Medical Journals

Cerebral Autoregulation is Preserved During Orthostatic Stress Superimposed with Systemic Hypotension.

Authors:
  • Guo Hong
  • Tierney Nancy
  • Schaller Frederic
  • Raven Peter B
  • Smith Scott A
  • Shi Xiangrong

From: Department of Integrative Physiology, University of North Texas Health Science Center, 3500 Camp Bowie Boulevard, Fort Worth, TX 76107, USA.

Journal of applied physiology (Bethesda, Md. : 1985)

  • Publish Date: Jun 2006
  • ISSN: 8750-7587
  • Volume: 100
  • Issue: 6
  • Pages: 1785-92
  • Medium: Print
  • Language: English
  • Citation (JAMA): Guo Hong, Tierney Nancy, Schaller Frederic, et al. Cerebral Autoregulation is Preserved During Orthostatic Stress Superimposed with Systemic Hypotension.. J. Appl. Physiol. Jun 2006;100:1785-92

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 (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.

Mesh Headings (Keywords): Adult, Blood Flow Velocity, Blood Pressure, Cardiac Output, Cerebral Cortex, Hemodynamics, Homeostasis, Humans, Hypocapnia, Hypotension, Hypotension, Orthostatic, Hypovolemia, Lower Body Negative Pressure, Male, Sympathetic Nervous System, Syncope


Check for Full Text / PubMed Unique Identifier (PMID): 16424075


This abstract is part of PubMed, a service of the U.S. National Library of Medicine. PubMed includes more than 17 million citations from MEDLINE and other life science journals for biomedical articles. See Copyright and Disclaimers.

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The data herein was last updated on July 8th, 2008 and may not reflect the most current and accurate data available from NLM.


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