant change in the arterial blood pressure in synchronized with the oscillatory LBNP. We conclude that the stochastic resonance, affecting both HR and MSNA, results from the interaction of noise with the signal in the brain stem, where the neuronal inputs from the arterial and cardiopulmonary baroreceptors first come together in the nucleus tractus solitarius. Also, these results indicate that the noise could induce functional improvement in human blood pressure regulatory system in overcoming given hypotensive stimuli.     

Cardiovascular Responses to Changes in Carotid Sinus Transmural Pressure in Man

To study the relative importance of cardiac and peripheral effector mechanisms in the carotid sinus baroreflex in man cardiovascular responses to equal changes of the carotid sinus transmural pressure (Ptm) in either direction of the normal were recorded and compared in eight physically well-trained young male volunteers. In both the supine and the 70d? head-up position, a decrease in Ptm produced a more potent reflex response of the systemic arterial pressure than did a similar increase in Ptm. Whereas the arterial pressure response to increased Ptm was due solely to a reduction in vascular resistance, a significant increase in cardiac output contributed to the more potent pressor response to a decrease in Ptm and thus to the predominantly antihypotensive properties that characterize the carotid sinus baroreceptor control system in man. However, since combined beta-adrenergic and parasympathetic blockade abolished the effect of reduced Ptm on cardiac output without greatly impairing the blood pressure response, it is concluded that adjustments in cardiac output are not of critical importance in the buffering function of the carotid sinus baroreceptors. Autonomic cardiac blockade exaggerated the fall in cardiac output on head-up tilt, the arterial pressure remaining unaffected due to a compensatory increase in systemic vascular resistance.     

Hemodynamic and hormonal responses to lower body negative pressure in men with varying profiles of strength and aerobic power

Hemodynamic, cardiac, and hormonal responses to lower-body negative pressure (LBNP) were examined in 24 healthy men to test the hypothesis that responsiveness of reflex control of blood pressure during orthostatic challenge is associated with interactions between strength and aerobic power. Subjects underwent treadmill tests to determine peak oxygen uptake ( O_2max) and isokinetic dynamometer tests to determine knee extensor strength. Based on predetermined criteria, subjects were classified into one of four fitness profiles of six subjects each, matched for age, height, and body mass: (a) low strength/average aerobic fitness, (b) low strength/high aerobic fitness, (c) high strength/average aerobic fitness, and (d) high strength/high aerobic fitness. Following 90 min of 0.11 rad (6°) head-down tilt (HDT), each subject underwent graded LBNP to –6.7 kPa or presyncope, with maximal duration 15 min, while hemodynamic, cardiac, and hormonal responses were measured. All groups exhibited typical hemodynamic, hormonal, and fluid shift responses during LBNP, with no intergroup differences between high and low strength characteristics. Subjects with high aerobic power exhibited greater (P < 0.05) stroke volume and lower (P < 0.05) heart rate, vascular peripheral resistance, and mean arterial pressure during rest, HDT, and LBNP. Seven subjects, distributed among the four fitness profiles, became presyncopal. These subjects showed greatest reduction in mean arterial pressure during LBNP, had greater elevations in vasopressin, and lesser increases in heart rate and peripheral resistance. Neither O_2max nor leg strength were associated with fall in arterial pressure or with syncopal episodes. We conclude that interactions between aerobic and strength fitness characteristics do not influence responses to LBNP challenge.     

Changes of elastic properties of central arteries during acute static exercise and lower body negative pressure

