The role of nitric oxide (NO) in cerebral autoregulation is controversial. The purpose of this study was to compare the effects on the lower limit of the cortical cerebral autoregulation of the inhibition of NO synthesis by Nω-nitro-L-arginine (L-NNA) infusion to saline and phenylephrine in pentobarbital-anaesthetized rats. Variations of the cortical cerebral blood flow (CBF), the cortical cerebrovascular resistances, the mean arterial pressure and the lower limit of cerebral autoregulation were compared in three groups: a group pre-treated with L-NNA (n = 8), a group pretreated with saline (n = 8) and a group pretreated with phenylephrine (n = 5). The laser-Doppler flowmetry continuously measured CBF. Controlled haemorrhage was performed after the intravenous infusion of L-NNA, saline, or phenylephrine. The lower limit of cerebral autoregulation of each rat was computed by the least-squares method. The lower limit of cerebral autoregulation was significantly higher after L-NNA infusion (74 ± 5 mm Hg) than after saline (43 ± 3 mm Hg; p < 0.01) or phenylephrine infusions (52 ± 5 mm Hg; p < 0.05). In conclusion, the role of NO on the cerebral autoregulation has been controversial; our results confirm the hypothesis that NO exerts a significant role in maintaining the lower limit of cerebral autoregulation in pentobarbital-anaesthetized rats.
The effect of head-upright tilting on the rate of cerebral autoregulation was studied in 12 healthy volunteers (nine men and three women; age range 20-36 years). The dynamics of cerebral autoregulation was determined from the rate of change in cerebral resistance (RoR) during a drop in arterial blood pressure induced by rapid deflation of a 3-min ischaemic thigh cuff and from the ratio of changes in cerebral blood flow and arterial blood pressure (CAI) during the recovery period after the drop in arterial blood pressure. The test was performed supine and with 40 degrees head-up tilt (40 degrees HUT). Middle cerebral artery mean blood flow velocity was measured by transcranial Doppler simultaneously with peripheral arterial blood pressure using Finapres. The thigh cuff deflation induced a larger drop in arterial pressure during 40 degrees HUT [median -28% (25 percentile -36, 75 percentile -19)] than in the supine position [-16% (-23, -15)] (P < 0.01) and in cerebral resistance [supine: -12% (-15, -6); 40 degrees HUT: -15% (-20, -12); P < 0.05]. There was no significant change in RoR [15% s-1 (12, 15)] and CAI [1.9 (1.5, 3.1)] measured supine and during 40 degrees HUT [RoR: 13% s-1 (12, 15); CAI: 1.3 (0.99, 1.9)]. During the drop in arterial pressure, the relationship between arterial blood pressure and systolic peak-to-peak interval exhibited an hysteresis loop, indicating a cardiopulmonary and/or baroreflex activation that was not observed with cerebral resistance. The rate of autoregulation is an intrinsic property of the cerebral vascular bed and is not affected by the vasodilator state in the range of arterial blood pressure changes induced by the tight cuff method.
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