Cerebral haemodynamic response to acute intracranial hypertension induced by head-down tilt


Bosone D., Ozturk V., Roatta S., Cavallini A., Tosi P., Micieli G.

FUNCTIONAL NEUROLOGY, vol.19, no.1, pp.31-35, 2004 (SCI-Expanded) identifier

  • Publication Type: Article / Article
  • Volume: 19 Issue: 1
  • Publication Date: 2004
  • Journal Name: FUNCTIONAL NEUROLOGY
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.31-35
  • Keywords: cerebral circulation, head-down tilt, posture, sympathetic nervous system, MEAN FLOW VELOCITY, PLASMA NOREPINEPHRINE, ORTHOSTATIC STRESS, HUMANS, ARTERY, PRESSURE, AUTOREGULATION, FAILURE
  • Dokuz Eylül University Affiliated: Yes

Abstract

The aim of this study was to evaluate, in a context of general inhibition of the sympathetic nervous system, the cerebral haemodynamic response to -30degrees head-down tilt (HDT), a manoeuvre that produces an increase in intracranial arterial pressure. Nineteen healthy subjects were studied according to the following protocol: 10 min lying in supine position, 10 min HDT, 10 min recovery. Inhibition of the sympathetic system was confirmed by the decrease in heart rate (-3.6 bpm) and arterial blood pressure (-5.9 mmHg, p<0.05) in the late phase of the test. Blood velocity and blood pusatility index initially increased (+3.2 cm s(-1) and +9% respectively, p<0.01) then returned towards baseline before the end of HDT, while the cerebrovascular resistance index (=arterial blood pressure/blood velocity) dropped significantly and remained below control level (-7%, p<0.01) throughout the test. The changes in both these indices were opposite to those reported in several sympathetic activation tests, such as the handgrip and cold pressor tests. Conversely, arterial pressure at cranial level increased during HDT (as it also does during sympathetic activation tests), due to the development of a hydrostatic pressure gradient between heart and brain levels. Therefore, the effects observed on the pulsatility and resistance indices are not secondary to the increase in intracranial arterial pressure. It is suggested that the changes in these cerebrovascular indices are mediated by a reduction of sympathetic tone that presumably involves the cerebral as well as the peripheral vascular bed.