958 resultados para Cerebral blood flow


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Introducción: La aparición de vasodilatación aislada de la arteria cerebral media en fetos pequeños para la edad gestacional sin otros cambios en el doppler puede interpretarse como fisiológica o podría ser la manifestación inicial de una restricción de crecimiento intrauterino de inicio tardío. Se pretende evaluar la asociación de la disminución del índice de pulsatibilidad de la arteria cerebral media, como predictor de desenlaces perinatales adversos, en fetos con bajo peso para edad gestacional. Metodología: Se realizó un estudio de cohorte analítica de temporalidad histórica para determinar si el hallazgo de disminución de la pulsatibilidad en el doppler de arteria cerebral media se asocia con el pronóstico perinatal adverso, en fetos pequeños para edad gestacional mediante un muestreo no probabilístico. Resultados: Se recolectaron un total de 325 flujometría doppler de fetos pequeños para edad gestacional. El riesgo de parto pretérmino fue RR 2.6 IC95% 1.6-4.1, de hospitalización fue RR 1.4 IC95%1.1-1.9 y de muerte fue 2.1 IC95%1.5-3.2 cuando hay índice de pulsatilidad alterada en la arteria cerebral media. La regresión logística mostró que el riesgo de desenlaces desfavorables con alteraciones en la arteria cerebral media fue de RR 4.2 IC95% 2.5-7.1 ajustado por edad materna, edad gestacional y bajo peso al nacer. Discusión Los pacientes expuestos presentan mayor riesgo de desenlaces desfavorables con diferencias significativas, no así en otros estudios publicados. El presente estudio muestra asociaciones significativas que debe ser evaluada con estudios más amplios.

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The changes that occur with age in the distribution of atherosclerotic lesions around arterial branch points challenge accepted theories relating disease to haemodynamic stresses. We investigated whether flow near branch points changes with age in a way that can account for the different lesion distributions. Flow around 20 branches from immature and mature aortas was investigated by examining the length:width ratio and orientation of endothelial nuclei; these properties depend on the magnitude and direction of near-wall flows, respectively. There were significant changes in the pattern of nuclear shape with age, consistent with a reversal in the pattern of shear around branches. In control regions away from branches, there were no such changes. The role of haemodynamic stresses in atherogenesis may require re-evaluation in the light of these results. (C) 2003 Elsevier Ireland Ltd. All rights reserved.

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The changes that occur with age in the distribution of atherosclerotic lesions around arterial branch points challenge accepted theories relating disease to haemodynamic stresses. We investigated whether flow near branch points changes with age in a way that can account for the different lesion distributions. Flow around 20 branches from immature and mature aortas was investigated by examining the length:width ratio and orientation of endothelial nuclei; these properties depend on the magnitude and direction of near-wall flows, respectively. There were significant changes in the pattern of nuclear shape with age, consistent with a reversal in the pattern of shear around branches. In control regions away from branches, there were no such changes. The role of haemodynamic stresses in atherogenesis may require re-evaluation in the light of these results.

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Neurovascular coupling in response to stimulation of the rat barrel cortex was investigated using concurrent multichannel electrophysiology and laser Doppler flowmetry. The data were used to build a linear dynamic model relating neural activity to blood flow. Local field potential time series were subject to current source density analysis, and the time series of a layer IV sink of the barrel cortex was used as the input to the model. The model output was the time series of the changes in regional cerebral blood flow (CBF). We show that this model can provide excellent fit of the CBF responses for stimulus durations of up to 16 s. The structure of the model consisted of two coupled components representing vascular dilation and constriction. The complex temporal characteristics of the CBF time series were reproduced by the relatively simple balance of these two components. We show that the impulse response obtained under the 16-s duration stimulation condition generalised to provide a good prediction to the data from the shorter duration stimulation conditions. Furthermore, by optimising three out of the total of nine model parameters, the variability in the data can be well accounted for over a wide range of stimulus conditions. By establishing linearity, classic system analysis methods can be used to generate and explore a range of equivalent model structures (e.g., feed-forward or feedback) to guide the experimental investigation of the control of vascular dilation and constriction following stimulation.

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Characterization of neural and hemodynamic biomarkers of epileptic activity that can be measured using noninvasive techniques is fundamental to the accurate identification of the epileptogenic zone (EZ) in the clinical setting. Recently, oscillations at gamma-band frequencies and above (N30 Hz) have been suggested to provide valuable localizing information of the EZ and track cortical activation associated with epileptogenic processes. Although a tight coupling between gamma-band activity and hemodynamic-based signals has been consistently demonstrated in non-pathological conditions, very little is known about whether such a relationship is maintained in epilepsy and the laminar etiology of these signals. Confirmation of this relationship may elucidate the underpinnings of perfusion-based signals in epilepsy and the potential value of localizing the EZ using hemodynamic correlates of pathological rhythms. Here, we use concurrent multi-depth electrophysiology and 2- dimensional optical imaging spectroscopy to examine the coupling between multi-band neural activity and cerebral blood volume (CBV) during recurrent acute focal neocortical seizures in the urethane-anesthetized rat. We show a powerful correlation between gamma-band power (25–90 Hz) and CBV across cortical laminae, in particular layer 5, and a close association between gamma measures and multi-unit activity (MUA). Our findings provide insights into the laminar electrophysiological basis of perfusion-based imaging signals in the epileptic state and may have implications for further research using non-invasive multi-modal techniques to localize epileptogenic tissue

