Associations between changes in precerebral blood flow and cerebral oximetry in the lower body negative pressure model of hypovolemia in healthy volunteers

Neurovascular coupling refers to the link between an increase in neural activity in response to a task and an increase in cerebral blood flow denoted “functional hyperemia.” Recent work on postural tachycardia syndrome indicated that increased oscillatory cerebral blood flow velocity (CBFv) was associated with reduced functional hyperemia. We hypothesized that a reduction in functional hyperemia could be causally produced in healthy volunteers by using oscillations in lower body negative pressure (OLBNP) to force oscillations in CBFv. CBFv was measured by transcranial Doppler ultrasound of the left middle cerebral artery. We used passive arm flexion applied during eight periodic 60-s flexion/60-s relaxation epochs to produce 120-s periodic changes in functional hyperemia (at 0.0083 Hz). We used −30 mmHg of OLBNP at 0.03, 0.05, and 0.10 Hz, the range for cerebral autoregulation, and measured spectral power of CBFv at all frequencies. Arm flexion power performed without OLBNP was compared with arm flexion power during OLBNP. OLBNP power performed in isolation was compared with power during OLBNP plus arm flexion. Cerebral flow velocity oscillations at 0.05 Hz reduced and at 0.10 Hz eliminated functional hyperemia, while 0.03 Hz did not reach significance. In contrast, arm flexion reduced OLBNP-induced oscillatory power at all frequencies. The interactions between OLBNP-driven CBFv oscillations and arm flexion-driven CBFv oscillations are reciprocal. Thus induced cerebral blood flow oscillations suppress functional hyperemia, and functional hyperemia suppresses cerebral blood flow oscillations. We conclude that oscillatory cerebral blood flow produces a causal reduction of functional hyperemia.

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Bradykinin has no acute effect on the response of forearm blood flow to sympathetic stimulation in man

Clinical Science ◽

10.1042/cs0780399 ◽

1990 ◽

Vol 78 (4) ◽

pp. 399-401 ◽

Cited By ~ 2

Author(s):

M. J. Cullen ◽

J. R. Cockcroft ◽

D. J. Webb

Keyword(s):

Blood Flow ◽

Angiotensin Ii ◽

Negative Pressure ◽

Enzyme Inhibitor ◽

Lower Body Negative Pressure ◽

Acute Effect ◽

Acute Administration ◽

Lower Body ◽

Resistance Vessels ◽

Sympathetic Responses

1. Six healthy male subjects received 0.9% (w/v) NaCl (saline) followed by incremental doses of bradykinin (1, 3 and 10 pmol/min), via the left brachial artery. Blood flow and the response of blood flow to lower-body negative pressure were measured in both forearms during infusion of saline and each dose of bradykinin. 2. Bradykinin produced a moderate and dose-dependent increase in blood flow in the infused, but not the non-infused, forearm. Lower-body negative pressure produced an approximately 15–20% reduction in blood flow in both forearms, and this response was unaffected by local infusion of bradykinin. 3. Bradykinin, in contrast to angiotensin II, had no acute effect on peripheral sympathetic responses to lower-body negative pressure. We conclude that, in forearm resistance vessels in man, withdrawal of angiotensin II, rather than accumulation of bradykinin, is likely to account for the attenuation of peripheral sympathetic responses after acute administration of a converting-enzyme inhibitor.

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Sustained increases in sympathetic outflow during prolonged lower body negative pressure in humans

Journal of Applied Physiology ◽

10.1152/jappl.1990.68.3.1004 ◽

1990 ◽

Vol 68 (3) ◽

pp. 1004-1009 ◽

Cited By ~ 41

Author(s):

M. J. Joyner ◽

J. T. Shepherd ◽

D. R. Seals

Keyword(s):

