Dissociated cerebral vasoparalysis in acute liver failure: A hypothesis of gradual cerebral hyperaemia

Background/Aims: Normally, cerebral blood flow responds to changes in the arterial carbon dioxide tension (PaCO 2) but not to changes in mean arterial pressure, commonly referred to as the cerebral CO 2-reactivity and autoregulation. In patients with fulminant hepatic failure and in the rat with thioacetamide-induced liver failure, autoregulation is absent, presumably due to cerebral vasoparalysis. Since also CO 2-reactivity may then be compromised, it was studied in patients with fulminant hepatic failure and rats with thioacetamide-induced liver failure. Methods: In ten patients (median age 32 (range 20–48) years)) and in ten age-matched volunteers, cerebral perfusion was evaluated by transcranial Doppler assessed mean flow velocity (V mean) in the middle cerebral artery during hypo- and hyper-capnia. In six rats with liver failure and in six control rats, cerebral blood flow was measured repeatedly by the intracarotid 133Xenon injection technique. Results: In the patients and volunteers, PaCO 2 was lowered from 33 (23–44) to 28 (23–39) mmHg by hypocapnia and raised to 40 (34–48) mmHg by hypercapnia or 5% CO 2 inhalation. During hypocapnia, the CO 2-reactivity did not differ significantly between patients and volunteers, 4.0 (1.1–7.4) vs. 3.0 (1.7–5.0)% mmHg −1, while it was reduced during hypercapnia in the patients, 2.2 (1.8–5.2) vs. 4.6 (3.0–8.0)% mmHg −1 ( p