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Cerebral Autoregulation (cerebral + autoregulation)
Selected AbstractsRegional cerebral blood flow autoregulation in patients with fulminant hepatic failureLIVER TRANSPLANTATION, Issue 6 2000Fin Stolze Larsen The absence of cerebral blood flow autoregulation in patients with fulminant hepatic failure (FHF) implies that changes in arterial pressure directly influence cerebral perfusion. It is assumed that dilatation of cerebral arterioles is responsible for the impaired autoregulation. Recently, frontal blood flow was reported to be lower compared with other brain regions, indicating greater arteriolar tone and perhaps preserved regional cerebral autoregulation. In patients with severe FHF (6 women, 1 man; median age, 46 years; range, 18 to 55 years), we tested the hypothesis that perfusion in the anterior cerebral artery would be less affected by an increase in mean arterial pressure compared with the brain area supplied by the middle cerebral artery. Relative changes in cerebral perfusion were determined by transcranial Doppler,measured mean flow velocity (Vmean), and resistance was determined by pulsatility index in the anterior and middle cerebral arteries. Cerebral autoregulation was evaluated by concomitant measurements of mean arterial pressure and Vmean in the anterior and middle cerebral arteries during norepinephrine infusion. Baseline Vmean was lower in the brain area supplied by the anterior cerebral artery compared with the middle cerebral artery (median, 47 cm/s; range, 21 to 62 cm/s v 70 cm/s; range 43 to 119 cm/s, respectively; P < .05). Also, vascular resistance determined by pulsatility index was greater in the anterior than middle cerebral artery (median, 1.02; range 1.00 to 1.37 v 0.87; range 0.75 to 1.48; P < .01). When arterial pressure was increased from 84 mm Hg (range 57 to 95 mm Hg) to 115 mm Hg (range, 73 to 130 mm Hg) during norepinephrine infusion, Vmean remained unchanged in 2 patients in the anterior cerebral artery, whereas it increased in the middle cerebral artery in all 7 patients. In the remaining patients, Vmean increased approximately 25% in both the anterior and middle cerebral arteries. Thus, this study could only partially confirm the hypothesis that autoregulation is preserved in the brain regions supplied by the anterior cerebral artery in patients with FHF. Although the findings of this small study need to be further evaluated, one should consider that autoregulation may be impaired not only in the brain region supplied by the middle cerebral artery, but also in the area corresponding to the anterior cerebral artery. [source] Impairment of cerebral autoregulation in diabetic patients with cardiovascular autonomic neuropathy and orthostatic hypotensionDIABETIC MEDICINE, Issue 2 2003B. N. Mankovsky Abstract Aims Impaired cerebrovascular reactivity and autoregulation has been previously reported in patients with diabetes mellitus. However, the contribution of cardiovascular diabetic autonomic neuropathy and orthostatic hypotension to the pathogenesis of such disturbances is not known. The purpose of this study was to evaluate cerebral blood flow velocity in response to standing in patients with diabetes and cardiovascular autonomic neuropathy with or without orthostatic hypotension. Methods We studied 27 patients with diabetes,eight had cardiovascular autonomic neuropathy and orthostatic hypotension (age 46.4 ± 13.5 years, diabetes duration 25.0 ± 11.0 years), seven had autonomic neuropathy without hypotension (age 47.3 ± 12.7 years, diabetes duration 26.4 ± 12.1 years), and 12 had no evidence of autonomic neuropathy (age 44.1 ± 13.8 years, diabetes duration 17.1 ± 10.2 years),and 12 control subjects (age 42.6 ± 9.7 years). Flow velocity was recorded in the right middle cerebral artery using transcranial Doppler sonography in the supine position and after active standing. Results Cerebral flow velocity in the supine position was not different between the groups studied. Active standing resulted in a significant drop of mean and diastolic flow velocities in autonomic neuropathy patients with orthostatic hypotension, while there were no such changes in the other groups. The relative changes in mean flow velocity 1 min after standing up were ,22.7 ± 16.25% in patients with neuropathy and orthostatic hypotension, +0.02 ± 9.8% in those with neuropathy without hypotension, ,2.8 ± 14.05% in patients without neuropathy, and ,9.2 ± 15.1% in controls. Conclusions Patients with diabetes and cardiovascular autonomic neuropathy with orthostatic hypotension show instability in cerebral blood flow upon active standing, which suggests impaired cerebral autoregulation. [source] Regulation of cerebral blood flow in mammals during chronic hypoxia: a matter of balanceEXPERIMENTAL PHYSIOLOGY, Issue 2 2010Philip N. Ainslie Respiratory-induced