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At least 19 recordsLinked to original sources
PubMed1986

Cardiovascular responses of women to lower body negative pressure.

Lower body negative pressure (LBNP) has provided a method for studying cardiovascular responses in men while simulating a return to the stresses of 1-G following space flight. In this study, we have monitored responses of women to the stresses provided by LBNP. There were 20 women, 23-43 years, each tested in the follicular and luteal phases of the menstrual cycle. Variables were recorded during supine control; at -30, -40, -50 mm Hg LBNP; immediately after pressure release; and after 5 min recovery. There were no significant differences in response to LBNP between the two menstrual phases. During LBNP calf circumference was enlarged; transthoracic impedance was increased; stroke volume, left ventricular ejection time, the Heather Index of contractility and systolic pressure were reduced; total peripheral resistance was elevated; and cardiac output fell despite a rise in heart rate. Differences in cardiovascular variables between 0 mm Hg LBNP and -50 mm Hg LBNP were generally similar to reported differences between supine and standing. The responses of these women to LBNP were qualitatively similar to those reported for the Apollo astronauts and other male subjects. These women appeared to compensate with a greater heart rate response; however, the net cardiovascular compensation as determined from arterial pressure appears to be similar in men and women.

Adult↗
PubMed1989

Sympathetic nerve activity in arm and leg muscles during lower body negative pressure in humans.

Nonhypotensive lower body negative pressure (LBNP) is reported to decrease forearm but not calf blood flow as measured by strain-gauge plethysmography. This suggests that unloading of cardiopulmonary receptors increases sympathetic outflow to arm but not to leg. To test this hypothesis we measured muscle sympathetic nerve activity (MSA) in the arm (radial nerve) and leg (peroneal nerve) simultaneously during LBNP. In eight healthy subjects, we measured heart rate, blood pressure, and radial and peroneal MSA during LBNP at 10 and 20 mmHg. There was no difference between radial and peroneal MSA at rest, and there were successive parallel increases of MSA in both nerves during LBNP at 10 and 20 mmHg. These data indicate that there are nearly identical increases of sympathetic outflow to the arm and leg during mild to moderate degrees of orthostatic stress.

Adult↗
PubMed1990

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.

Adult↗
PubMed1978

Influence of lower body negative pressure upon arginine vasopressin release.

Lower body negative pressure (9-12 kPa) was applied to ten normal subjects. Large increases in plasma arginine vasopression concentration occurred only in subjects that experienced syncopal symptoms and developed hypotension. Blood samples obtained from the superior vena cava at 1/2 min intervals during application of negative pressure showed that maximal plasma vasopressin concentrations occurred with hypotension. Chromatography of the presyncopal plasma on Sephadex G-25 gave a large peak which eluted in the position of synthetic arginine vasopressin.

Adult↗
PubMed1979

Cardiovascular responses to lower body negative pressure in normal subjects and in patients with diabetes mellitus.

The cardiovascular responses of non-diabetic and diabetic subjects to lower body negative pressure at 1.3, 2.7, and 5.3 kPa (10, 20, and 40 mmHg) were measured. The diabetics fell into two groups--those showing little change in systolic blood pressure with lower body negative pressure at 5.3 kPa (40 mmHg) and those showing falls greater than 2.7 kPa (20 mmHg). The patterns of response in the former group of diabetics and in the non-diabetics were similar. The diabetics who showed a fall in systolic blood pressure with lower body negative pressure nonetheless responded with a forearm vasoconstriction indicating that the vasomotor dysfunction was localised to some other vascular bed. In one subject forearm vasodilatation occurred with lower body negative pressure at 5.3 kPa (40 mmHg) although his response to milder levels of lower body negative pressure appeared normal. It is suggested that the integrity of vasomotor reflexes is most reliably tested by exposure to stepped increases in lower body negative pressure.

Adolescent↗
PubMed1990

Effect of a central redistribution of fluid volume on response to lower-body negative pressure.

