Influence of sympathoexcitation at high altitude on cerebrovascular function and ventilatory control in humans

2012 ◽  
Vol 113 (7) ◽  
pp. 1058-1067 ◽  
Author(s):  
P. N. Ainslie ◽  
S. J. E. Lucas ◽  
J.-L. Fan ◽  
K. N. Thomas ◽  
J. D. Cotter ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
High Altitude ◽  
Function Analysis ◽  
Low Frequency ◽  
Cerebrovascular Reactivity ◽  
Adrenergic Blockade ◽  
Ventilatory Control ◽  
Phase Lead ◽  
Arterial Blood ◽  
Transfer Function Analysis

We sought to determine the influence of sympathoexcitation on dynamic cerebral autoregulation (CA), cerebrovascular reactivity, and ventilatory control in humans at high altitude (HA). At sea level (SL) and following 3–10 days at HA (5,050 m), we measured arterial blood gases, ventilation, arterial pressure, and middle cerebral blood velocity (MCAv) before and after combined α- and β-adrenergic blockade. Dynamic CA was quantified using transfer function analysis. Cerebrovascular reactivity was assessed using hypocapnia and hyperoxic hypercapnia. Ventilatory control was assessed from the hypercapnia and during isocapnic hypoxia. Arterial Pco2 and ventilation and its control were unaltered following blockade at both SL and HA. At HA, mean arterial pressure (MAP) was elevated ( P < 0.01 vs. SL), but MCAv remained unchanged. Blockade reduced MAP more at HA than at SL (26 vs. 15%, P = 0.048). At HA, gain and coherence in the very-low-frequency (VLF) range (0.02–0.07 Hz) increased, and phase lead was reduced (all P < 0.05 vs. SL). Following blockade at SL, coherence was unchanged, whereas VLF phase lead was reduced (−40 ± 23%; P < 0.01). In contrast, blockade at HA reduced low-frequency coherence (−26 ± 20%; P = 0.01 vs. baseline) and elevated VLF phase lead (by 177 ± 238%; P < 0.01 vs. baseline), fully restoring these parameters back to SL values. Irrespective of this elevation in VLF gain at HA ( P < 0.01), blockade increased it comparably at SL and HA (∼43–68%; P < 0.01). Despite elevations in MCAv reactivity to hypercapnia at HA, blockade reduced ( P < 0.05) it comparably at SL and HA, effects we attributed to the hypotension and/or abolition of the hypercapnic-induced increase in MAP. With the exception of dynamic CA, we provide evidence of a redundant role of sympathetic nerve activity as a direct mechanism underlying changes in cerebrovascular reactivity and ventilatory control following partial acclimatization to HA. These findings have implications for our understanding of CBF function in the context of pathologies associated with sympathoexcitation and hypoxemia.

Dynamic modulation of cerebrovascular resistance as an index of autoregulation under tilt and controlled Pet CO2

2002 ◽  
Vol 283 (3) ◽  
pp. R653-R662 ◽  
Author(s):  
Michael R. Edwards ◽  
J. Kevin Shoemaker ◽  
Richard L. Hughson
Keyword(s):  
Transfer Function ◽  
Function Analysis ◽  
Low Frequency ◽  
Mean Flow ◽  
Low Frequencies ◽  
Cerebrovascular Autoregulation ◽  
Cerebrovascular Resistance ◽  
Arterial Blood ◽  
Transfer Function Analysis ◽  
Frequency Changes

Transfer function analysis of the arterial blood pressure (BP)-mean flow velocity (MFV) relationship describes an aspect of cerebrovascular autoregulation. We hypothesized that the transfer function relating BP to cerebrovascular resistance (CVRi) would be sensitive to low-frequency changes in autoregulation induced by head-up tilt (HUT) and altered arterial Pco 2. Nine subjects were studied in supine and HUT positions with end-tidal Pco 2(Pet CO2 ) kept constant at normal levels: +5 and −5 mmHg. The BP-MFV relationship had low coherence at low frequencies, and there were significant effects of HUT on gain only at high frequencies and of Pco 2 on phase only at low frequencies. BP → CVRi had coherence >0.5 from very low to low frequencies. There was a significant reduction of gain with increased Pco 2 in the very low and low frequencies and with HUT at the low frequency. Phase was affected by Pco 2 in the very low frequencies. Transfer function analysis of BP → CVRi provides direct evidence of altered cerebrovascular autoregulation under HUT and higher levels of Pco 2.

