Cerebral autoregulation is preserved during orthostatic stress superimposed with systemic hypotension

Hong Guo, Nancy Tierney, Frederic Schaller, Peter B. Raven, Scott A. Smith, Xiangrong Shi

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Abstract

We sought to determine whether cerebral autoregulation (CA) is compromised during orthostatic stress superimposed with systemic hypotension. Transient systemic hypotension was produced by deflation of thigh cuffs previously inflated to suprasystolic pressure, combined with or without lower body negative pressure (LBNP). Cardiac output (CO) decreased from a baseline of 5.0 ± 0.5 l/min by -8.3 ± 1.7, -19.2 ± 2.0, and -30.6 ± 3.4% during LBNP of -15, -30, and -50 Torr, respectively. Mean arterial pressure (MAP) was maintained during LBNP, despite decreases in systolic and pulse pressures. Middle cerebral arterial blood flow velocity (V MCA ) decreased significantly from a baseline of 64 ± 3 to 58 ± 4 cm/s (-9.7 ± 2.4%) at -50 Torr of LBNP. The reduction in V MCA was associated with a decrease in regional cerebral O 2 saturation. However, the percent decrease in V MCA was markedly less than that of CO. This suggests that the magnitude of the change in V MCA (an index of cerebral blood flow) is less than would be predicted, given the decrease in CO. Transient systemic hypotension decreased MAP by -21 ± 2, -24 ± 2, -28 ± 3, and -26 ± 3% at rest and during LBNP of -15, -30, and -50 Torr, respectively. Likewise, this acute hypotension resulted in decreases in V MCA of -20 ± 2, -21 ± 2, -24 ± 25, and -19 ± 2% and regional cerebral O 2 saturation of -5 ± 1, -6 ± 1, -6 ± 1, and -7 ± 2% at rest and during LBNP of -15, -30, and -50 Torr, respectively. Complete recovery of V MCA to baseline values following transient hypotension (ranging from 5 to 8 s) occurred significantly earlier compared with MAP (from 10 to 12 s). No subjects experienced syncope during acute hypotension. We conclude that CA is preserved during LBNP, superimposed with transient systemic hypotension, despite the decrease in V MCA associated with sustained central hypovolemia in normal healthy individuals. This preserved CA is vital for the prevention of orthostatic syncope.

Original languageEnglish
Pages (from-to)1785-1792
Number of pages8
JournalJournal of Applied Physiology
Volume100
Issue number6
DOIs
StatePublished - 1 Jun 2006

Fingerprint

Lower Body Negative Pressure
Hypotension
Homeostasis
Cerebrovascular Circulation
Cardiac Output
Arterial Pressure
Syncope
Blood Pressure
Hypovolemia
Blood Flow Velocity
Thigh
Pressure

Keywords

  • Blood flow velocity
  • Cerebral oxygenation
  • Lower body negative pressure
  • Sympathetic nerve activity
  • Syncope

Cite this

Guo, Hong ; Tierney, Nancy ; Schaller, Frederic ; Raven, Peter B. ; Smith, Scott A. ; Shi, Xiangrong. / Cerebral autoregulation is preserved during orthostatic stress superimposed with systemic hypotension. In: Journal of Applied Physiology. 2006 ; Vol. 100, No. 6. pp. 1785-1792.
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abstract = "We sought to determine whether cerebral autoregulation (CA) is compromised during orthostatic stress superimposed with systemic hypotension. Transient systemic hypotension was produced by deflation of thigh cuffs previously inflated to suprasystolic pressure, combined with or without lower body negative pressure (LBNP). Cardiac output (CO) decreased from a baseline of 5.0 ± 0.5 l/min by -8.3 ± 1.7, -19.2 ± 2.0, and -30.6 ± 3.4{\%} during LBNP of -15, -30, and -50 Torr, respectively. Mean arterial pressure (MAP) was maintained during LBNP, despite decreases in systolic and pulse pressures. Middle cerebral arterial blood flow velocity (V MCA ) decreased significantly from a baseline of 64 ± 3 to 58 ± 4 cm/s (-9.7 ± 2.4{\%}) at -50 Torr of LBNP. The reduction in V MCA was associated with a decrease in regional cerebral O 2 saturation. However, the percent decrease in V MCA was markedly less than that of CO. This suggests that the magnitude of the change in V MCA (an index of cerebral blood flow) is less than would be predicted, given the decrease in CO. Transient systemic hypotension decreased MAP by -21 ± 2, -24 ± 2, -28 ± 3, and -26 ± 3{\%} at rest and during LBNP of -15, -30, and -50 Torr, respectively. Likewise, this acute hypotension resulted in decreases in V MCA of -20 ± 2, -21 ± 2, -24 ± 25, and -19 ± 2{\%} and regional cerebral O 2 saturation of -5 ± 1, -6 ± 1, -6 ± 1, and -7 ± 2{\%} at rest and during LBNP of -15, -30, and -50 Torr, respectively. Complete recovery of V MCA to baseline values following transient hypotension (ranging from 5 to 8 s) occurred significantly earlier compared with MAP (from 10 to 12 s). No subjects experienced syncope during acute hypotension. We conclude that CA is preserved during LBNP, superimposed with transient systemic hypotension, despite the decrease in V MCA associated with sustained central hypovolemia in normal healthy individuals. This preserved CA is vital for the prevention of orthostatic syncope.",
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Cerebral autoregulation is preserved during orthostatic stress superimposed with systemic hypotension. / Guo, Hong; Tierney, Nancy; Schaller, Frederic; Raven, Peter B.; Smith, Scott A.; Shi, Xiangrong.