We studied cardiovascular responses to lower-body negative pressure (LBNP) following 1 hour (h) of 6 degrees head-down tilt to determine whether a redistribution of blood volume toward the central circulation modifies the subsequent response to orthostatic stress. Responses of 12 men, ages 30-39 years, were evaluated by electrocardiography, impedance cardiography, sphygmomanometry, and measurement of calf circumference. During the LBNP that followed head-down tilt--as compared with control LBNP (no preceding head-down tilt)--subjects had smaller stroke volume and cardiac output, greater total peripheral resistance, and less calf enlargement. These differences reflect differences in the variables immediately preceding LBNP. Magnitudes of the responses from pre-LBNP to each pressure stage of the LBNP procedure did not differ between protocols. Mean and diastolic arterial pressures were slightly elevated after LBNP-control, but they fell slightly during LBNP post-tilt. These cardiovascular responses to simulated gravitational stress following head-down tilt may reflect the manner in which adaptation to microgravity affects subsequent responses to orthostatic stress on return to Earth.

Adult↗
PubMedDate not supplied

[Oxygen status and regional blood flow in the gingival mucosa as affected by lower body negative pressure].

Five test subjects were exposed to lower body negative pressure (LBNP). During exposure their regional circulation and oxygen balance of the gingival mucosa were measured and electrocardiography and kinetocardiography were performed to calculate parameters of the left heart function. The study showed a distinct correlation between LBNP tolerance and the level of compensatory reactions of the gingival mucosa blood flow and the cardiovascular system as a whole. The subjects with a high LBNP tolerance showed well pronounced regional compensatory reactions of the gingival mucosa that were not accompanied by significant changes in the left heart function. The subjects with a moderate tolerance exhibited either weak or no regional compensatory reactions of the gingival mucosa and significant changes in the left heart function.

Adult↗
PubMed1985

Lower body negative pressure in the tranquilized rat.

The application of lower body negative pressure (LBNP) to tranquilized rats was assessed as an experimental technique to evaluate the response of the cardiovascular system to hypotension. After pilot studies had demonstrated that diazepam (600 micrograms X kg-1, i.v.) had no significant influence on the pressor response to unilateral carotid occlusion in unanesthetized and unrestrained rats, subsequent rats were tranquilized. When LBNP was applied, the decline in central venous pressure was linearly related to the level of negative pressure as was the initial fall in mean arterial pressure (MAP). Pulse-interval was highly correlated with the initial fall of MAP. The results indicate that the application of LBNP in the tranquilized rat can effectively produce systemic hypotension and elicit cardiovascular reflexes similar to those reported for other animals in response to LBNP, including humans.

Animals↗
PubMed1989

Circulatory and respiratory responses to lower body negative pressure in man.

Circulatory and ventilatory responses to lower body negative pressure (LBNP) were simultaneously investigated in 8 healthy men before, during, and after the application of -20, -40, and -60 mmHg pressure. Minute ventilation (VE) decreased during LBNP due to a fall in respiratory frequency with sustained tidal volume. The cardiac output (Q) was reduced in proportion to the applied LBNP exposure, while VE decreased to almost the same level at all LBNP applications. In spite of decreased VE, end-tidal PO2 and PCO2 were increased and decreased, respectively, indicating a relative alveolar hyperventilation. The ventilation equivalent for O2 (VE/VO2) increased, while the cardiac output equivalent for O2 (Q/VO2) decreased. The relation between VE/VO2 and Q/VO2 showed a significant negative correlation (r = -0.93, p less than 0.01). The veno-arterial CO2 concentration difference (CvCO2--CaCO2) increased with LBNP, due to a fall in CaCO2 with constant CvCO2. The constant CvCO2 indicated a constant tissue acid-base balance. These observations suggest the existence of a ventilatory mechanism improving the efficiency of respiration in order to compensate for the sustained LBNP depression of Q at a given gas exchange.

Adult↗
PubMed1986

Differential effects of lower body negative pressure on forearm and calf blood flow.

Modest degrees of lower body negative pressure (less than 20 mmHg) cause a reflex constriction of forearm resistance vessels attributable to a decrease in activity of cardiopulmonary mechanoreceptors. In the present study, we sought to determine whether the calf vessels respond similarly. Left forearm and right calf blood flows were measured simultaneously by strain-gauge plethysmography in 10 healthy volunteers. Forearm flows decreased significantly from control during negative pressures of 10, 15, or 20 mmHg, whereas calf flows did not decrease significantly until 20 mmHg; at 10, 15, and 20 mmHg, decreases in forearm flow were significantly greater than those of the calf. Similar results were obtained in a second series of experiments in which venous pooling in the right leg during lower body negative pressure was prevented by enclosing it in a boot. At 40 mmHg, or after a Valsalva maneuver, both forearm and calf vessels constricted markedly and to the same degree. It appears that the reflex reduction in blood flow to the skeletal muscles of the limbs resulting from deactivation of the low-pressure intrathoracic mechanoreceptors is directed primarily to the arm.