The aim of this investigation was to determine the acute effects of isometric fatiguing handgrip (IFHG) and lower body negative pressure (LBNP) on indices of central arterial stiffness. Thirteen subjects were studied. Renal blood velocity (Duplex Ultrasound) and blood pressure (Finapres) were monitored during IFHG and LBNP at −30 and −50 mmHg. Radial pulse-wave forms were recorded by applanation tonometry. Central aortic waveforms and other hemodynamic parameters were assessed using the Sphygmocor software. Renal vascular resistance index (RVRI; mean BP/renal blood velocity) was used as index of sympathetic nervous system (SNS) engagement. RVRI increased during both IFHG and LBNP indicating that SNS was engaged; however, BP increased only during the IFHG. Pulse-wave analysis showed that during the IFHG protocol the transit time of the pulse wave decreased and the peripheral pulse pressure/nonaugmented central pulse pressure ratio increased from baseline. Both of these measurements suggest an increase in central large artery stiffness. During LBNP no changes in the indices of central stiffness were noted, in spite of a similar level of sympathetic system engagement. Heart rate increased during both protocols, whereas augmentation index increased during the IFHG protocol and decreased during the LBNP. Our major conclusion was that blood pressure rather than sympathetic activity seems to play the major role in modulating the elastic properties of the central arteries. The decrease in augmentation index during the LBNP protocol can be attributed to the increased heart rate, given that there is a negative correlation between these two parameters.     

Hemodynamic similarities between the trigeminal and aortic vasodepressor responses

The hemodynamic changes associated with hypotension elicited by electrical stimulation of the spinal trigeminal complex (trigeminal depressor response, TDR) or the aortic nerve (aortic depressor reflex, ADR) were compared in rabbits anesthetized with urethan. The hypotension associated with each response was accompanied by bradycardia, a marked fall in total peripheral resistance, a small decrease in cardiac output, and a nonuniform decrease in regional vascular resistances, with the order of magnitude of the decrease being femoral greater than mesenteric greater than renal arterial resistance. In individual experiments the percent decrease in heart rate, total peripheral resistance, or regional resistances was plotted against the percent fall in arterial pressure to obtain a pair of regression lines during the TDR and ADR. There was no significant difference in the slope or y-intercept of the regression line between the TDR and ADR for all of the hemodynamic variables examined. In both responses, however, the slope of the femoral resistance/arterial pressure relationship was significantly greater than that of the renal resistance/arterial pressure relationship. We conclude that the TDR is characterized by a pattern of hemodynamic changes similar to that of the ADR.     

Training mode does not affect orthostatic tolerance in chronically exercising subjects

This study tested the hypotheses that trained swimmers would have greater orthostatic tolerance than runners and, if present, it would be due to differences in their autonomic and hemodynamic responses to graded central hypovolemia. Twenty intercollegiate male athletes [11 runners and 9 swimmers; V˙O_2max =70.0 (1.6) vs 69.5 (2.6) ml·kg⁻¹·min⁻¹, respectively] underwent graded lower body negative pressure (LBNP) to presyncope. The swimmers were heavier [80.5 (1.9) vs 70.3 (1.9) kg, P<0.05], with larger resting cardiac [4.44 (0.29) vs 3.68 (0.18) l·min⁻¹·m⁻²] and total peripheral conductance [0.056 (0.04) vs 0.044 (0.02) units·m⁻²] indices. Neither spontaneous cardiac baroreflex sensitivity (sequence method) nor heart rate variability (spectral analysis) differed significantly between groups at rest. LBNP tolerance did not differ between groups, with an index value of 51 (2) kPa·min for the runners and 54 (4) kPa·min for the swimmers [383 (16) vs 402 (32) mmHg·min] , although the swimmers had larger declines in pulse pressure and tended (P=0.078) to have larger declines in total peripheral conductance index in the last completed stage of LBNP. These responses did not differ between groups in the last 2 min of LBNP. Neither the heart rate, mean arterial pressure nor forearm vascular conductance responses differed between groups throughout. Changes in heart rate variability indices did not differ significantly between groups, with similar declines in the high frequency component and increases in the low frequency/high frequency ratio. These data suggest that swim training does not lead to greater orthostatic tolerance than run training, and responses to maximal LBNP do not differ between swimmers and runners. Moreover, neither heart rate nor the autonomic modulation of the heart rate response to LBNP are affected by training modality. Electronic Publication     

Onset of mild lower body negative pressure induces transient change in mean arterial pressure in humans

