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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 N^ω-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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Transcranial Doppler (TCD) determined cerebral blood flow velocity and laser Doppler flowmetry (LDF) measured cortical perfusion were simultaneously assessed during hypotensive haemorrhage in 15 anaesthetized rabbits. Systolic (Fsys), diastolic (Fdia) and mean (Fmean) blood flow velocities were recorded into the intracranial internal carotid (ICA) and basilar artery (BA). Resistance (RI = Fsys-Fdia/Fsys) and pulsatility (PI = Fsys-Fdia/Fmean) indices were calculated. Step decreases of 10 mmHg of mean arterial pressure (MAP) from 80 to less than 30 mmHg provoked a fall of LDF signal below 50 mmHg. Blood velocities decreased into BA below 40 mmHg, and below 50 mmHg into ICA indicating regional differences in cerebral autoregulation. Cortical resistances (resLDF = MAP/LDF) fell below 60 mmHg whereas RI and PI increased when MAP decreased into BA below 40 mmHg and ICA below 50 mmHg. A weak correlation was found between Fmean and LDF (BA: r = 0.55, P < 0.01 and ICA = 0.46, P < 0.01). Both RI and PI were poorly correlated to resLDF into BA (RI-resLDF: r = -0.39, P < 0.01; PI-resLDF: r = -0.39, P < 0.01) and ICA (RI-resLDF: r = -0.18, ns; PI-resLDF: r = -0.22, ns). Pulse pressure (systolic-diastolic pressure) correlated with RI (ICA: r = -0.62, P < 0.001; BA: r = -0.61, P < 0.001) and PI (ICA: r = -0.61, P < 0.001; BA: r = -0.62, P < 0.001). In conclusion, during haemorrhagic shock, TCD correlates with LDF and indicates regional differences in autoregulatory settings. However, Doppler indices do not reflect the changes in cerebral resistances because they are influenced by the changes in pulsatile pressure.

The purpose of this work was to show that regulation of the blood flow to the cochlea by the sympathetic nervous system occurs in humans at the level of the cochlear microcirculation during increases in blood pressure and that its involvement depends on the pressure level. Eight anaesthetized patients undergoing tympanoplasty for hearing disease took part in a pharmacological protocol of stimulation and inhibition of the autonomic nervous system (ANS) to provide variations in systolic blood pressure (BPS) and cochlear blood flow (CBF). The CBF was measured by laser-Doppler flowmetry. Changes in autonomic nerve activity were brought about by changes in baroreceptor activity (BR) initiated by the injection of an alpha adrenergic agent before and after sympathetic and parasympathetic blockade. The CBF variations (delta CBF) were plotted against BPS increases at each stage of the ANS inhibition. The BR diminished significantly after alpha blockade, after alpha and beta blockade, and after alpha and beta blockade and atropine, by 50% (P < 0.01), 29% (P < 0.05), and 95% (P < 0.001) respectively. The BPS increased significantly (P < 0.01) by 36 (SD 9)%, 47 (SD 1)%, and 67 (SD 16)% respectively. The CBF response to an increase in BPS exhibited two opposing variations in the patients: CBF decreased significantly in one group, and increased significantly in the other group. In both groups, delta CBF decrease and delta CBF increase, respectively, were significant after ANS blockade; even so the decrease and increase, respectively, levelled off at BPS around 160 mmHg before ANS blockade. For BPS below 160 mmHg, correlations between delta CBF and BPS were significant before inhibition and after inhibition of ANS. For BPS below 160 mmHg, BPS and delta CBF were not correlated before inhibition of ANS, and were significantly correlated after inhibition of ANS. For BPS below 160 mmHg, CBF response to the BPS increase was the same before and after ANS blockade, i.e. ANS control did not predominate: even so, for BPS above 160 mmHg, the CBF response to BPS increase was different before and after ANS blockade: CBF varied significantly after ANS blockade as it varied for BPS below 160 mmHg, while it remained constant before ANS blockade that elicited ANS control of CBF. In conclusion, sympathetic nerve regulation via its vasomotor tone at the level of cochlear microcirculation occurred markedly when the blood pressure was above 160 mmHg; the autonomic nervous system would appear to control the cochlear blood flow against large variations in blood flow in response to hypertensive phenomena.

Since general anesthesia has been shown to attenuate endothelium-dependent vasodilation, it was of interest to verify whether general anesthesia would modify skin vasodilation in response to local pressure application, which is endothelium dependent. To study the effect of general anesthesia on pressure-induced vasodilation development, we examined the effects of low- and high-dose isoflurane. Skin blood flow was measured by laser Doppler flowmetry during 11.1 Pa s^–1 increases in locally applied pressure in anesthetized rats treated with low or high doses of isoflurane. Following the administration of low doses of isoflurane, skin blood flow increased from baseline, with increasing local pressure application (+37 ± 10% at 2.0 kPa). The increase in skin blood flow was absent in rats treated with high doses (–20 ± 5% at 2.0 kPa), even when the anesthesia-induced hypotension was corrected by gelofusine infusion (–20 ± 10% at 2.0 kPa). Whereas sodium-nitroprusside-induced vasodilation developed following low and high doses of isoflurane, acetylcholine-induced vasodilation was impaired with high doses compared to low doses. These data show that pressure-induced vasodilation is abolished with high doses of anesthetics. It is not the anesthesia-induced hypotension, but the depth of anesthesia, which can lead to the disappearance of pressure-induced vasodilation by an alteration in endothelial function.

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