Sympathetic cardiac influence and arterial blood pressure instability

Previous studies have suggested that sympathetic cardiac blockade enhances baroreflex function, whereas parasympathetic blockade diminishes baroreflex sensitivity and elicits arterial blood pressure (ABP) instability. The aim of this project was to test the hypothesis that sympathetic cardiac blockade was beneficial in maintaining ABP stability during orthostatic challenge. In 8 young healthy subjects, measurements were taken before and after sympathetic cardiac blockade (beta1-adrenoceptor blockade via metoprolol) in combination with or without parasympathetic blockade (atropine) at rest and during lower body negative pressure (LBNP). Arterial blood samples were obtained to evaluate plasma renin activity (PRA) and norepinephrine (NE). Power spectral analyses were performed on heart rate (HR) and ABP variability. LBNP -50 Torr significantly decreased systolic blood pressure (SBP, -6+/-3 mm Hg) and increased PRA (from 0.72+/-0.23 to 1.75+/-0.24 ng ml(-1) h(-1)) and NE (from 1.02+/-0.11 to 2.13+/-0.32 pg ml(-1)). Low frequency (LF, 0.04-0.12 Hz) SBP and diastolic blood pressure (DBP) variability were significantly augmented by LBNP (4.1+/-1.6 vs. 10.8+/-3.0 mm Hg2, and 3.1+/-1.0 vs. 7.9+/-1.9 mm Hg2, respectively). Following metoprolol, arterial baroreflex sensitivity (assessed by the slope of HR interval to SBP during injection with 1 mug kg(-1) phenylephrine) increased significantly (9.9+/-2.2 to 19.6+/-4.1 ms mm Hg(-1)). With beta1-adrenoceptor blockade, LBNP still decreased SBP (-10+/-2 mm Hg) and increased NE, but did not significantly augment PRA (0.59+/-0.22 vs. 1.03+/-0.18 ng ml(-1) h(-1)), or LF SBP and DBP variability (3.3+/-0.6 vs. 5.7+/-1.3 mm Hg2, and 3.1+/-0.7 vs. 5.4+/-1.1 mm Hg2, respectively). The increased PRA during LBNP remained non-significant following metoprolol combined with atropine, whereas the augmented LF SBP (2.6+/-0.7 vs. 9.9+/-2.8 mm Hg2) and DBP (2.5+/-0.7 vs. 11.1+/-3.0 mm Hg2) variability were significantly accentuated compared to both metoprolol alone and control conditions, accompanied by a greater delta SBP (-17+/-7 mm Hg) and significantly diminished baroreflex gain (0.91+/-0.05 ms/mm Hg). These data suggested that removal of sympathetic cardiac influence improved cardiovascular stability as indicated by a diminished LF ABP variability, which was related to an enhanced cardiac responsiveness.     

Cerebrospinal fluid nitrite/nitrate correlated with oxyhemoglobin and outcome in patients with subarachnoid hemorrhage

The findings of various studies reporting temporal changes in CSF total nitrite/nitrate (NOx) levels after subarachnoid hemorrhage (SAH) vary considerably. The study group comprised 10 patients with SAH and 10 control subjects. Total nitrite/nitrate concentration was measured by a vanadium-based assay with the colorimetric Griess reaction. CSF oxyhemoglobin level was assessed by spectrophotometry. After an initial peak (22.6+/-10.1 microM) within first 24 h after SAH, CSF NOx decreased gradually during the period of observation. There was a significant correlation between CSF concentrations of NOx and OxyHb in the entire observation period (R=0.87, p<0.001). When the impact of bleeding into CSF was considered, patients with very good outcome [Glasgow Outcome Scale (GOS)=5] had significantly lower CSF NOx (11.1+/-1.3 microM) than those with worse outcome (GOS<5) (21.8+/-11.2 microM, p<0.01). In conclusion, this study demonstrates that after aneurysm rupture CSF NOx levels correlate with OxyHb. We suggest this as a novel interpretation of other variable findings in relation to NO metabolites in the central nervous system (CNS) post SAH, and hence it could usefully be incorporated into the planning of future studies, correlating NOx with clinical outcome.     

Nonlinear analysis of blood cell flux fluctuations in the rat brain cortex during stepwise hypotension challenge.

