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Departments of 1Integrative Physiology and 2Internal Medicine, University of North Texas Health Science Center, Fort Worth, Texas; 3Department of Physical Therapy, University of Texas Southwestern Medical Center, Dallas, Texas; and 4College of Sports Science, South China Normal University, Guangzhou, China
Submitted 11 June 2005 ; accepted in final form 12 January 2006
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.
blood flow velocity; cerebral oxygenation; lower body negative pressure; sympathetic nerve activity; syncope
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