Effects of hyperglycemia on the cerebrovascular response to rhythmic handgrip exercise

2007 ◽  
Vol 293 (1) ◽  
pp. H467-H473 ◽  
Author(s):  
Yu-Sok Kim ◽  
Rikke Krogh-Madsen ◽  
Peter Rasmussen ◽  
Peter Plomgaard ◽  
Shigehiko Ogoh ◽  
...  
Keyword(s):  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Function Analysis ◽  
Low Frequency ◽  
Resistance Index ◽  
Handgrip Exercise ◽  
Dynamic Relationship ◽  
Hyperglycemic Clamp ◽  
Transfer Function Analysis

Dynamic cerebral autoregulation (CA) is challenged by exercise and may become less effective when exercise is exhaustive. Exercise may increase arterial glucose concentration, and we evaluated whether the cerebrovascular response to exercise is affected by hyperglycemia. The effects of a hyperinsulinemic euglycemic clamp (EU) and hyperglycemic clamp (HY) on the cerebrovascular (CVRI) and systemic vascular resistance index (SVRI) responses were evaluated in seven healthy subjects at rest and during rhythmic handgrip exercise. Transfer function analysis of the dynamic relationship between beat-to-beat changes in mean arterial pressure and middle cerebral artery (MCA) mean blood flow velocity ( Vmean) was used to assess dynamic CA. At rest, SVRI decreased with HY and EU ( P < 0.01). CVRI was maintained with EU but became reduced with HY [11% (SD 3); P < 0.01], and MCA Vmean increased ( P < 0.05), whereas brain catecholamine uptake and arterial Pco2 did not change significantly. HY did not affect the normalized low-frequency gain between mean arterial pressure and MCA Vmean or the phase shift, indicating maintained dynamic CA. With HY, the increase in CVRI associated with exercise was enhanced (19 ± 7% vs. 9 ± 7%; P < 0.05), concomitant with a larger increase in heart rate and cardiac output and a larger reduction in SVRI (22 ± 4% vs. 14 ± 2%; P < 0.05). Thus hyperglycemia lowered cerebral vascular tone independently of CA capacity at rest, whereas dynamic CA remained able to modulate cerebral blood flow around the exercise-induced increase in MCA Vmean. These findings suggest that elevated blood glucose does not explain that dynamic CA is affected during intense exercise.

Impaired cerebral haemodynamic function associated with chronic traumatic brain injury in professional boxers

2012 ◽  
Vol 124 (3) ◽  
pp. 177-189 ◽  
Author(s):  
Damian M. Bailey ◽  
Daniel W. Jones ◽  
Andrew Sinnott ◽  
Julien V. Brugniaux ◽  
Karl J. New ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Function Analysis ◽  
Transcranial Doppler Ultrasound ◽  
Cerebrovascular Reactivity ◽  
Cerebral Hypoperfusion ◽  
Mechanical Trauma ◽  
Neurocognitive Dysfunction ◽  
Arterial Blood ◽  
Transfer Function Analysis

The present study examined to what extent professional boxing compromises cerebral haemodynamic function and its association with CTBI (chronic traumatic brain injury). A total of 12 male professional boxers were compared with 12 age-, gender- and physical fitness-matched non-boxing controls. We assessed dCA (dynamic cerebral autoregulation; thigh-cuff technique and transfer function analysis), CVRCO2 (cerebrovascular reactivity to changes in CO2: 5% CO2 and controlled hyperventilation), orthostatic tolerance (supine to standing) and neurocognitive function (psychometric tests). Blood flow velocity in the middle cerebral artery (transcranial Doppler ultrasound), mean arterial blood pressure (finger photoplethysmography), end-tidal CO2 (capnography) and cortical oxyhaemoglobin concentration (near-IR spectroscopy) were continuously measured. Boxers were characterized by fronto-temporal neurocognitive dysfunction and impaired dCA as indicated by a lower rate of regulation and autoregulatory index (P<0.05 compared with controls). Likewise, CVRCO2 was also reduced resulting in a lower CVRCO2 range (P<0.05 compared with controls). The latter was most marked in boxers with the highest CTBI scores and correlated against the volume and intensity of sparring during training (r=−0.84, P<0.05). These impairments coincided with more marked orthostatic hypotension, cerebral hypoperfusion and corresponding cortical de-oxygenation during orthostatic stress (P<0.05 compared with controls). In conclusion, these findings provide the first comprehensive evidence for chronically impaired cerebral haemodynamic function in active boxers due to the mechanical trauma incurred by repetitive, sub-concussive head impact incurred during sparring training. This may help explain why CTBI is a progressive disease that manifests beyond the active boxing career.