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Rationale: There has recently been increasing interest in the potential of flavanols, plant derived compounds found in foods such as fruit and vegetables, to ameliorate age-related cognitive decline. Research suggests that cocoa flavanols improve memory and learning, possibly as a result of their anti-inflammatory and neuroprotective effects. These effects may be mediated by increased cerebral blood flow (CBF), thus stimulating neuronal function. Objectives: The present study employed arterial spin labelling (ASL) functional magnetic resonance imaging (FMRI) to explore the effect of a single acute dose of cocoa flavanols on regional CBF. Methods: CBF was measured pre and post consumption of low (23mg) or high (494mg) 330ml equicaloric flavanol drinks matched for caffeine, theobromine, taste and appearance according to a randomised counterbalanced crossover double-blind design in eight males and ten females, aged 50-65 years. Changes in perfusion from pre to post consumption were calculated as a function of each drink. Results: Significant increases in regional perfusion across the brain were observed following consumption of the high flavanol drink relative to the low flavanol drink, particularly in the anterior cingulate cortex (ACC) and the central opercular cortex of the parietal lobe. Conclusions: Consumption of cocoa flavanol improves regional cerebral perfusion in older adults. This provides evidence for a possible acute mechanism by which cocoa flavanols are associated with benefits for cognitive performance.

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Purpose: To obtain cerebral perfusion territories of the left, the right. and the posterior circulation in humans with high signal-to-noise ratio (SNR) and robust delineation. Materials and Methods: Continuous arterial spin labeling (CASL) was implemented using a dedicated radio frequency (RF) coil. positioned over the neck, to label the major cerebral feeding arteries in humans. Selective labeling was achieved by flow-driven adiabatic fast passage and by tilting the longitudinal labeling gradient about the Y-axis by theta = +/- 60 degrees. Results: Mean cerebral blood flow (CBF) values in gray matter (GM) and white matter (WM) were 74 +/- 13 mL center dot 100 g(-1) center dot minute(-1) and 14 +/- 13 mL center dot 100 g(-1) center dot minute(-1), respectively (N = 14). There were no signal differences between left and right hemispheres when theta = 0 degrees (P > 0.19), indicating efficient labeling of both hemispheres. When theta = +60 degrees, the signal in GM on the left hemisphere, 0.07 +/- 0.06%, was 92% lower than on the right hemisphere. 0.85 +/- 0.30% (P < 1 x 10(-9)). while for theta = -60 degrees, the signal in the right hemisphere. 0.16 +/- 0.13%, was 82% lower than on the contralateral side. 0.89 +/- 0.22% (P < 1 x 10(-10)). Similar attenuations were obtained in WM. Conclusion: Clear delineation of the left and right cerebral perfusion territories was obtained, allowing discrimination of the anterior and posterior circulation in each hemisphere.

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The study examined the implication of the renin-angiotensin system (RAS) in regulation of splanchnic blood flow and glucose production in exercising humans. Subjects cycled for 40 min at 50% maximal O2 consumption (VO2 max) followed by 30 min at 70% VO2 max either with [angiotensin-converting enzyme (ACE) blockade] or without (control) administration of the ACE inhibitor enalapril (10 mg iv). Splanchnic blood flow was estimated by indocyanine green, and splanchnic substrate exchange was determined by the arteriohepatic venous difference. Exercise led to an ~20-fold increase (P < 0.001) in ANG II levels in the control group (5.4 ± 1.0 to 102.0 ± 25.1 pg/ml), whereas this response was blunted during ACE blockade (8.1 ± 1.2 to 13.2 ± 2.4 pg/ml) and in response to an orthostatic challenge performed postexercise. Apart from lactate and cortisol, which were higher in the ACE-blockade group vs. the control group, hormones, metabolites, VO2, and RER followed the same pattern of changes in ACE-blockade and control groups during exercise. Splanchnic blood flow (at rest: 1.67 ± 0.12, ACE blockade; 1.59 ± 0.18 l/min, control) decreased during moderate exercise (0.78 ± 0.07, ACE blockade; 0.74 ± 0.14 l/min, control), whereas splanchnic glucose production (at rest: 0.50 ± 0.06, ACE blockade; 0.68 ± 0.10 mmol/min, control) increased during moderate exercise (1.97 ± 0.29, ACE blockade; 1.91 ± 0.41 mmol/min, control). Refuting a major role of the RAS for these responses, no differences in the pattern of change of splanchnic blood flow and splanchnic glucose production were observed during ACE blockade compared with controls. This study demonstrates that the normal increase in ANG II levels observed during prolonged exercise in humans does not play a major role in the regulation of splanchnic blood flow and glucose production.

