Transcranial doppler sonography during acute 80°head-down tilt (HDT) for the assessment of cerebral autoregulation in humans

Cerebrovascular hemodynamics during postural changes have been sparsely investigated despite the fact that abnormal responses may contribute to the risk of stroke. The aim of this study was to determine the effect of acute 80°head-down tilt (HDT) on Cerebrovascular hemodynamics in humans using transcranial Doppler sonography (TCD). In 13 healthy volunteers (2 female, 11 male, age 19-37 years, mean age 26.8 years) left midcerebral artery blood flow velocities (CBFVs) were continuously monitored using TCD during 180 sec in horizontal position and during 60 sec of 80°HDT. Simultaneously, systolic, diastolic, mean CBFVs, pulsatility index (PI), heart rate, beat- to-beat blood pressure (BP) and transcutaneous pCO₂ were measured. In five volunteers, the procedure was repeated the next day to test the repeatability of the results. Mean BP increased slightly, but not significantly during tilt (from 80.5± 7.7 mmHg to 85.9± 14.1 mmHg; p> 0.05). Heart 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 pCO₂ was within physiological ranges during the whole procedure (mean pCO₂ minimum 39.5± 2.9 mmHg, mean pCO₂ maximum 42.2±3.3 mmHg). Mean CBFV did not change significantly during tilt (from 70.1±19.1 cmsec^-1 to 66.6±14.1 cm sec^-1; p > 0.05). PI, however, increased significantly with a more pronounced increase during the first 20 sec than the last 40 sec of tilt (PI(supine) 0.92 ± 0.11; PI(tilt(0-20sec)) 1.15 ± 0.18; PI(tilt(21-60sec)) 1.03 ± 0.16; p = 0.001; p = 0.017). The HDT results were found to be reproducible in the five volunteers. During 80°-HDT mean BP and pCO₂ did not change significantly. This observation combined with the significant decrease in heart rate during the first 20 sec of HDT, suggests that there is no sympathetic activation. The significant PI increase during HDT indicates a vasoconstriction of the cerebral resistance vessels. We assume that this vasoconstriction is due to the myogenic mechanism of cerebrovascular autoregulation triggered by a rapid, passive intracranial blood volume influx during HDT.