Persistence of baroreceptor control of cerebral blood flow velocity at a simulated altitude of 5000 m

Passino, Claudio; Cencetti, Simone; Spadacini, Giammario; Quintana, R.; Parker, Daryl; Robergs, Robert; Appenzeller, Otto; Bernardi, Luciano

doi:10.1097/hjh.0b013e32826f49a3

Cited by 3 publications

(3 citation statements)

References 23 publications

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“…To minimize respiratory-related modulation of heart rate, the 5-s pulses of neck suction were delivered to the carotid sinus during controlled breathing. Specifically, participants were instructed to breathe along to a metronome set at ~15 breaths/min, consistent with work published previously (23,26,39,49). Respiration was assessed by use of a Piezo Respiratory Belt Transducer (MLT1132; ADInstruments, Colorado Springs, CO).…”

Section: Methodsmentioning

confidence: 99%

Sympathetically mediated increases in cardiac output, not restraint of peripheral vasodilation, contribute to blood pressure maintenance during hyperinsulinemia

Limberg

Smith

Soares

et al. 2020

American Journal of Physiology-Heart and Circulatory Physiology

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We examined the role of sympathetic activation in restraining vasodilatory responses to hyperinsulinemia and sustaining blood pressure in healthy adults. Data are reported from two separate experimental protocols in humans and one experimental protocol in isolated arteries from mice. Contrary to our hypothesis, the present findings support the idea that during hyperinsulinemia, a sympathetically mediated increase in cardiac output, rather than restraint of peripheral vasodilation, is the principal contributor to the maintenance of systemic blood pressure.

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Section: Methodsmentioning

confidence: 99%

Sympathetically mediated increases in cardiac output, not restraint of peripheral vasodilation, contribute to blood pressure maintenance during hyperinsulinemia

Limberg

Smith

Soares

et al. 2020

American Journal of Physiology-Heart and Circulatory Physiology

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“…The interpretation of this phase angle is controversial: while some investigators consider it a marker of dynamic autoregulation [18], others have previously suggested that it may instead depend upon the autonomic control of the cerebral vessels [19,36]. A larger phase angle implicates the intervention of some modulating factor (either intrinsic to the vessels or with the implication of the autonomic nervous system), whereas a smaller angle indicates a more passive transmission between main arteries and blood vessels.…”

Section: Autonomic Disturbances In Copd Patientsmentioning

confidence: 99%

Autonomic and cerebrovascular abnormalities in mild COPD are worsened by chronic smoking

Bernardi¹,

Casucci²,

Haider³

et al. 2008

European Respiratory Journal

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Patients with chronic obstructive pulmonary disease (COPD) may develop hypercapnia and hypoxia, two main determinants of cerebral blood flow. The current authors tested whether cerebrovascular regulation was altered in mild COPD, modified by manoeuvres acutely improving autonomic cardiovascular modulation or influenced by smoking habit.In 15 eucapnic normoxic mild COPD patients (eight smokers) and 28 age-matched controls (14 smokers), midcerebral artery blood flow velocity (MCFV), end-tidal carbon dioxide tension (PET,CO 2 ), arterial oxygen saturation (Sa,O 2 ), ECG and blood pressure at rest were monitored during progressive hypercapnic hyperoxia, isocapnic hypoxia, slow breathing and oxygen administration. MCFV, arterial baroreflex and dynamic MCFV-blood pressure relationships were compared by phase analysis.COPD and control smokers showed higher MCFV (when corrected for PET,CO 2 ), lower cerebrovascular resistance index and lower sensitivity to hypercapnia than nonsmokers, with equal sensitivity to Sa,O 2 and similar phase analysis. Arterial baroreflex was depressed in all COPD patients. Slow breathing and oxygen administration improved baroreflex sensitivity and reduced MCFV in all COPD patients.Patients with mild chronic obstructive pulmonary disease show autonomic dysfunction. Chronic smoking induces cerebral vasodilation and impairs cerebrovascular control. All abnormalities can be partly corrected by improving the cardio-and cerebrovascular autonomic modulation, suggesting that functional autonomic abnormalities are already present at an early stage of disease.

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“…Marple [45] and applied in many previous studies assessing PA as a parameter of cerebral autoregulation [10,24,25,29,30,40,43,46].…”

Section: Methodsmentioning

confidence: 99%

Partial pharmacologic blockade shows sympathetic connection between blood pressure and cerebral blood flow velocity fluctuations

Hilz

Marthol²,

Liu

et al. 2016

Journal of the Neurological Sciences

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Cerebral autoregulation (CA) dampens transfer of blood pressure (BP)-fluctuations onto cerebral blood flow velocity (CBFV). Thus, CBFV-oscillations precede BP-oscillations. The phase angle (PA) between sympathetically mediated low-frequency (LF: 0.03-0.15Hz) BP- and CBFV-oscillations is a measure of CA quality. To evaluate whether PA depends on sympathetic modulation, we assessed PA-changes upon sympathetic stimulation with and without pharmacologic sympathetic blockade. In 10 healthy, young men, we monitored mean BP and CBFV before and during 120-second cold pressor stimulation (CPS) of one foot (0°C ice-water). We calculated mean values, standard deviations and sympathetic LF-powers of all signals, and PAs between LF-BP- and LF-CBFV-oscillations. We repeated measurements after ingestion of the adrenoceptor-blocker carvedilol (25mg). We compared parameters before and during CPS, without and after carvedilol (analysis of variance, post-hoc t-tests, significance: p<0.05). Without carvedilol, CPS increased BP, CBFV, BP-LF- and CBFV-LF-powers, and shortened PA. Carvedilol decreased resting BP, CBFV, BP-LF- and CBFV-LF-powers, while PAs remained unchanged. During CPS, BPs, CBFVs, BP-LF- and CBFV-LF-powers were lower, while PAs were longer with than without carvedilol. With carvedilol, CPS no longer shortened resting PA. Sympathetic activation shortens PA. Partial adrenoceptor blockade abolishes this PA-shortening. Thus, PA-measurements provide a subtle marker of sympathetic influences on CA and might refine CA evaluation.

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Persistence of baroreceptor control of cerebral blood flow velocity at a simulated altitude of 5000 m

Abstract: During acute exposure to high altitude, cerebral blood flow is still modulated by the autonomic nervous system through the baroreflex, whose sensitivity is not affected by changes in CO2 and oxygen saturation levels.

Cited by 3 publications

References 23 publications

Sympathetically mediated increases in cardiac output, not restraint of peripheral vasodilation, contribute to blood pressure maintenance during hyperinsulinemia

Sympathetically mediated increases in cardiac output, not restraint of peripheral vasodilation, contribute to blood pressure maintenance during hyperinsulinemia

Autonomic and cerebrovascular abnormalities in mild COPD are worsened by chronic smoking

Partial pharmacologic blockade shows sympathetic connection between blood pressure and cerebral blood flow velocity fluctuations

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