Blood flow through a region of interest in the brain cortex (cerebral blood flow (CBF)) as measured by laser-Doppler flowmetry (LDF) shows a complex temporal pattern, which can be either merely random or a manifestation of segmental chaotic dynamics of vasomotion-induced flowmotion in the arterial tree, a deterministic phenomenon; or that of a fractal, self-similar correlation order that emerges from the set of segmental perfusion events on statistical ground. Fractal content (F%) was determined by coarse-graining spectral analysis and their self-similar exponent, H, estimated by bridge-detrended Scaled Windowed Variance (bdSWV) method and a variant of the power Spectral Density method ((low)PSD(w,e)). Chaotic dynamics were assessed by computing the correlation dimension (D(corr)) and the largest Lyapunov exponent (lambda(max)) on unfiltered raw and surrogate datasets. In 10 Sprague-Dawley rats anesthetized by halothane, CBF was measured through the thinned calvarium by the LDF method. Blood pressure (BP) was reduced from 100 to 40 mm Hg in steps of 20 mm Hg maintained for 2 mins by the lower body negative pressure method. Fractal and chaotic patterns coexisted in tissue perfusion. CBF did not show autoregulation. At every BP step, F% remained high (72% to 88%) and was independent of BP. Laser-Doppler flowmetry signals proved to be nonstationary fractional Brownian motions. Their H's by bdSWV and (low)PSD(w,e) (0.29+/-0.006 and 0.25+/-0.012, respectively) were independent of BP. Neither D(corr) nor lambda(max) varied with hypotension. Their values were characteristic of a chaotic system, but surrogate data analysis rendered some of them inconclusive. Hence, CBF fluctuations can be regarded as a robust phenomenon that is not abolished even by sustained hypotension at 40 mm Hg.     

Effect of prolonged head-down bed rest on complex cardiovascular dynamics

We postulated that a change in complex dynamics of the cardiovascular system could be involved in the orthostatic intolerance observed after simulated weightlessness. Supine recordings of 1024 consecutive pulse intervals and systolic blood pressures were obtained on 7 subjects adapted to a 42 day head-down bed rest (day 22 and 42) but also before and 6 days after head-down bed rest (-6 degrees). Coarse graining spectral analysis was used to extract the non-harmonic (fractal) component from each time series. The power spectral densities of this fractal component are inversely proportional to their frequency (1/f beta). We fitted an inverse power law estimate to the fractal component to determine the spectral exponent beta. The complex dynamics of blood pressure and heart rate variability were also analyzed by correlation dimension and non-linear prediction. Bed rest induced orthostatic intolerance in 4 subjects. There was a significant increase in the spectral exponent beta of RR-interval variability during and after head-down bed rest (before: 1.039 +/- 0.090; during: 1.552 +/- 0.080 and 1.547 +/- 0.100; after: 1.428 +/- 0.040). Analysis of the blood pressure dynamics indicated lower correlation dimensions during head-down bed rest and higher coefficients of predictability after head-down bed rest. Complexity alterations of RR-interval and blood pressure variability were not linked with one another during head-down bed rest. These alterations seemed to be correlated with the orthostatic intolerance observed after bed rest. These results suggest a change of the integration level of cardiovascular autonomic regulation.     

Low-dose atropine amplifies cardiac vagal modulation and increases dynamic baroreflex function in humans

It has been previously known that low-dose atropine (LDA) enhances vagal outflow to the heart. To demonstrate the importance of vagal cardiac modulation in arterial blood pressure (ABP) stability, we evaluated the effect of vagal cardiac stimulation with administration of LDA on ABP fluctuation during dynamic hypertensive and hypotensive stimuli. We assessed changes in RR interval (RRI), ABP, power spectral densities of heart rate variability (HRV) and ABP variability, and spontaneous baroreflex sensitivity (BRS) in 16 healthy volunteers before and after administration of LDA (2 microg/kg). Transient hypertension was induced by phenylephrine (2 microg/kg), whereas hypotension was induced by bilateral thigh cuff deflation after a 3-min suprasystolic occlusion. LDA elicited bradycardia and significantly increased high-frequency (HF, 0.15-0.4 Hz) power of HRV and spontaneous BRS, as determined by transfer function analysis. The increase in systolic blood pressure (SBP) after phenylephrine administration was significantly attenuated by LDA (16+/-2 to 11+/-3 mmHg, P<0.005) and was associated with the augmented reflex bradycardia, whereas the decrease in SBP after cuff deflation was not affected (14+/-5 to 13+/-5 mmHg) with the augmented reflex tachycardia. Increases of HF HRV were correlated significantly and negatively with the increased SBP induced by phenylephrine before and after LDA (r=-0.502, P<0.05). These data suggest that the increased vagal cardiac function induced by LDA augments HR buffering effects, and is important in minimizing arterial pressure fluctuation during dynamic hypertensive stimuli.     