Adult↗
PubMed1987

Fluid shifts and endocrine responses during lower body negative pressure and dynamic arm exercise.

The use of lower body negative pressure (LBNP) is proposed as a means of reducing the effect of spaceflight on body water loss by stimulation of renin angiotensin aldosterone system (RAAS) activity. Seven subjects were successively submitted to LBNP exposure, arm cranking physical exercise, and to a combination of both procedures (LBNP + arm cranking) in order to check whether this combination enhances RAAS activity. The results showed that exposure to 40 min of LBNP to a level of -40 mm Hg was a more potent stimulus for renin secretion than submaximal and maximal arm cranking. The combination of LBNP with exercise does not further enhance the RAAS activity induced by LBNP alone. These data suggest that the fluid shift toward the lower body induced by LBNP counteracts triggering of renin secretion due to physical exercise.

Adult↗
PubMed1992

Carotid arterial haemodynamics after mild degrees of lower-body negative pressure in man.

1. Pulsatile changes in the diameter of the common carotid artery were studied transcutaneously using an echo-tracking technique in 15 normal subjects: eight subjects before and during application of graded lower-body negative pressure from -5 to -15 mmHg, and seven subjects before and during weight-bearing head-up tilt at 30 and 60 degrees. 2. In concomitant studies of changes in forearm vascular resistance, it was seen that mild lower-body negative pressure produced deactivation of cardiopulmonary receptors without changes in systemic blood pressure or heart rate. 3. After lower-body negative pressure, a significant decrease in carotid arterial diastolic diameter [from 0.662 +/- 0.028 to 0.624 +/- 0.033 cm (lower-body negative pressure -10 mmHg) and 0.640 +/- 0.030 cm lower-body negative pressure -15 mmHg), P < 0.001 and < 0.05] was observed. 4. After head-up tilt, carotid arterial diameter was also significantly decreased at 30 and 60 degrees, whereas a significant increase in heart rate occurred only at 60 degrees and mean blood pressure did not change. 5. The study provides evidence that the geometry of the arterial wall is substantially modified by non-invasive manoeuvres such as head-up tilting and lower-body negative pressure. The latter is assumed to selectively deactivate human cardiopulmonary receptors, but the present data suggest that local changes may also influence carotid baroreceptors.

Adult↗
PubMed1985

Effects of diltiazem on hormonal and hemodynamic responses to lower body negative pressure and tilt in patients with mild to moderate systemic hypertension.

Mean arterial blood pressure, forearm vascular resistance, plasma norepinephrine, plasma renin activity and aldosterone responses to graded lower body negative pressure and tilt at 80 degrees were examined in 10 men with mild to moderate essential hypertension before and after 12 weeks of diltiazem (240 to 360 mg/day) therapy. Diltiazem therapy lowered basal supine systolic and diastolic blood pressures without affecting basal heart rate. Mean arterial blood pressure and forearm vascular resistance were decreased from 114 +/- 1.5 to 105 +/- 1 mm Hg, p less than 0.01 and from 29.3 +/- 3.5 to 18.9 +/- 2.1 units, p less than 0.01, respectively. Diltiazem therapy had no effect on basal supine levels of norepinephrine, plasma renin activity or aldosterone, nor on the responses of these hormones to lower body negative pressure. Diltiazem did decrease the forearm vascular resistance responses to lower body negative pressure and tilt. Diltiazem abolished an orthostatic increase (10 +/- 0.3 mm Hg) in mean arterial blood pressure and this was associated with a greater plasma norepinephrine response to tilt. These results suggest that diltiazem decreases vascular resistance through a reduction in the postjunctional effects of norepinephrine on vascular smooth muscle.

Adult↗
PubMed1990

Atrial natriuretic factor attenuates sympathetic reflexes during lower body negative pressure in normal men.

