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
Y1 - 2006/6
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 (VMCA) 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 VMCA was associated with a decrease in regional cerebral O2 saturation. However, the percent decrease in VMCA was markedly less than that of CO. This suggests that the magnitude of the change in VMCA (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 VMCA of -20 ± 2, -21 ± 2, -24 ± 25, and -19 ± 2% and regional cerebral O2 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 VMCA 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 VMCA 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 (VMCA) 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 VMCA was associated with a decrease in regional cerebral O2 saturation. However, the percent decrease in VMCA was markedly less than that of CO. This suggests that the magnitude of the change in VMCA (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 VMCA of -20 ± 2, -21 ± 2, -24 ± 25, and -19 ± 2% and regional cerebral O2 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 VMCA 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 VMCA 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
KW - Syncope
UR - http://www.scopus.com/inward/record.url?scp=33744930324&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=33744930324&partnerID=8YFLogxK
U2 - 10.1152/japplphysiol.00690.2005
DO - 10.1152/japplphysiol.00690.2005
M3 - Article
C2 - 16424075
AN - SCOPUS:33744930324
SN - 8750-7587
VL - 100
SP - 1785
EP - 1792
JO - Journal of applied physiology
JF - Journal of applied physiology
IS - 6
ER -