Beneficial effect of hydrogen-rich saline on cerebral vasospasm after experimental subarachnoid hemorrhage in rats

Cerebral vasospasm (CV) remains a common and devastating complication in patients with subarachnoid hemorrhage (SAH). Despite its clinical significance and extensive research, the underlying pathogenesis and therapeutic perspectives of CV remain incompletely understood. Recently, it has been suggested that molecular hydrogen (H(2)) can selectively reduce levels of hydroxyl radicals (·OH) and ameliorate oxidative and inflammatory injuries to organs in many models. However, whether H(2) can ameliorate CV after SAH is still unknown. This study was designed to evaluate the efficacy of H(2) in preventing SAH-induced CV. Experimental SAH was induced in Sprague-Dawley rats using cisterna magna blood injection. Hydrogen-rich saline (HS) was injected intraperitoneally (5 ml/kg) immediately and at 24 hr after injury. All rats were sacrificed 48 hr after the neurological examination scores had been recorded following SAH. Levels of oxidative stress and inflammation were evaluated. Basilar artery vasospasm was assessed by histological examination using light and transmission electron microscopy. HS treatment significantly improved neurological outcomes and attenuated morphological vasospasm of the basilar artery after SAH. In addition, we found that the beneficial effects of HS treatment on SAH-induced CV were associated with decreased levels of lipid peroxidation, increased activity of antioxidant enzymes, and reduced levels of proinflammatory cytokines in the basilar artery. These results indicate that H(2) has the potential to be a novel therapeutic strategy for the treatment of CV after SAH, and its neuroprotective effect might be partially mediated via limitation of vascular inflammation and oxidative stress.     

Fractal and noisy CBV dynamics in humans: influence of age and gender.

The complexity of spontaneous cerebral blood volume (CBV) fluctuations can emerge from random, fractal, or chaotic processes. Our aims were to define the contribution of these patterns to the observed complexity and to evaluate the effect of age and gender on it. The total hemoglobin content as the measure of CBV was monitored by near-infrared spectroscopy on volunteers (men n = 19, age = 20 to 78 years; women n = 23, age = 21 to 79 years). Random and fractal patterns were distinguished by the spectral index (beta). Chaos was identified by surrogate analysis of the correlation dimension (a static chaotic parameter, the dimension of the correlation integral) and the largest Lyapunov exponent (a dynamic chaotic parameter, the rate of exponential divergence of the system states from a perturbed initial condition over the chaotic attractor). In spontaneous CBV fluctuations, both fast random and slow fractal dynamics are present separately in their spectra by a cutoff frequency, f'. Below f' the pattern is fractal, in that power rises inversely with frequency as 1/f(beta). f' decreases with age in men and women alike (F1: up to 0.12+/-0.06 Hz versus F2: up to 0.05+/-0.04 Hz at P = 0.015, and M1: up to 0.16+/-0.05 Hz versus M2: up to 0.11+/-0.04 Hz at P = 0.044). Neither pre- nor postmenopausal age groups (1 and 2, respectively) showed a (low)beta gender difference. Surrogate analysis showed that CBV dynamics cannot be characterized on the grounds of deterministic chaos. Cerebral blood volume fluctuates in a complex, bimodal manner in humans, in that the fast dynamics has no structure, while the slow dynamics exhibits a self-similar, that is, fractal temporal structure. The range of fluctuation amplitudes produced by fractal dynamics is always larger than that of random fluctuations, and it shrinks with an altered structuring in aging women only.     

