Background. In the healthy state, dynamic cerebral autoregulatory function is enhanced during acute vasopressor-induced hypertension, which may comprise a neuroprotective mechanism during increases in blood pressure by preventing cerebral hyperperfusion and subsequent vasogenic cerebral oedema (1). Given that sepsis may be associated with vasogenic cerebral oedema (2), we sought to investigate whether this adaptive enhancement of dynamic cerebral autoregulation during hypertensionis affected by lipopolysaccharide (LPS) infusion, a human-experimental model of the systemic inflammatory response during the very early stages of sepsis.Methods. Nine healthy male volunteers aged 23 (mean; SD, 2) were included. Dynamic cerebral autoregulation was assessed by transfer function analysis of spontaneous oscillations between mean arterial blood pressure (MAP) and middle cerebral artery blood flow velocity (MCAv) in the low frequency range (0.07-0.20 Hz) using transcranial Doppler ultrasound (3). This was performed during normotension and noradrenaline-induced hypertension with an intended MAP-increase of ~30 mmHg both before and after a four-hour LPS infusion (total dose, 2 ng kg-1). The subjects were poikilopcapnic throughout. Data were analysed by Wilcoxon’s signed-rank test and p-values were adjusted by Holm’s sequential Bonferroni correction.Results. LPS induced a systemic inflammatory response which was associated with fever and hyperventilation.A concurrent decrease in gain and an increase in phase, indicating improved dynamic autoregulation, were present (Table). Before LPS, hypertension was associated with a decrease in gain with no effect on phase, whereas neither was affected by hypertension following LPS infusion (Table). Conclusion. Dynamic autoregulation is likely enhanced by both fever and hyperventilation after LPS infusion (4). The present findings suggest that acute noradrenaline-induced hypertension does cause any further enhancement in dynamic autoregulation under these circumstances. The latter may be an early sign of underlying cerebrovascular dysfunction, and thus be relevant to the neuropathology of sepsis.