scholarly journals Dexmedetomidine Weakens Dynamic Cerebral Autoregulation as Assessed by Transfer Function Analysis and the Thigh Cuff Method

2008 ◽  
Vol 109 (4) ◽  
pp. 642-650 ◽  
Author(s):  
Yojiro Ogawa ◽  
Ken-ichi Iwasaki ◽  
Ken Aoki ◽  
Wakako Kojima ◽  
Jitsu Kato ◽  
...  
Keyword(s):  
Steady State ◽  
Transfer Function ◽  
Arterial Pressure ◽  
Cerebral Autoregulation ◽  
Function Analysis ◽  
Low Frequency ◽  
High Dose ◽  
Frequency Range ◽  
Transfer Function Analysis ◽  
Dynamic Cerebral Autoregulation

Background Dexmedetomidine, which is often used in intensive care units in patients with compromised circulation, might induce further severe decreases in cerebral blood flow (CBF) with temporal decreases in arterial pressure induced by various stimuli if dynamic cerebral autoregulation is not improved. Therefore, the authors hypothesized that dexmedetomidine strengthens dynamic cerebral autoregulation. Methods Fourteen healthy male subjects received placebo, low-dose dexmedetomidine (loading, 3 microg x kg(-1) x h(-1) for 10 min; maintenance, 0.2 microg x kg(-1) x h(-1) for 60 min), and high-dose dexmedetomidine (loading, 6 microg x kg(-1) x h(-1) for 10 min; maintenance, 0.4 microg x kg(-1) x h(-1) for 60 min) infusions in a randomized, double-blind, crossover study. After 70 min of drug administration, dynamic cerebral autoregulation was estimated by transfer function analysis between arterial pressure variability and CBF velocity variability, and the thigh cuff method. Results Compared with placebo, steady state CBF velocity and mean blood pressure significantly decreased during administration of dexmedetomidine. Transfer function gain in the very-low-frequency range increased and phase in the low-frequency range decreased significantly, suggesting alterations in dynamic cerebral autoregulation in lower frequency ranges. Moreover, the dynamic rate of regulation and percentage restoration in CBF velocity significantly decreased when a temporal decrease in arterial pressure was induced by thigh cuff release. Conclusion Contrary to the authors' hypothesis, the current results of two experimental analyses suggest together that dexmedetomidine weakens dynamic cerebral autoregulation and delays restoration in CBF velocity during conditions of decreased steady state CBF velocity. Therefore, dexmedetomidine may lead to further sustained reductions in CBF during temporal decreases in arterial pressure.

scholarly journals Lack of correlation between cerebral vasomotor reactivity and dynamic cerebral autoregulation during stepwise increases in inspired CO2 concentration

2016 ◽  
Vol 120 (12) ◽  
pp. 1434-1441 ◽  
Author(s):  
Sung-Moon Jeong ◽  
Seon-Ok Kim ◽  
Darren S. DeLorey ◽  
Tony G. Babb ◽  
Benjamin D. Levine ◽  
...  
Keyword(s):  
Transfer Function ◽  
Cerebral Autoregulation ◽  
Function Analysis ◽  
Low Frequency ◽  
Frequency Range ◽  
Vasomotor Reactivity ◽  
Arterial Blood ◽  
Transfer Function Analysis ◽  
Cerebral Vasomotor Reactivity ◽  
Dynamic Cerebral Autoregulation