Hemispheric asymmetry and temporal profiles of cerebral pressure autoregulation in head injury

A moving correlation index (Mx-ABP) between arterial blood pressure (ABP) and mean middle cerebral artery blood flow velocity (CBFV) can be used to monitor dynamic cerebrovascular autoregulation (CA) after traumatic brain injury (TBI). In this study we examined hemispheric CA asymmetry and temporal CA profiles, their relationship with ABP and CBFV, and their prognostic relevance. Mx-ABP was calculated for each hemisphere in 25 TBI patients second-daily for as long as they were receiving sedation and analgesia. Forty-nine recordings were obtained, between one and six per patient. Four time periods were defined: immediate - postinjury days (PID) 0 and 1; early - PID 2 and 3; intermediate - PID 4 and 5, and late - PID 6 and later. GOS was estimated at discharge, GOS 4 and 5 were considered favorable (15 patients) and GOS 1-3 unfavorable outcome (10 patients). A Mx difference >0.2 was classified as hemispheric asymmetry (HA). HA was observed at least once in 12 of the 25 patients (48%) and in 18 of 49 recordings (37%). It was observed during all time periods: 35%, 43%, 25%, 43%, respectively, and was not related to outcome. There was no difference in mean CBFV or ABP between patients with and without HA. HA was not related to interhemispheric CBFV differences. A significant improvement in Mx was seen over time. Hemispheric CA asymmetry is common after traumatic brain injury. It does not bear significant clinical or predictive relevance, and it is unrelated to CBFV or ABP. CA is most profoundly disturbed during the immediate postinjury phase and improves gradually during the ICU course. Further studies are needed to investigate CA during post ICU recovery and rehabilitation.     

血糖变异性与重症脑出血患者神经功能恢复的相关性

目的 探讨血糖变异性对重症急性脑出血患者神经功能恢复的影响及血糖变异性在重症脑出血患者发病时间轴上的表现特点。方法 选取2018年1月1日-2019年7月1日收入河南科技大学第一附属医院重症外科的脑出血患者,根据患者入院30 d后改良Rankin(Modified Rankin scale,mRS)评分将患者分为神经功能恢复良好组(mRS≤2分),和神经功能恢复不良组(mRS>2分)(残疾/死亡),比较2组入院时高血糖、平均血糖、血糖标准差、入院24 h内血糖变异性(CV1)、入院1～3 d血糖变异性(CV2)、入院3～7 d血糖变异性(CV3)、入院7 d内血糖平均变异性(CV7)、最低血糖水平以及其他临床资料,应用多变量logistic回归分析确定入院30 d后神经功能恢复的独立预测因素。结果 单因素分析显示年龄、CV1、CV3、CV7、最低血糖水平、血糖标准差是影响重症脑出血患者神经功能恢复的相关因素(P<0.05); 多因素logistic逐步回归模型分析显示血糖标准差、CV1、CV3、CV7、最低血糖水平能独立预测重症脑出血患者神经功能的恢复情况; 神经功能恢复良好组和神经功能恢复不良组患者的血糖变异性在入院24 h内、入院1～3 d和入院3～7 d时间轴上的变化特点不同(F=5.000,P=0.029),进一步分析可以看出神经功能恢复不良组的血糖变异性平均幅度较神经功能恢复良好组高,但2组在时间轴上的变化趋势基本相同,均在急性期(入院1～3 d)呈线性上升趋势,之后趋于下降; 组内效应显示患者的血糖变异性在3个时间段上的变化具有显著差异(F=11.663,P<0.001)。结论 血糖标准差、CV1、CV3、CV7、最低血糖水平是影响重症脑出血患者神经功能恢复的独立危险因素; 在重症脑出血患者超急性期、急性期、亚急性期过程中血糖变异性的变化具有显著差异,临床工作中重症脑出血患者应在入院早期密切监测血糖,并积极干预,减小血糖波动范围,以期减少不良预后的发生。     

Spontaneous oscillations of arterial blood pressure, cerebral and peripheral blood flow in healthy and comatose subjects.

