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Objective: The aim of the present study was to determine whether cerebral autoregulation is absent in patients with end-stage liver disease., Design: A prospective physiological study., Methods: Thirty patients, 15 female (median age 50 years, range 33-74), with biopsy-proven cirrhosis (4 Child-Pugh class B, 26 Child-Pugh class C), had their cerebral perfusion evaluated using mean flow velocity (Vmean) in the middle cerebral artery as measured by transcranial Doppler sonography. Mean arterial pressure (MAP) was raised by intravenous noradrenaline (5-30 microg/min). Nine patients had no clinical signs of hepatic encephalopathy (HE), three were in HE stage 1, four in HE stage 2, four in HE stage 3 and ten in HE stage 4, respectively., Results: Cerebral autoregulation was impaired in 13 patients, as Vmean increased from 47 (26-88) to 60 (36-109) cm/s during a rise in MAP from 61 (47-99) to 82 (65-121) mmHg. Vmean remained unchanged (preserved cerebral autoregulation) at 56 (30-119) cm/s in 17 patients when MAP was raised from 74 (59-90) to 95 (81-129) mmHg. Cerebral autoregulation was lost in 8/10 patients with HE stage 4 and only in 2/9 patients without HE (P = 0.023). The duration of HE stage 1-4 before the autoregulation study was identical for patients with preserved cerebral autoregulation compared to patients with impaired cerebral autoregulation, 5 (2-30) versus 6 (2-35) days, respectively. Baseline values of MAP were significantly lower in patients with no cerebral autoregulation compared to patients with preserved cerebral autoregulation, 61 (47-99) versus 74 (59-90) mmHg (P = 0.012). All other baseline values in the two groups were similar, including PaCO2, albumin, bilirubin, international normalization ratio, galactose elimination capacity, Child-Pugh class and age., Conclusion: Cerebral autoregulation is preserved in most patients with end-stage liver disease. In patients with hepatic encephalopathy and low MAP, however, cerebral autoregulation is impaired.