Cerebral vasomotor reactivity (CVMR) and dynamic cerebral autoregulation (CA) are measured extensively in clinical and research studies. However, the relationship between these measurements of cerebrovascular function is not well understood. In this study, we measured changes in cerebral blood flow velocity (CBFV) and arterial blood pressure (BP) in response to stepwise increases in inspired CO2 concentrations of 3 and 6% to assess CVMR and dynamic CA in 13 healthy young adults [2 women, 32 ± 9 (SD) yr]. CVMR was assessed as percentage changes in CBFV (CVMRCBFV) or cerebrovascular conductance index (CVCi, CVMRCVCi) in response to hypercapnia. Dynamic CA was estimated by performing transfer function analysis between spontaneous oscillations in BP and CBFV. Steady-state CBFV and CVCi both increased exponentially during hypercapnia; CVMRCBFV and CVMRCVCi were greater at 6% (3.85 ± 0.90 and 2.45 ± 0.79%/mmHg) than at 3% CO2 (2.09 ± 1.47 and 0.21 ± 1.56%/mmHg, P = 0.009 and 0.005, respectively). Furthermore, CVMRCBFV was greater than CVMRCVCi during either 3 or 6% CO2 ( P = 0.017 and P < 0.001, respectively). Transfer function gain and coherence increased in the very low frequency range (0.02-0.07 Hz), and phase decreased in the low-frequency range (0.07–0.20 Hz) when breathing 6%, but not 3% CO2. There were no correlations between the measurements of CVMR and dynamic CA. These findings demonstrated influences of inspired CO2 concentrations on assessment of CVMR and dynamic CA. The lack of correlation between CVMR and dynamic CA suggests that cerebrovascular responses to changes in arterial CO2 and BP are mediated by distinct regulatory mechanisms.

Alterations in cerebral dynamics at high altitude following partial acclimatization in humans: wakefulness and sleep

2007 ◽  
Vol 102 (2) ◽  
pp. 658-664 ◽  
Author(s):  
Philip N. Ainslie ◽  
Katie Burgess ◽  
Prajan Subedi ◽  
Keith R. Burgess
Keyword(s):  
Blood Pressure ◽  
Sleep Apnea ◽  
High Altitude ◽  
Cerebral Autoregulation ◽  
Central Sleep Apnea ◽  
Cerebrovascular Reactivity ◽  
Arterial Blood ◽  
Transfer Function Analysis ◽  
Low Altitude ◽  
Dynamic Cerebral Autoregulation

We tested the hypothesis that, following exposure to high altitude, cerebrovascular reactivity to CO2 and cerebral autoregulation would be attenuated. Such alterations may predispose to central sleep apnea at high altitude by promoting changes in brain Pco2 and thus breathing stability. We measured middle cerebral artery blood flow velocity (MCAv; transcranial Doppler ultrasound) and arterial blood pressure during wakefulness in conditions of eucapnia (room air), hypocapnia (voluntary hyperventilation), and hypercapnia (isooxic rebeathing), and also during non-rapid eye movement (stage 2) sleep at low altitude (1,400 m) and at high altitude (3,840 m) in five individuals. At each altitude, sleep was studied using full polysomnography, and resting arterial blood gases were obtained. During wakefulness and polysomnographic-monitored sleep, dynamic cerebral autoregulation and steady-state changes in MCAv in relation to changes in blood pressure were evaluated using transfer function analysis. High altitude was associated with an increase in central sleep apnea index (0.2 ± 0.4 to 20.7 ± 23.2 per hour) and an increase in mean blood pressure and cerebrovascular resistance during wakefulness and sleep. MCAv was unchanged during wakefulness, whereas there was a greater decrease during sleep at high altitude compared with low altitude (−9.1 ± 1.7 vs. −4.8 ± 0.7 cm/s; P < 0.05). At high altitude, compared with low altitude, the cerebrovascular reactivity to CO2 in the hypercapnic range was unchanged (5.5 ± 0.7 vs. 5.3 ± 0.7%/mmHg; P = 0.06), while it was lowered in the hypocapnic range (3.1 ± 0.7 vs. 1.9 ± 0.6%/mmHg; P < 0.05). Dynamic cerebral autoregulation was further reduced during sleep ( P < 0.05 vs. low altitude). Lowered cerebrovascular reactivity to CO2 and reduction in both dynamic cerebral autoregulation and MCAv during sleep at high altitude may be factors in the pathogenesis of breathing instability.