Slow and rhythmic spontaneous oscillations of cerebral and peripheral blood flow occur within frequencies of 0.5-3 min-1 (0.008-0.05 Hz, B-waves) and 3-9 min-1 (0.05-0.15 Hz, M-waves). The generators and pathways of such oscillations are not fully understood. We compared the coefficient of variance (CoV), which serves as an indicator for the amplitude of oscillations and is calculated as the percent standard deviation of oscillations within a particular frequency band from the mean, to study the impairment of generators or pathways of such oscillations in normal subjects and comatose patients in a controlled fashion. With local ethic committee approval, data were collected from 19 healthy volunteers and nine comatose patients suffering from severe traumatic brain injury (n = 3), severe subarachnoid hemorrhage (n = 3), and intracerebral hemorrhage (n = 3). Cerebral blood flow velocities were measured by transcranial Doppler ultrasound (TCD), peripheral vasomotion by finger tip laser Doppler flowmetry (LDF), and ABP by either non-invasive continuous blood pressure recordings (Finapres method) in control subjects, or by direct radial artery recordings in comatose patients. Each recording session lasted approximately 20-30 min. Data were stored in the TCD device for offline analysis of CoV. For CoV in the cerebral B-wave frequency range there was no difference between coma patients and controls, however there was a highly significant reduction in the amplitude of peripheral B-wave LDF and ABP vasomotion (3.8 +/- 2.1 vs. 28.2 +/- 16.1 for LDF, p < 0.001; and 1.2 +/- 0.7 vs. 4.6 +/- 2.8 for ABP, p < 0.001). This observation was confirmed for spontaneous cerebral and peripheral oscillations in the M-wave frequency range. The CoV reduction in peripheral LDF and ABP oscillations suggest a severe impairment of the proposed sympathetic pathway in comatose patients. The preservation of central TCD oscillations argues in favor of different pathways and/or generators of cerebral and peripheral B- and M-waves.     

Variability of motor unit discharge and force fluctuations across a range of muscle forces in older adults

Variability of motor unit discharge is a likely contributor to the greater force fluctuations observed in old adults at low muscle forces. We sought to determine whether the variability of motor unit discharge rate underlies the fluctuations in force during steady contractions across a range of forces in young (n = 11) and old (n = 14) adults. The coefficient of variation (CV) for discharge rate and force were measured during a force-matching task as the first dorsal interosseous muscle performed isometric contractions. The recruitment thresholds of the 78 motor units ranged from 0.04% to 34% of maximal voluntary contraction (MVC) force. The CV for discharge rate ranged from 7.6% to 46.2% and was greater (P < 0.05) for old adults (21.5% +/- 7.7%) than young adults (17.3% +/- 8.1%). Although the CV for force was similar for young and old subjects (2.53% +/- 1.6%) across all target forces, it was greater for old adults at the lowest forces. Furthermore, there was a positive relation (r2 = 0.20, P < 0.001) between the CV for force and the CV for discharge rate across the range of recruitment thresholds. This relation was significant for old adults (r2 = 0.30, P < 0.001), but not for young adults (r2 = 0.06, P > 0.05). Thus, the normalized variability (CV) of motor unit discharge was greater in old adults and was related to the amplitude of force fluctuations across a broader range of forces than previously examined. These findings underscore the contribution of variability of motor unit activity to motor output in normal human aging.     

S-100B and NSE: markers of initial impact of subarachnoid haemorrhage and their relation to vasospasm and outcome.

S100-B and neuron specific enolase (NSE) are known predictors of outcome in head injured and stroke patients. This study was conducted to test the hypothesis that S-100B and NSE can predict the development of vasospasm and outcome within the first 3 days after subarachnoid haemorrhage (SAH). Fifty-one SAH patients (mean age 51+/-11 years, male : female ratio 1.0 : 1.6, mean World Federation of Neurological Surgeons [WFNS] Grade 3+/-1.5) were included in the study. S100-B and NSE were recorded in venous blood across the first 3 days post-SAH. Vasospasm was diagnosed if mean blood flow velocity of the middle cerebral artery was greater than 120 cm/s and Lindegaard ratio >3. Glasgow Outcome Score (GOS) and cranial CT scans were recorded at 6 months. Normal, intermediate and high S-100B values were seen in 24%, 51% and 25% of patients, respectively. In patients with S-100B>1 microg/L, Fisher Grade 4 and WFNS 4-5 were both seen in 77% of cases. S-100B was significantly higher in those patients who did not develop vasospasm. In addition, S-100B values were significantly higher in those patients who died than in those with unfavourable or favourable outcome. NSE was normal, intermediate and high in 82%, 8% and 10% of patients, respectively. Patients with WFNS 4-5 and/or Fisher Grade 4 had significantly higher NSE values than all others. Across the first 3 days after SAH, measuring S-100B is useful to predict outcome and vasospasm.     

