SIMULTANEOUS CEREBROVASCULAR AND CARDIOVASCULAR-RESPONSES DURING PRESYNCOPE

Background and Purpose Presyncope, characterized by symptoms and signs indicative of imminent syncope, can be aborted in many situations bef ore loss of consciousness occurs. The plasticity of cerebral autoregul ation in healthy humans and its behavior during this syncopal prodrome are unclear, although systemic hemodynamic instability has been sugge sted as a key factor in the precipitation of syncope. Using lon er bod y negative pressure (LBNP) to simulate central hypovolemia, we previou sly observed falling mean Bow velocities (MFVs) with maintained mean a rterial blood pressure (MABP). These findings, and recent reports sugg esting increased vascular tone within the cerebral vasculature at pres yncope, cannot be explained by the classic static cerebral autoregulat ion curve; neither san they be totally explained by a recent suggestio n of a rightward shift in this curve. Methods Four male and five femal e healthy volunteers were exposed to presyncopal LBNP to evaluate thei r cerebrovascular and cardiovascular responses by use of continuous ac quisition of MFV from the right middle cerebral artery with transcrani al Doppler sonography, MABP (Finapres), and heart rate (EGG). Results At presyncope, MFV dropped on average by 27.3+/-14% of its baseline va lue (P<.05), while MABP remained at 2.0+/-27% above its baseline level . Estimated cerebrovascular resistance increased during LBNP. The perc entage change from baseline to presyncope in MFV and MABP revealed con sistent decreases in MFV before MABP. Conclusions increased estimated cerebrovascular resistance, falling MFV, and constant MABP are evidenc e of an increase in cerebral vascular tone with falling flow, suggesti ng a downward shift in the cerebral autoregulation curve. Cerebral ves sels may have a differential sensitivity to sympathetic drive or more than one type of sympathetic innervation. Future work to induce dynami c changes in MABP during LBNP may help in assessing the plasticity of the cerebral autoregulation mechanism.