Cerebral hypoperfusion during hypoxic exercise following two different hypoxic exposures: independence from changes in dynamic autoregulation and reactivity

2008 ◽  
Vol 295 (5) ◽  
pp. R1613-R1622 ◽  
Author(s):  
Philip N. Ainslie ◽  
Michael Hamlin ◽  
John Hellemans ◽  
Peter Rasmussen ◽  
Shigehiko Ogoh
Keyword(s):  
Near Infrared ◽  
Cerebral Oxygenation ◽  
Function Analysis ◽  
Low Frequency ◽  
Cerebrovascular Reactivity ◽  
Cerebral Hypoperfusion ◽  
Cerebrovascular Function ◽  
Transfer Function Analysis ◽  
End Tidal ◽  
Hypoxic Exercise

We examined the effects of exposure to 10–12 days intermittent hypercapnia [IHC: 5:5-min hypercapnia (inspired fraction of CO2 0.05)-to-normoxia for 90 min ( n = 10)], intermittent hypoxia [IH: 5:5-min hypoxia-to-normoxia for 90 min ( n = 11)] or 12 days of continuous hypoxia [CH: 1,560 m ( n = 7)], or both IH followed by CH on cardiorespiratory and cerebrovascular function during steady-state cycling exercise with and without hypoxia (inspired fraction of oxygen, 0.14). Cerebrovascular reactivity to CO2 was also monitored. During all procedures, ventilation, end-tidal gases, blood pressure, muscle and cerebral oxygenation (near-infrared spectroscopy), and middle cerebral artery blood flow velocity (MCAv) were measured continuously. Dynamic cerebral autoregulation (CA) was assessed using transfer-function analysis. Hypoxic exercise resulted in increases in ventilation, hypocapnia, heart rate, and cardiac output when compared with normoxic exercise ( P < 0.05); these responses were unchanged following IHC but were elevated following the IH and CH exposure ( P < 0.05) with no between-intervention differences. Following IH and/or CH exposure, the greater hypocapnia during hypoxic exercise provoked a decrease in MCAv ( P < 0.05 vs. preexposure) that was related to lowered cerebral oxygenation ( r = 0.54; P < 0.05). Following any intervention, during hypoxic exercise, the apparent impairment in CA, reflected in lowered low-frequency phase between MCAv and BP, and MCAv-CO2 reactivity, were unaltered. Conversely, during hypoxic exercise following both IH and/or CH, there was less of a decrease in muscle oxygenation ( P < 0.05 vs. preexposure). Thus IH or CH induces some adaptation at the muscle level and lowers MCAv and cerebral oxygenation during hypoxic exercise, potentially mediated by the greater hypocapnia, rather than a compromise in CA or MCAv reactivity.

Cerebrovascular reactivity and dynamic autoregulation in tetraplegia

2010 ◽  
Vol 298 (4) ◽  
pp. R1035-R1042 ◽  
Author(s):  
Luke C. Wilson ◽  
James D. Cotter ◽  
Jui-Lin Fan ◽  
Rebekah A. I. Lucas ◽  
Kate N. Thomas ◽  
...  
Keyword(s):  
Transfer Function ◽  
Cerebral Oxygenation ◽  
Function Analysis ◽  
Plasma Catecholamines ◽  
Peripheral Resistance ◽  
Cardiovascular Function ◽  
Cerebrovascular Reactivity ◽  
Arterial Blood ◽  
Transfer Function Analysis ◽  
Cord Injury

Humans with spinal cord injury have impaired cardiovascular function proportional to the level and completeness of the lesion. The effect on cerebrovascular function is unclear, especially for high-level lesions. The purpose of this study was to evaluate the integrity of dynamic cerebral autoregulation (CA) and the cerebrovascular reactivity in chronic tetraplegia (Tetra). After baseline, steady-state hypercapnia (5% CO2) and hypocapnia (controlled hyperventilation) were used to assess cerebrovascular reactivity in 6 men with Tetra (C5–C7 lesion) and 14 men without [able-bodied (AB)]. Middle cerebral artery blood flow velocity (MCAv), cerebral oxygenation, arterial blood pressure (BP), heart rate (HR), cardiac output (Q̇; model flow), partial pressure of end-tidal CO2 (PetCO2), and plasma catecholamines were measured. Dynamic CA was assessed by transfer function analysis of spontaneous fluctuations in BP and MCAv. MCAv pulsatility index (MCAv PI) was calculated as (MCAvsystolic − MCAvdiastolic)/MCAvmean and standardized by dividing by mean arterial pressure (MAP). Resting BP, total peripheral resistance, and catecholamines were lower in Tetra ( P < 0.05), and standardized MCAv PI was ∼36% higher in Tetra ( P = 0.003). Resting MCAv, cerebral oxygenation, HR, and PetCO2 were similar between groups ( P > 0.05). Although phase and transfer function gain relationships in dynamic CA were maintained with Tetra ( P > 0.05), coherence in the very low-frequency range (0.02–0.07 Hz) was ∼21% lower in Tetra ( P = 0.006). Full (hypo- and hypercapnic) cerebrovascular reactivity to CO2 was unchanged with Tetra ( P > 0.05). During hypercapnia, standardized MCAv PI reactivity was enhanced by ∼78% in Tetra ( P = 0.016). Despite impaired cardiovascular function, chronic Tetra involves subtle changes in dynamic CA and cerebrovascular reactivity to CO2. Changes are evident in coherence at baseline and MCAv PI during baseline and hypercapnic states in chronic Tetra, which may be indicative of cerebrovascular adaptation.