Changes in nitric oxide production and cerebral blood flow before development of hyperbaric oxygen-induced seizures in rats

The predictive value of increase in cerebral blood flow (CBF) was examined to detect hyperbaric oxygen (HBO(2))-induced electrical discharge in artificially ventilated rats at three PaCO(2) levels under 5 atmospheric pressures. The possible involvement of NO production in the mechanism of the increase in CBF was also assessed by measurement of major NO metabolites (NO(2)(-) plus NO(3)(-)) using a microdialysis technique at the left parietal cortex during HBO(2) exposure. The onset times of electrical discharge, measured in the right frontal region, were significantly prolonged and shortened in the low PaCO(2) group (79+/-21 min) and high PaCO(2) group (27+/-7 min), respectively, compared to that in the normal PaCO(2) group (37+/-5 min). Increase in CBF (200% of the pre-exposure level) was observed in every animal and was sustained until the appearance of electrical discharge. The onset time of increase in CBF was closely related to that of electrical discharge (R(2)=0.987), and the durations of increase in CBF were almost identical (11-14 min in mean) regardless of the PaCO(2) level. The level of NO(2)(-) plus NO(3)(-) was unaffected by the initiation of HBO(2) exposure and simultaneously increased up to 246+/-59% of control level with the onset of increase in CBF. There was a close relationship between changes in CBF and levels of NO(2)(-) plus NO(3)(-) (R(2)=0.544). These results indicate that monitoring of CBF is useful for the prediction of electrical discharge in artificially ventilated rats regardless of their PaCO(2) levels and that the increase in NO production is related to the mechanism of increase in CBF.     

Spontaneous blood pressure oscillations and cerebral autoregulation

The relationship between spontaneous oscillations in cerebral blood flow velocity (CBFV) and arterial blood pressure (ABP) was analysed in normal subjects in order to evaluate whether these relationships provide information about cerebral autoregulation. CBFV was measured using transcranial Doppler sonography and continuous ABP and heart rate using Finapres in 50 volunteers. Measurements were made over 5 min in a supine position and 6 min in a tilted position. Coefficients of variation were calculated using power- and cross-spectral analysis in order to quantify amplitudes within two frequency ranges: 3–9 cycles per min (cpm) (M-waves); and 9–20 cpm (R-waves). Correlations, coherence values, phase angle shifts and gains were also computed between corresponding waves in CBFV and in ABP. A clear correlation was seen for M-waves and R-waves between CBFV and ABP and coherence values were large enough to calculate phase angle shifts and gains. Phase angles for M-waves were larger and gains lower than was the case for R-waves, either tilted or supine. These data are consistent with a highpass filter model of cerebral autoregulation. Relatively high CBFV/ABP gain values (between 1.4 and 2.0) suggest that the principle of frequency-dependent vascular input impedances has to be considered in addition to autoregulatory feedback mechanisms. Spontaneous ABP oscillations in the M-wave and R-wave ranges may serve as a basis for continuous autoregulation monitoring.     

Conditions That May Determine Blood Vessel Phenotype in Tissues Grafted to Brain

The hypothesis, that a blood vessel's phenotype is determined by the tissue it vascularizes and not by the vessel's source, does not hold for tissue beyond a certain period of development. In mature skeletal muscle grafted to choroid plexus of adult and 2-week-old rats, some vessels were choroidal or fenestrated (FV) rather than, according to the hypothesis, continuous (CV), like those of muscle. In E14 fetal muscle placed on the choroid plexus, 80% of the grafts' capillaries were CV, like those of muscle. Most choroidal FV that entered the grafts were apparently changed to CV. By E16, about 70% of the graft vessels remained as FV rather than being converted. Thus, FV were changed to CV by a hypothetical conversion factor made, apparently, by E14 grafts but not by E16 grafts. In grafts from [³H]thymidine-labeled donors, an appreciable number of CV in E14 grafts were identified as intrinsic to the muscle. When hosts were labeled to verify the origin of FV in their nonlabeled donor grafts, only a few FV, to date, were tagged. The FV must have come from host choroid plexus, the only available source of graft FV. Vascular endothelial growth factor (VEGF) might convert CV into FV, yet VEGF and the mRNA for its receptor were present in choroid plexus but not in the grafts. Therefore, VEGF is not a conversion factor. The purported factor that changes FV to CV may be expressed in E14 muscle grafts but diminishes by fetal age E16 and beyond.     