changes in the partial pressures of arterial carbon dioxide and oxygen play a major role in cerebral blood flow (CBF) regulation. Elevations in (hypercapnia) lead to vasodilatation and increases in CBF, whereas reductions in (hypocapnia) lead to vasoconstriction and decreases in CBF. A fall in (hypoxia) below a certain threshold (<40,45 mmHg) also produces cerebral vasodilatation. Upon initial exposure to hypoxia, CBF is elevated via a greater relative degree of hypoxia compared with hypocapnia. At this point, hypoxia-induced elevations in blood pressure and loss of cerebral autoregulation, stimulation of neuronal pathways, angiogenesis, release of adenosine, endothelium-derived NO and a variety of autocoids and cytokines are additional factors acting to increase CBF. Following 2,3 days, however, the process of ventilatory acclimatization results in a progressive rise in ventilation, which increases and reduces , collectively acting to attenuate the initial rise in CBF. Other factors acting to lower CBF include elevations in haematocrit, sympathetic nerve activity and local and endothelium-derived vasoconstrictors. Hypoxia-induced alterations of cerebrovascular reactivity, autoregulation and pulmonary vascular tone may also affect CBF. Thus, the extent of change in CBF during exposure to hypoxia is dependent on the balance between the myriad of vasodilators and constrictors derived from the endothelium, neuronal innervations and perfusion pressure. This review examines the extent and mechanisms by which hypoxia regulates CBF. Particular focus will be given to the marked influence of hypoxia associated with exposure to high altitude and chronic lung disease. The associated implications of these hypoxia-induced integrative alterations for the regulation of CBF are discussed, and future avenues for research are proposed. [source] Remifentanil and the brainACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 3 2008V. FODALE Background and aim: Remifentanil is an ultra-short-acting opioid, increasingly used today in neuroanesthesia and neurointensive care. Its characteristics make remifentanil a potentially ideal agent, but previous data have cast a shadow on this opioid, supporting potentially toxic effects on the ischemic brain. The aim of the present concise review is to survey available up-to-date information on the effects of remifentanil on the central nervous system. Method: A MEDLINE search within the past seven years for available up-to-date information on remifentanil and brain was performed. Results: Concise up-to-date information on the effects of remifentanil on the central nervous system was reported, with a particular emphasis on the following topics: cerebral metabolism, electroencephalogram, electrocorticography, motor-evoked potentials, regional cerebral blood flow, cerebral blood flow velocity, arterial hypotension and hypertension, intracranial pressure, cerebral perfusion pressure, cerebral autoregulation, cerebrovascular CO2 reactivity, cerebrospinal fluid, painful stimulation, analgesia and hyperalgesia, neuroprotection, neurotoxicity and hypothermia. Conclusion: The knowledge of the influence of remifentanil on brain functions is crucial before routine use in neuroanesthesia to improve anesthesia performance and patient safety as well as outcome. [source] Regional cerebral blood flow autoregulation in patients with fulminant hepatic failureLIVER TRANSPLANTATION, Issue 6 2000Fin Stolze Larsen The absence of cerebral blood flow autoregulation in patients with fulminant hepatic failure (FHF) implies that changes in arterial pressure directly influence cerebral perfusion. It is assumed that dilatation of cerebral arterioles is responsible for the impaired autoregulation. Recently, frontal blood flow was reported to be lower compared with other brain regions, indicating greater arteriolar tone and perhaps preserved regional cerebral autoregulation. In patients with severe FHF (6 women, 1 man; median age, 46 years; range, 18 to 55 years), we tested the hypothesis that perfusion in the anterior cerebral artery would be less affected by an increase in mean arterial pressure compared with the brain area supplied by the middle cerebral artery. Relative changes in cerebral perfusion were determined by transcranial Doppler,measured mean flow velocity (Vmean), and resistance was determined by pulsatility index in the anterior and middle cerebral arteries. Cerebral autoregulation was evaluated by concomitant measurements of mean arterial pressure and Vmean in the anterior and middle cerebral arteries during norepinephrine infusion. Baseline Vmean was lower in the brain area supplied by the anterior cerebral artery compared with the middle cerebral artery (median, 47 cm/s; range, 21 to 62 cm/s v 70 cm/s; range 43 to 119 cm/s, respectively; P < .05). Also, vascular resistance determined by pulsatility