Interindividual relationships between blood pressure and cerebral blood flow variability with intact and blunted cerebrovascular control

2013 ◽  
Vol 114 (7) ◽  
pp. 888-895 ◽  
Author(s):  
Yu-Chieh Tzeng ◽  
Braid A. MacRae
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Flow Velocity ◽  
Function Analysis ◽  
Low Frequency ◽  
Flow Variability ◽  
Very Low Frequency ◽  
Arterial Blood ◽  
Transfer Function Analysis

The relationships between blood pressure variability (BPV) and cerebral blood flow variability (CFV) across individuals in the presence of intact and blunted cerebrovascular control are poorly understood. This study sought to characterize the interindividual associations between spontaneous BPV and CFV under conditions of normal and blunted [calcium channel blockade (CCB)] cerebrovascular control in healthy humans. We analyzed blood pressure and flow velocity data from 12 subjects treated with CCB (60 mg oral nimodipine) and 11 subjects treated with a placebo pill. Spontaneously occurring fluctuations in mean arterial blood pressure (MAP) and middle cerebral artery flow velocity (MCAvmean; transcranial Doppler) were characterized using power spectral and transfer function analysis in the very-low- (0.02–0.07 Hz), low- (0.07–0.20 Hz), and high-frequency (0.20–0.40 Hz) ranges. Across our study sample, MAP and MCAvmean power were positively correlated in all three frequency ranges, both before ( R2 = 0.34–0.67, all P < 0.01) and after CCB ( R2 = 0.53–0.61, all P < 0.02). Compared with placebo, CCB reduced very-low-frequency MAP ( P < 0.05) and MCAvmean power ( P < 0.01) and the low-frequency cross-spectral phase angle ( P < 0.05). The magnitude of change in MAP and MCAvmean power with CCB (i.e., change scores) was positively related in the very-low-frequency range. Collectively, these findings indicate that CFV may be an explanatory factor in the association between elevated BPV and adverse cerebrovascular outcomes and support the possibility of using CCB to improve hemodynamic stability under resting conditions.

Inhibition of NO synthesis minimally affects the dynamic baroreflex regulation of sympathetic nerve activity

1997 ◽  
Vol 272 (5) ◽  
pp. H2446-H2452 ◽  
Author(s):  
H. Miyano ◽  
T. Kawada ◽  
T. Shishido ◽  
T. Sato ◽  
M. Sugimachi ◽  
...  
Keyword(s):  
Transfer Function ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Carotid Sinus ◽  
Function Analysis ◽  
Corner Frequency ◽  
Nerve Activity ◽  
Carotid Sinus Baroreflex ◽  
Transfer Function Analysis

The purpose of this investigation was to examine the role of nitric oxide (NO) in the dynamic baroreflex regulation of cardiac sympathetic nerve activity. In anesthetized rabbits, we imposed random pressure perturbations on the isolated carotid sinuses before and after the intravenous administration of NG-monomethyl-L-arginine. We characterized the dynamic properties relating carotid sinus pressure input to sympathetic nerve activity by means of a transfer function analysis. NG-monomethyl-L-arginine decreased the corner frequency of the transfer function (0.100 +/- 0.054 vs. 0.074 +/- 0.035 Hz; P < 0.05), whereas other parameters such as the steady-state gain and transmission lag time remained unchanged. Although cursory examination of these findings would suggest a possible contribution of NO in the dynamic baroreflex regulation of sympathetic nerve activity, quantitative assessment of the transfer function reveals only a minimal effect on the baroreflex regulation of arterial pressure, particularly under closed-loop conditions. We conclude that NO noticeably affects the dynamic baroreflex regulation of sympathetic nerve activity. However, it may not significantly affect arterial pressure regulation through central modulation of the carotid sinus baroreflex.

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