Changes in the arterial fraction of human cerebral blood volume during hypercapnia and hypocapnia measured by positron emission tomography.

Hypercapnia induces cerebral vasodilation and increases cerebral blood volume (CBV), and hypocapnia induces cerebral vasoconstriction and decreases CBV. Cerebral blood volume measured by positron emission tomography (PET) is the sum of three components, that is, arterial, capillary, and venous blood volumes. Changes in arterial blood volume (V(a)) and CBV during hypercapnia and hypocapnia were investigated in humans using PET with H(2)(15)O and (11)CO. Arterial blood volume was determined from H(2)(15)O PET data by means of a two-compartment model that takes V(a) into account. Baseline CBV and values during hypercapnia and hypocapnia in the cerebral cortex were 0.034+/-0.003, 0.038+/-0.003, and 0.031+/-0.003 mL/mL (mean+/-s.d.), respectively. Baseline V(a) and values during hypercapnia and hypocapnia were 0.015+/-0.003, 0.025+/-0.011, and 0.007+/-0.003 mL/mL, respectively. Cerebral blood volume changed significantly owing to changes in PaCO(2), and V(a) changed significantly in the direction of CBV changes. However, no significant change was observed in venous plus capillary blood volume (=CBV-V(a)). This indicates that changes in CBV during hypercapnia and hypocapnia are caused by changes in arterial blood volume without changes in venous and capillary blood volume.     

Interobserver and within-subject variances of T2-relaxation time and 1H-metabolite ratios in the normal hippocampus

PURPOSE: To investigate the magnetic resonance (MR) reproducibility of normal hippocampal volume (HV), temporal lobe volume (TLV), transversal relaxation time (T(2)) and (1)H-MR spectroscopy ((1)H-MRS) metabolite ratios. MATERIALS AND METHODS: Two sets of HV, TLV, T(2) and MR spectroscopic metabolite signal ratios were determined in 27 healthy volunteers. HV and TLV were measured with a T(1)-weighted MR sequence; whereas T(2) measurements were performed with conventional spin-echo (CSE) and fast spin-echo (FSE) MR imaging sequences. The interobserver and within-subject variances of T(2) measurements were estimated. RESULTS: Estimated right and left HV coefficients of variation (CV)=0.13. FSE T(2) measurements showed no significant differences in the interobserver (CV=0.02) and within-subject variances (CV=0.02). Measurements showed no differences in the interobserver (CV=0.02) and within-subject (CV=0.04) variances for the CSE T(2) of the right and left hippocampi. Metabolite ratios between N-acetyl aspartate (NAA) and creatine (Cr), choline (Cho) and creatine, and NAA and choline plus creatine (Cho + Cr) for the right hippocampus were 2.29+/-0.19, 1.52+/-0.14 and 0.91+/-0.05, respectively. Metabolite ratios for the left hippocampus were 2.18+/-0.10, 1.48+/-0.10 and 0.88+/-0.06, respectively. CONCLUSIONS: HV, TLV, T(2) and (1)H MRS metabolite ratio measurements showed fair reproducibility with small CVs, and no differences in the interobserver and within-subject variances, including no differences between right and left TLV, and in the right and left T(2).     

Dynamics of cerebral blood flow autoregulation in hypertensive patients

In hypertensive patients, the upper and lower limits of cerebral autoregulation are shifted to higher levels. However, the dynamics of cerebral autoregulation in hypertensive patients are less well known. We compared the dynamics of cerebral autoregulation in 21 treated hypertensive patients (13 men and 8 women; mean age: 48.9+/-13.6 years) and in 21 normotensive subjects (13 men and 8 women; mean age: 51+/-14.5 years) by transcranial Doppler (TCD) of the middle cerebral artery (MCA) during the acute decrease in blood pressure induced by standing up after 2 min in squatting position. MCA maximal outline blood flow velocity (FV), blood pressure (Finapres) and end-tidal PCO2 were continuously monitored and computerised. A cerebral vascular resistance index (CR) was calculated as follows: mean arterial BP/MCA mean FV with normalised changes in CR per second during the blood pressure decrease (CR slope). The CR slope reflecting the rate of cerebral autoregulation did not differ between the two groups and within the hypertensive patients [well controlled (8 patients) and not controlled (13 patients)]. The time to maximum decrease of CR (T1) and the time to full recovery of CR after the initial drop (T2) were also similar in the two groups (controls T1: 11.3+/-3.1 s, T2: 12+/-5.9 s; hypertensive T1: 11.7+/-2.5 s, T2: 10.7+/-4.5 s) and within hypertensive patients. These findings suggest that the dynamics of cerebral autoregulation are well preserved in hypertensive patients, with no difference according to the efficiency of treatment of hypertension.     