Mild (0 to –20 mmHg) lower body negative pressure (LBNP) has traditionally been considered to elicit reflex responses mediated by cardiopulmonary baroreceptors only, without any arterial baroreflex involvement. Mild LBNP has therefore frequently been used to study the influence of cardiopulmonary baroreceptors on the human circulatory system. In a previous study we found that mean arterial pressure (MAP) was transiently but strongly affected by rapid (0.3 s) onset and release of –20 mmHg LBNP. In the present study we tested whether MAP is also transiently affected by slow onset and release of –20 mmHg LBNP. A group of 12 subjects participated in this study, which was approved by the local Ethics Committee. Heart rate, stroke volume, cardiac output, MAP, total peripheral resistance, acral and non-acral skin blood flow, and blood flow velocity in the brachial artery were continuously recorded during the pre-LBNP period, during LBNP and during the post-LBNP period. The LBNP was gradually applied and released over a 15 s period. The main finding was that MAP was transiently but strongly affected by the gradual onset of LBNP as mild as –20 mmHg. During onset of LBNP MAP was significantly (P=0.003) lower than MAP in the pre-LBNP period. This shows that not only the cardiopulmonary baroreceptors but also the arterial baroreceptors must be activated during mild LBNP. Electronic Publication     

The contribution of alterations in cardiac output to changes in arterial pressure reflexly evoked from the carotid sinus in the rabbit.

1. The reflex cardiovascular effects of changes in pressure within the vascularly isolated carotid sinus were examined in seventeen anaesthetized rabbits. The opposite sinus was denervated and both aortic nerves were divided, 2. Comparison of the mean values at sinus pressures of 40 and 200 mmHg showed a large reduction in systemic arterial pressure from 126 to 58 mmHg and a moderate reduction in heart rate, from 287 to 253 beats min-1. Cardiac output, measured by thermal dilution, showed only a small change, a fall from 160 to 148 ml. min-1 kg-1. 3. By contrast with this reduction in cardiac output of just over 7%, total peripheral resistance, derived by dividing mean arterial pressure by cardiac output, was halved, falling from 0-48 to 0-41 mmHg ml.-1 min kg. 4. Thus in the anaesthetized rabbit changes in cardiac output make only a small contribution to the changes in systemic pressure evoked by alterations in carotid sinus pressure. Changes in total peripheral resistance are principally responsible for the effect on systemic pressure. 5. Though the changes in output of the heart were small, there were considerable changes in the work done by the left ventricle which was approximately halved when carotid sinus pressure was raised from 40 to 200 mmHg.     

Cardiovascular Response to Graded Lower Body Negative Pressure in Young and Elderly Man

Lower body negative pressure (LBNP) reduces central venous pressure (CVP) and cardiac output. The elderly are reported to have a limited capacity to increase cardiac output by increasing heart rate (HR), are especially dependent on end diastolic volume to maintain stroke volume and therefore should be especially vulnerable to LBNP. The present study compared the effects of LBNP in the young and old. Stroke volume was assessed non-invasively as stroke distance (SD) by aortovelography. Two groups of healthy male volunteers were studied: eight young (29.7 +/- 2.0 years, mean +/- S.E.M.) and nine old (70.1 +/- 0.9 years). LBNP was applied progressively at 17.5, 35 and 50 mmHg in 20 min steps, with measurements taken during each steady state. There were similar, significant, falls in CVP in both groups. SD fell significantly in both groups from respective control values of 24.8 +/- 1.6 and 16.6 +/- 0.9 cm to 12.5 +/- 1.3 and 8.9 +/- 0.4 cm at a LBNP of 50 mmHg. Although SD in the elderly was significantly lower than in the young, the LBNP-induced changes were not different between groups. Both groups produced similar significant increases in vascular resistance, HR, plasma vasopressin (AVP) and noradrenaline. Mean arterial blood pressure (MBP) and plasma adrenaline did not change significantly. Therefore healthy old men respond to LBNP in a similar manner to the young, although MBP and SD are regulated around different baselines in the two groups.