Blood Flow ◽

Negative Pressure ◽

Lower Body Negative Pressure ◽

Partial Recovery ◽

Sympathetic Outflow ◽

Lower Body ◽

Control Value ◽

Arterial Blood ◽

Change In Mean ◽

Cardiopulmonary Baroreceptors

The purpose of this study was to determine whether prolonged unloading of cardiopulmonary baroreceptors with lower body negative pressure (LBNP) causes constant increases in sympathetic outflow to skeletal muscles. Eight healthy subjects underwent a 20-min control period followed by 20 min of 15-mmHg LBNP. This pressure was selected because it did not cause any significant change in mean arterial blood pressure (sphygmomanometry) or heart rate, suggesting that the cardiopulmonary baroreceptors were selectively unloaded and the activity of the arterial baroreceptors was unchanged. Muscle sympathetic nerve activity in the peroneal nerve (MSNA, microneurography) increased from an average of 21.8 +/- 1.7 bursts/min over the last 5 min of control to 29.0 +/- 2.9 bursts/min during the 1st min of LBNP (P less than 0.05 LBNP vs. control). The increase in MSNA observed during the 1st min was sustained throughout LBNP. Forelimb blood flow (plethysmography) decreased abruptly at the onset of the LBNP from a control value of 4.3 +/- 0.5 ml.min-1.100 ml-1 to 2.5 +/- 0.2 at the 1st min; the flow then increased and remained significantly above this value, but below the control value, throughout LBNP. Similar blood flow findings were obtained in additional studies, when the hand circulation was excluded during the flow measurements. Forearm skin blood flow (laser Doppler) also decreased abruptly at the onset of LBNP and was followed by partial recovery, but these changes were too small to account for all the increases in limb blood flow over the course of LBNP.(ABSTRACT TRUNCATED AT 250 WORDS)

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Effect of acute hypoxemia on cerebral blood flow velocity control during lower body negative pressure

Physiological Reports ◽

10.14814/phy2.13594 ◽

2018 ◽

Vol 6 (4) ◽

pp. e13594 ◽

Cited By ~ 3

Author(s):

Noud van Helmond ◽

Blair D. Johnson ◽

Walter W. Holbein ◽

Humphrey G. Petersen-Jones ◽

Ronée E. Harvey ◽

...

Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Flow Velocity ◽

Negative Pressure ◽

Blood Flow Velocity ◽

Cerebral Blood Flow Velocity ◽

Lower Body Negative Pressure ◽

Lower Body ◽

Velocity Control

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Comparison of two indices for forearm noradrenaline release in humans

Clinical Science ◽

10.1042/cs0990363 ◽

2000 ◽

Vol 99 (5) ◽

pp. 363-369 ◽

Cited By ~ 6

Author(s):

Gerard A. RONGEN ◽

Jacques W. M. LENDERS ◽

Paul SMITS ◽

John S. FLORAS

Keyword(s):

Blood Flow ◽

Sodium Nitroprusside ◽

Noradrenaline Release ◽

Negative Pressure ◽

Forearm Blood Flow ◽

Lower Body Negative Pressure ◽

Lower Body ◽

Release Of Noradrenaline ◽

Appearance Rate

Although there is as yet no method which measures directly the neuronal release of noradrenaline in humans in vivo, the isotope dilution technique with [3H]noradrenaline has been applied to estimate forearm neuronal noradrenaline release into plasma. Two different equations have been developed for this purpose: one to estimate the spillover of noradrenaline into the venous effluent, and a modified formula (often referred to as the appearance rate) which may reflect more closely changes in the neuronal release of noradrenaline into the synaptic cleft, particularly during interventions that alter forearm blood flow. The present study was performed to compare the effects of two interventions known to exert contrasting actions on neuronal forearm noradrenaline release and forearm blood flow. Intra-arterial infusion of sodium nitroprusside at doses without systemic effect increases forearm blood flow, but not neuronal noradrenaline release. In contrast, lower-body negative pressure at -25 mmHg causes forearm vasoconstriction by stimulating neuronal noradrenaline release. During sodium nitroprusside infusion, forearm noradrenaline spillover increased from 1.1±0.3 to 2.2±1.0 pmol·min-1·100 ml-1 (P < 0.05), whereas the forearm noradrenaline appearance rate was unchanged. Lower-body negative pressure did not affect the forearm noradrenaline spillover rate, but increased the forearm noradrenaline appearance rate from 3.4±0.4 pmol·min-1·100 ml-1 at baseline to 5.0±0.9 pmol·min-1·100 ml-1 (P < 0.05). These results indicate that the noradrenaline appearance rate provides the better approximation of changes in forearm neuronal noradrenaline release in response to stimuli which alter local blood flow.

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

Journal of Applied Physiology ◽

10.1152/jappl.1986.61.3.994 ◽

1986 ◽

Vol 61 (3) ◽

pp. 994-998 ◽

Cited By ~ 24

Author(s):

L. K. Essandoh ◽

D. S. Houston ◽

P. M. Vanhoutte ◽

J. T. Shepherd

Keyword(s):

Blood Flow ◽

Negative Pressure ◽

Skeletal Muscles ◽

Lower Body Negative Pressure ◽

Valsalva Maneuver ◽

Lower Body ◽

Blood Flows ◽

Resistance Vessels ◽

Series Of Experiments ◽

The Right

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.

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