蛛网膜下腔出血并迟发性脑血管痉挛大鼠脑能量代谢与脑血流量变化的实验研究

目的探讨实验性蛛网膜下腔出血导致的迟发性脑血管痉挛时脑能量代谢的变化规律，及其与皮质脑血流量（CBF）变化的相关性。方法50只雄性SD大鼠随机分为对照组和蛛网膜下腔出血第1、3、5、7天组．应用非抗凝自体动脉血枕大池两次注血法制备蛛网膜下腔出血大鼠模型；另5只大鼠用于颅内血液大体分布的观察。应用微透析仪监测各组大鼠脑组织间液中葡萄糖（Glu）、乳酸（Lac）及丙酮酸（Pyr）含量，并计算乳酸／丙酮酸比值；激光多普勒血流仪监测各组大鼠皮质脑血流量；于光学显微镜及透射电子显微镜下观察基底动脉血管壁的病理学改变。结果（1）5只用于观察颅内血液大体分布的大鼠中4只蛛网膜下腔出血模型鼠血液主要分布于基底池、脚间池及额叶底面，亚甲蓝与血液混合物主要沉积于颅底．同时在脑室及纵裂池亦可见血液分布；余1只注入人工脑脊液后未发生颅内出血及血液沉积。表明蛛网膜下腔出血动物模型制备成功。（2）与对照组相比，蛛网膜下腔出血组大鼠葡萄糖及丙酮酸含量明显降低（P〈0．01）；乳酸／丙酮酸比值明显升高（P〈0．01），以第5、7天组升高最为明显（P〈0．01）；第5天组乳酸含量亦明显升高（P〈0．01）。（3）激光多普勒监测显示，蛛网膜下腔出血组大鼠脑血流量减少率高于对照组（P〈0．05），其中第5天组减少最为显著。与其他各亚组比较差异有统计学意义（尸〈0．05）；脑血流量变化与乳酸／丙酮酸比值、乳酸水平的改变呈正相关（r=0．721，0．477；均P〈0．01），与葡萄糖、丙酮酸水平的改变呈负相关（r=-0．447，-0．579；均P〈0．01）。结论微透析指标与脑血流量变化具有一致性，可作为蛛网膜下腔出血脑组织间液生化指标的动态监测，用于预测迟发性脑血管痉挛的发生。     

Monitoring cerebral autoregulation after head injury. Which component of transcranial Doppler flow velocity is optimal?

Background

Cerebral autoregulation assessed using transcranial Doppler (TCD) mean flow velocity (FV) in response to various physiological challenges is predictive of outcome after traumatic brain injury (TBI). Systolic and diastolic FV have been explored in other diseases. This study aims to evaluate the systolic, mean and diastolic FV for monitoring autoregulation and predicting outcome after TBI.

Methods

300 head-injured patients with blood pressure (ABP), intracranial pressure (ICP), cerebral perfusion pressure (CPP), and FV recordings were studied. Autoregulation was calculated as a correlation of slow changes in diastolic, mean and systolic components of FV with CPP (Dx, Mx, Sx, respectively) and ABP (Dxa, Mxa, Sxa, respectively) from 30 consecutive 10?s averaged values. The relationship with age, severity of injury, and dichotomized 6?months outcome was examined.

Results

Association with outcome was significant for Mx and Sx. For favorable/unfavorable and death/survival outcomes Sx showed the strongest association (F?=?20.11; P?=?0.00001 and F?=?13.10; P?=?0.0003, respectively). Similarly, indices derived from ABP demonstrated the highest discriminatory value when systolic FV was used (F?=?12.49; P?=?0.0005 and F?=?5.32; P?=?0.02, respectively). Indices derived from diastolic FV demonstrated significant differences (when calculated using CPP) only when comparing between fatal and non-fatal outcome.

Conclusions

Systolic flow indices (Sx and Sxa) demonstrated a stronger association with outcome than the mean flow indices (Mx and Mxa), irrespective of whether CPP or ABP was used for calculation.