index was greater in the anterior than middle cerebral artery (median, 1.02; range 1.00 to 1.37 v 0.87; range 0.75 to 1.48; P < .01). When arterial pressure was increased from 84 mm Hg (range 57 to 95 mm Hg) to 115 mm Hg (range, 73 to 130 mm Hg) during norepinephrine infusion, Vmean remained unchanged in 2 patients in the anterior cerebral artery, whereas it increased in the middle cerebral artery in all 7 patients. In the remaining patients, Vmean increased approximately 25% in both the anterior and middle cerebral arteries. Thus, this study could only partially confirm the hypothesis that autoregulation is preserved in the brain regions supplied by the anterior cerebral artery in patients with FHF. Although the findings of this small study need to be further evaluated, one should consider that autoregulation may be impaired not only in the brain region supplied by the middle cerebral artery, but also in the area corresponding to the anterior cerebral artery. [source] Dynamic cerebral autoregulation in healthy adolescentsACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 4 2002M. S. Vavilala Background: There is little information on the limits of cerebral autoregulation and the autoregulatory capacity in children. The aim of this study was to compare dynamic cerebral autoregulation between healthy adolescents and adults. Methods: Seventeen healthy volunteers 12,17 years (n = 8) and 25,45 years (n = 9) were enrolled in this study. Bilateral mean middle cerebral artery flow velocities (Vmca; (cm/s)) were measured using transcranial Doppler ultrasonography (TCD). Mean arterial blood pressure (MAP) and end-tidal carbon dioxide were measured continuously during dynamic cerebral autoregulation studies. Blood pressure cuffs were placed around both thighs and inflated to 30 mmHg above the systolic blood pressure for 3 min and then rapidly deflated, resulting in transient systemic hypotension. The change of Vmca to change in MAP constitutes the autoregulatory response, and the speed of this response was quantified using computer model parameter estimation. The dynamic autoregulatory index (ARI) was averaged between the two sides. Results: Adolescents had significantly lower ARI (3.9 ± 2.1 vs. 5.3 ± 0.8; P=0.05), and higher Vmca (75.2 ± 15.2 vs. 57.6 ± 15.0; P<0.001) than adults. Conclusion: The autoregulatory index is physiologically lower in normal adolescents 12,17 years of age than in adults. [source] Altered free radical metabolism in acute mountain sickness: implications for dynamic cerebral autoregulation and blood,brain barrier functionTHE JOURNAL OF PHYSIOLOGY, Issue 1 2009D. M. Bailey We tested the hypothesis that dynamic cerebral autoregulation (CA) and blood,brain barrier (BBB) function would be compromised in acute mountain sickness (AMS) subsequent to a hypoxia-mediated alteration in systemic free radical metabolism. Eighteen male lowlanders were examined in normoxia (21% O2) and following 6 h passive exposure to hypoxia (12% O2). Blood flow velocity in the middle cerebral artery (MCAv) and mean arterial blood pressure (MAP) were measured for determination of CA following calculation of transfer function analysis and rate of regulation (RoR). Nine subjects developed clinical AMS (AMS+) and were more hypoxaemic relative to subjects without AMS (AMS,). A more marked increase in the venous concentration of the ascorbate radical (A,,), lipid hydroperoxides (LOOH) and increased susceptibility of low-density lipoprotein (LDL) to oxidation was observed during hypoxia in AMS+ (P < 0.05 versus AMS,). Despite a general decline in total nitric oxide (NO) in hypoxia (P < 0.05 versus normoxia), the normoxic baseline plasma and red blood cell (RBC) NO metabolite pool was lower in AMS+ with normalization observed during hypoxia (P < 0.05 versus AMS,). CA was selectively impaired in AMS+ as indicated both by an increase in the low-frequency (0.07,0.20Hz) transfer function gain and decrease in RoR (P < 0.05 versus AMS,). However, there was no evidence for cerebral hyper-perfusion, BBB disruption or neuronal,parenchymal damage as indicated by a lack of change in MCAv, S100, and neuron-specific enolase. In conclusion, these findings suggest that AMS is associated with altered redox homeostasis and disordered CA independent of barrier disruption. [source] Autoregulation of the cerebral circulation during sleep in newborn lambsTHE JOURNAL OF PHYSIOLOGY, Issue 3 2005Daniel A. Grant Autoregulation is a vital protective mechanism that maintains stable cerebral blood flow as cerebral perfusion pressure changes. We contrasted cerebral autoregulation across sleep,wake states, as little is known about its effectiveness during sleep. Newborn lambs (n= 9) were instrumented to measure cerebral blood flow (flow probe on the superior sagittal sinus) and cerebral perfusion pressure, then studied during active sleep (AS), quiet sleep (QS) and quiet wakefulness (QW). We generated cerebral autoregulation curves by inflating an occluder cuff around the brachiocephalic artery thereby lowering cerebral perfusion pressure. Baseline cerebral blood flow was higher (P < 0.05) and cerebral vascular resistance lower (P < 0.05) in AS than in QW (76 ± 8% and 133 ± 15%, respectively, of the AS value, mean ±s.d.) and in QS (66 ± 11% and 158 ± 30%). The autoregulation curve in AS differed from that in QS and QW in three key respects: firstly, the plateau was elevated relative to QS and QW (P < 0.05); secondly, the lower limit of the curve (breakpoint) was higher (P < 0.05) in AS (50 mmHg) than QS (45 mmHg); and thirdly, the slope of the descending limb below the breakpoint was greater (P < 0.05) in AS than QS (56% of AS) or QW (56% of AS). Although autoregulation functions in AS, the higher breakpoint and greater slope of the descending limb may place the brain at risk for vascular compromise should hypotension occur. [source] Quantitative study on cerebral blood volume determined by a near-infrared spectroscopy during postural change in childrenACTA PAEDIATRICA, Issue 3 2009Yasuko Taeja Kim Abstract Aim: To investigate changes in cerebral blood volume during standing in healthy children with or without abnormal cardiovascular responses. Methods: We studied 53 children (age, 10,15 years). Cerebral oxygenated haemoglobin (oxy-Hb) and deoxygenated Hb (deoxy-Hb) were non-invasively and continuously measured using near-infrared spectroscopy (NIRS) (NIRO 300, Hamamatsu Photomedics, Shizuoka, Japan) during active standing. Beat-to-beat arterial pressure was monitored by Portapres. Results: Of 49 children with complete data acquisition, 33 had a normal cardiovascular response to the test (Group I) and 16 showed an abnormal response (Group II); nine with instantaneous orthostatic hypotension, three with postural tachycardia syndrome, three with neutrally mediated syncope and one with delayed orthostatic hypotension. At the onset of standing, Group II showed a significantly larger fall of oxy-Hb than Group I did (,2.9 ± 2.8 ,mol/L vs. ,6.4 ± 7.2 ,mol/L, respectively, p < 0.05). During min 1 to 7 of standing, with one exception, changes in oxy-Hb were normally distributed over the level of ,4 ,mol/L in Group I. Group II also showed a significantly marked decrease in oxy-Hb compared to Group I. Decreases in oxy-Hb were not correlated with blood pressure changes. Conclusion: This study shows that precise change in cerebral blood volume caused by orthostatic stress can be determined by NIRS in children in a quantitative manner of NIRS. Children with abnormal circulatory responses to standing showed a significant reduction of oxy-Hb compared with normal counterparts, suggesting impairment of cerebral autoregulation in these children. [source] Importance of calcitonin gene-related peptide, adenosine and reactive oxygen species in cerebral autoregulation under normal and diseased conditionsCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 1-2 2004Hwa Kyoung Shin Summary 1.,Mechanisms regulating cerebral circulation, including autoregulation of cerebral blood flow (CBF), have been widely investigated. Vasodilators such as nitric oxide, prostacyclin, calcitonin gene-related peptide (CGRP) and K+ channel openers are well known to have important roles in the physiological and pathophysiological control of CBF autoregulation. In the present review, the focus is on the mechanism(s) of altered CBF autoregulation after traumatic brain injury and subarachnoid haemorrhage (SAH) and on the effect of adenovirus-mediated transfer of Cu/Zn superoxide dismutase (SOD)-1 in amelioration of impaired CBF autoregulation. 2.,The roles of CGRP and adenosine are particularly emphasized, both being implicated in the autoregulatory vasodilation of the pial artery in response to hypotension. 3.,After fluid percussion injury, production of NADPH oxidase-derived superoxide anion and activation of tyrosine kinase links the inhibition of K+ channels to impaired autoregulatory vasodilation in response to acute hypotension and alterations in CBF autoregulation in rat pial artery. 4.,Subarachnoid haemorrhage during the acute stage causes an increase in NADPH oxidase-dependent superoxide formation in cerebral vessels in association with activated tyrosine phosphorylation-coupled increased expression of gp91phox mRNA and membrane translocation of Rac protein, thereby resulting in a significant reduction of autoregulatory vasodilation. 5.,Fluid percussion injury and SAH-induced overproduction of superoxide anion in cerebral vessels contributes to the impairment of CBF autoregulation and administration of recombinant adenovirus-mediated transfer of the Cu/Zn SOD-1 gene effectively ameliorates the impairment of CBF autoregulation of the pial artery. 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