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Loss of cerebro-vascular autoregulation during head-up tilt.

Clark CL, Evans JE, Leonelli FM, Patwardhan AB, Knapp CF.

FASEB J. 1999 Mar 15; 13: A1049.

University of Kentucky, Lexington 40506, USA.

The pathophysiology of neurocardiogenic syncope(NCS), a condition characterized by episodic orthostatic intolerance, remains unclear. It is unknown whether an abnormal regulation of cerebral blood flow(CBF) contributes to the pathophysiology of NCS. We compared changes in the correlation between cerebro-vascular resistance(CVR) and blood pressure(BP) in a group of controls(C) and NCS patients(PTS) during head-up tilt (HUT). Four C and four NCS PTS were studied supine (20 min) and during 30 min 80 degrees HUT. Control subjects maintained Blood Pressure(BP) throughout HUT, while PTS became syncopal at 11 +/- 6 min. Both BP(Finapres) and CBF(Transcranial Doppler) were continuously monitored. Pulsatility Index(PI) of CBF was calculated as an index of CVR. The relationship between Mean BP(MBP) and PI was quantified using cross correlation(CC), computed from 90 second data segments taken at rest(R), beginning(S1) and end(S2) of HUT. Group and HUT effects were tested using 2 factor ANOVA. The PTS showed a significant (p<.05) increase in the magnitude of CC between MBP and PI during S2. There was also a significant increase in CC between R and S2 time segments for both groups. Spectral powers confirmed oscillations within MBP and PI at same frequencies. Our findings suggest that the normal response to HUT is a progressive increase in cerebro-vascular resistance, in keeping with an increase in sympathetic mediated vasoconstriction similar to that observed in peripheral circulation. This response, particularly marked in NCS PTS, overrides the compensatory vasodilatation which is expected in an autoregulating vascular bed.

Publication Types:
  • Meeting Abstracts
Keywords:
  • Blood Pressure
  • Blood Vessels
  • Cerebral Arteries
  • Cerebrovascular Circulation
  • Homeostasis
  • Humans
  • Middle Cerebral Artery
  • Syncope, Vasovagal
  • Vascular Resistance
  • Vasoconstriction
Other ID:
  • 20603648
UI: 102194958

From Meeting Abstracts




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