Jg. Heckmann et al., Transcranial Doppler sonography during acute 80 degrees head-down tilt (HDT) for the assessment of cerebral autoregulation in humans, NEUROL RES, 21(5), 1999, pp. 457-462
Cerebrovascular hemodynamics during postural changes have been sparsely inv
estigated despite the fact that abnormal responses may contribute to the ri
sk of stroke. The aim of this study was to determine the effect of acute 80
degrees head-down tilt (HDT) on cerebrovascular hemodynamics in humans usi
ng transcranial Doppler sonography (TCD). In 13 healthy volunteers (2 femal
e, 11 male, age 19-37 years, mean age 26.8 years) left midcerebral artery b
lood flow velocities (CBFVs) were continuously monitored using TCD during 1
80 sec in horizontal position and during 60 sec of 80 degrees HDT. Simultan
eously, systolic, diastolic, mean CBFVs, pulsatility index (PI) heart rate,
beat-to-beat blood pressure (BP) and transcutaneous pCO(2) were measured.
In five volunteers, the procedure was repeated the next day to test the rep
eatability of the results. Mean BP increased slightly, but not significantl
y during tilt (from 80.5 +/- 7.7 mmHg to 85.9 +/- 14.1 mmHg; p > 0.05). Hea
rt rate decreased significantly during the first 20 sec of HDT (from 66.8 /- 9.9 min(-1) to 60 +/- 11 min(-1) p < 0.05). Transcutaneous pCO(2) was wi
thin physiological ranges during the whole procedure (mean pCO(2) minimum 3
9.5 +/- 2.9 mmHg, mean pCO(2) max,mum 42.2 +/- 3.3 mmHg). Mean CBFV did not
change significantly during tilt (from 70.1 +/- 79.1 cm sec(-1) to 66.6 +/
- 14.1 cm sec(-1); p > 0.05). PI, however, increased significantly with a m
ore pronounced increase during the first 20 sec than the last 40 sec of til
t (PIsupine 0.92 +/- 0.11; PItilt(0-20 sec) 1.15 +/- 0.18; PItilt(21-60 sec
) 1.03 +/- 0.16; p = 0.001; p = 0017). The HDT results were found to be rep
roducible in the five volunteers. During 80 degrees-HDT mean BP and pCO(2)
did nor change significantly. This observation combined with the significan
t decrease in heart rate during the first 20 sec of HDT, suggests that ther
e is no; sympathetic activation. The significant PI increase during HDT ind
icates a vasoconstriction of the cerebral resistance vessels. We assume tha
t this vasoconstriction is due to the myogenic mechanism of cerebrovascular
autoregulation triggered by a rapid, passive intracranial blood volume inf
lux during HDT.