In: Journal of Applied Physiology, Vol. 100, No. 6, 01.06.2006, p. 1785-1792.

Research output: Contribution to journalArticleResearchpeer-review

TY - JOUR

T1 - Cerebral autoregulation is preserved during orthostatic stress superimposed with systemic hypotension

AU - Guo, Hong

AU - Tierney, Nancy

AU - Schaller, Frederic

AU - Raven, Peter B.

AU - Smith, Scott A.

AU - Shi, Xiangrong

PY - 2006/6/1

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N2 - We sought to determine whether cerebral autoregulation (CA) is compromised during orthostatic stress superimposed with systemic hypotension. Transient systemic hypotension was produced by deflation of thigh cuffs previously inflated to suprasystolic pressure, combined with or without lower body negative pressure (LBNP). Cardiac output (CO) decreased from a baseline of 5.0 ± 0.5 l/min by -8.3 ± 1.7, -19.2 ± 2.0, and -30.6 ± 3.4% during LBNP of -15, -30, and -50 Torr, respectively. Mean arterial pressure (MAP) was maintained during LBNP, despite decreases in systolic and pulse pressures. Middle cerebral arterial blood flow velocity (V MCA ) decreased significantly from a baseline of 64 ± 3 to 58 ± 4 cm/s (-9.7 ± 2.4%) at -50 Torr of LBNP. The reduction in V MCA was associated with a decrease in regional cerebral O 2 saturation. However, the percent decrease in V MCA was markedly less than that of CO. This suggests that the magnitude of the change in V MCA (an index of cerebral blood flow) is less than would be predicted, given the decrease in CO. Transient systemic hypotension decreased MAP by -21 ± 2, -24 ± 2, -28 ± 3, and -26 ± 3% at rest and during LBNP of -15, -30, and -50 Torr, respectively. Likewise, this acute hypotension resulted in decreases in V MCA of -20 ± 2, -21 ± 2, -24 ± 25, and -19 ± 2% and regional cerebral O 2 saturation of -5 ± 1, -6 ± 1, -6 ± 1, and -7 ± 2% at rest and during LBNP of -15, -30, and -50 Torr, respectively. Complete recovery of V MCA to baseline values following transient hypotension (ranging from 5 to 8 s) occurred significantly earlier compared with MAP (from 10 to 12 s). No subjects experienced syncope during acute hypotension. We conclude that CA is preserved during LBNP, superimposed with transient systemic hypotension, despite the decrease in V MCA associated with sustained central hypovolemia in normal healthy individuals. This preserved CA is vital for the prevention of orthostatic syncope.

AB - We sought to determine whether cerebral autoregulation (CA) is compromised during orthostatic stress superimposed with systemic hypotension. Transient systemic hypotension was produced by deflation of thigh cuffs previously inflated to suprasystolic pressure, combined with or without lower body negative pressure (LBNP). Cardiac output (CO) decreased from a baseline of 5.0 ± 0.5 l/min by -8.3 ± 1.7, -19.2 ± 2.0, and -30.6 ± 3.4% during LBNP of -15, -30, and -50 Torr, respectively. Mean arterial pressure (MAP) was maintained during LBNP, despite decreases in systolic and pulse pressures. Middle cerebral arterial blood flow velocity (V MCA ) decreased significantly from a baseline of 64 ± 3 to 58 ± 4 cm/s (-9.7 ± 2.4%) at -50 Torr of LBNP. The reduction in V MCA was associated with a decrease in regional cerebral O 2 saturation. However, the percent decrease in V MCA was markedly less than that of CO. This suggests that the magnitude of the change in V MCA (an index of cerebral blood flow) is less than would be predicted, given the decrease in CO. Transient systemic hypotension decreased MAP by -21 ± 2, -24 ± 2, -28 ± 3, and -26 ± 3% at rest and during LBNP of -15, -30, and -50 Torr, respectively. Likewise, this acute hypotension resulted in decreases in V MCA of -20 ± 2, -21 ± 2, -24 ± 25, and -19 ± 2% and regional cerebral O 2 saturation of -5 ± 1, -6 ± 1, -6 ± 1, and -7 ± 2% at rest and during LBNP of -15, -30, and -50 Torr, respectively. Complete recovery of V MCA to baseline values following transient hypotension (ranging from 5 to 8 s) occurred significantly earlier compared with MAP (from 10 to 12 s). No subjects experienced syncope during acute hypotension. We conclude that CA is preserved during LBNP, superimposed with transient systemic hypotension, despite the decrease in V MCA associated with sustained central hypovolemia in normal healthy individuals. This preserved CA is vital for the prevention of orthostatic syncope.

KW - Blood flow velocity

KW - Cerebral oxygenation

KW - Lower body negative pressure

KW - Sympathetic nerve activity

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