To assess further the effects of atrial natriuretic factor on autonomic nervous system reflexes in normal humans, the hemodynamic and neurohormonal responses to lower body negative pressure were measured at control and during infusions of atrial natriuretic factor and nitroglycerin in nine normal male subjects. The control -20 mm Hg lower body negative pressure was characterized by significant reductions in right atrial and pulmonary wedge pressures, as well as stroke volume and cardiac output. This was associated with a reflex increase in forearm vascular resistance and plasma norepinephrine. During the infusion of atrial natriuretic factor, the same -20 mm Hg lower body negative pressure produced a larger decrease in mean arterial pressure of 7.9 +/- 3.9 mm Hg (p less than 0.05), as well as a larger decrease in stroke volume (41.3 +/- 4.2 ml/beat) and cardiac output (2.0 +/- 0.3 L/min). Atrial natriuretic factor infusion did not affect the increase in forearm vascular resistance during lower body negative pressure, but did attenuate the increase in plasma norepinephrine. To control for nonspecific vasodilator actions, lower body negative pressure was also repeated during nitroglycerin infusion. Nitroglycerin infusion did not significantly change the responses of blood pressure, cardiac output, stroke volume, forearm vascular resistance, or plasma norepinephrine during lower body negative pressure. Thus, these data demonstrate that atrial natriuretic factor infusion can attenuate sympathetic nervous system reflexes evoked during lower body negative pressure. These inhibitory effects on the sympathetic nervous system may contribute to many of the observed hemodynamic actions of atrial natriuretic factor.

Aged↗
PubMed1992

Subcutaneous and skeletal muscle vascular responses in human limbs to lower body negative pressure.

Cardiopulmonary baroreceptor unloading in humans comparably increases sympathetic discharge to skeletal muscle in the forearm and calf, but blood flow studies have disclosed differential rather than uniform vasomotor responses in the extremities. The aim of the present study was to address the issue of differential effects of orthostatic stress on forearm and calf vascular adjustment and to extend previous studies by determining changes in vascular responses separately in various vascular beds of the limbs. The local [133Xenon] washout method was used for recording blood flow rates in subcutaneous tissue and skeletal muscle. Simultaneous recordings from the forearm and calf were performed in 11 healthy young males during lower body negative pressure at -10 mmHg. Heart rate, arterial mean and pulse pressures did not change during lower body negative pressure. In the forearm blood flow rates decreased significantly, in subcutaneous tissue by 16 +/- 2% (mean +/- SEM) and in skeletal muscle by 16 +/- 1%. In the calf lower body negative pressure induced a significant decrease in blood flow rates of 17 +/- 3% in subcutaneous tissue and of 30 +/- 2% in skeletal muscle. This vasoconstriction in calf skeletal muscle was consistently disclosed in both legs and was about the same magnitude in each calf when studied with the one leg exposed to lower body negative pressure and the other outside the lower body negative pressure chamber. These findings suggest that during unloading of cardiopulmonary afferents, reflex sympathetic activation as an important autonomic adjustment to orthostatic stress is accompanied by uniform vasoconstriction in subcutaneous and skeletal muscle vascular beds of human limbs.

Adult↗
PubMed1990

Haemodynamics of leg veins during a 30-days-6 degrees head-down bedrest with and without lower body negative pressure.

Venous distensibility of the lower limbs was assessed in six healthy men who were submitted twice successively to 1 month of -6 degrees head-down bedrest, with and without lower body negative pressure (LBNP) (LBNP subjects and control subjects, respectively). Venous capacity (delta Vv,max, in ml.100 ml-1) of the legs was determined by mercury strain gauge plethysmography with venous occlusion. Plethysmographic measurements were made on each subject before (Dc), during (D6 and D20) and after (5th day of recovery, D+5) bedrest. During bedrest, LBNP was applied daily, several times a day to the subjects submitted to this procedure. Results showed a gradual increase in Vv,max (ml.100 ml-1) throughout the bedrest, both in the control group [delta Vv,max = 2.11 SD 0.54 at Dc, 2.69 SD 0.29 at D6, 4.39 SD 2.08 at D20, 2.39 SD 0.69 at D+5, P less than 0.001 (ANOVA)] and in the LBNP group [delta Vv,max = 2.07 SD 0.71 at Dc, 2.85 SD 1.19 at D6, 3.75 SD 1.74 at D20, 2.43 SD 0.94 at D+5, P less than 0.001 (ANOVA)], without significant LBNP effect. These increases were of the same order as those encountered during spaceflight. It is concluded that -6 degrees head-down bedrest is a good model to simulate the haemodynamic changes induced by exposure to weightlessness and that LBNP did not seem to be a good technique to counteract the adverse effects of weightlessness on the capacitance vessels of the lower limbs. This latter conclusion raises the question of the role and magnitude of leg venous capacitance in venous return and cardiac regulation.

Adult↗