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OBJECTIVE: We have previously shown in humans that local infusion of a nitric oxide synthase (NOS) inhibitor into the femoral artery attenuates the increase in leg glucose uptake during exercise without influencing total leg blood flow. However, rodent studies examining the effect of NOS inhibition on contraction-stimulated skeletal muscle glucose uptake have yielded contradictory results. This study examined the effect of local infusion of an NOS inhibitor on skeletal muscle glucose uptake (2-deoxyglucose) and capillary blood flow (contrast-enhanced ultrasound) during in situ contractions in rats.

RESEARCH DESIGN AND METHODS: Male hooded Wistar rats were anesthetized and one hindleg electrically stimulated to contract (2 Hz, 0.1 ms) for 30 min while the other leg rested. After 10 min, the NOS inhibitor NG-nitro-L-arginine methyl ester (L-NAME) (arterial concentration of 5 µmol/l) or saline was infused into the epigastric artery of the contracting leg.

RESULTS: Local NOS inhibition had no effect on blood pressure, heart rate, or muscle contraction force. Contractions increased (P < 0.05) skeletal muscle NOS activity, and this was prevented by L-NAME infusion. NOS inhibition caused a modest significant (P < 0.05) attenuation of the increase in femoral blood flow during contractions, but importantly there was no effect on capillary recruitment. NOS inhibition attenuated (P < 0.05) the increase in contraction-stimulated skeletal muscle glucose uptake by ~35%, without affecting AMP-activated protein kinase (AMPK) activation.

CONCLUSIONS: NOS inhibition attenuated increases in skeletal muscle glucose uptake during contraction without influencing capillary recruitment, suggesting that NO is critical for part of the normal increase in skeletal muscle fiber glucose uptake during contraction.

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This study examined forearm blood flow (FBF) in individuals with chronic heart failure (CHF) at rest, moderate exercise, and following limb occlusion. FBF was measured by venous occlusion plethysmography in CHF patients (n = 43) and healthy age-matched volunteers (n = 8) at rest and during exercise consisting of intermittent isometric hand squeezing at 15, 30, and 45% of maximum voluntary contraction (MVC). Peak vasodilatory capacity was also determined following the release of an occluding arm cuff. FBF was lower in CHF patients during exercise and during peak reactive hyperemia (PRH) compared to healthy volunteers, but there was no significant difference between groups at rest. Peak vasodilatory capacity was significantly higher in healthy volunteers than the CHF group ((30.6 ± 8.6 ml±100 mL-1±min-1 and 18.3 ± 6.9 ml±100 mL-1±min-1, respectively). Local blood flow stimulation in response to exercise or limb occlusion is reduced in individuals with CHF, however, there was no difference in resting flows between the two groups, suggesting vasodilatory medication may restore resting blood flow to healthy values.

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Thirty-nine CHF patients (New York Heart Association Functional Class = 2.3±0.5; left ventricular ejection fraction 28%±7%; age 65±11 years; 33:6 male:female) underwent 2 identical series of tests, 1 week apart, for strength and endurance of the knee and elbow extensors and flexors, VO2peak, HRV, FBF at rest, and FBF activated by forearm exercise or limb ischemia. Patients were then randomized to 3 months of resistance training (EX, n = 19), consisting of mainly isokinetic (hydraulic) ergometry, interspersed with rest intervals, or continuance with usual care (CON, n = 20), after which they underwent repeat endpoint testing. Combining all 4 movement patterns, strength increased for EX by 21±30% (mean±SD, P<.01) after training, whereas endurance improved 21±21% (P<.01). Corresponding data for CON remained almost unchanged (strength P<.005, endurance P<.003 EX versus CON). VO2peak improved in EX by 11±15% (P<.01), whereas it decreased by 10±18% (P<.05) in CON (P<.001 EX versus CON). The ratio of low-frequency to high-frequency spectral power fell after resistance training in EX by 44±53% (P<.01), but was unchanged in CON (P<.05 EX versus CON). FBF increased at rest by 20±32% (P<.01), and when stimulated by submaximal exercise (24±32%, P<.01) or limb ischemia (26±45%, P<.01) in EX, but not in CON (P<.01 EX versus CON).

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An isolated, perfused salmon tail preparation showed oxyconformance at low oxygen delivery rates. Addition of pig red blood cells to the perfusing solution at a haematocrit of 5 or 10% allowed the tail tissues to oxyregulate. Below ca. 60 ml O2 kg−1 h−1 of oxygen delivery (DO2), VO2 was delivery dependent. Above this value additional oxygen delivery did not increase VO2 of resting muscle above ca. 35 ml O2 kg−1 h−1. Following electrical stimulation, VO2 increased to ca. 65 ml O2 kg−1 h−1, with a critical DO2 of ca. 150 ml O2 kg−1 h−1. Dorsal aortic pressure fell to 69% of the pre-stimulation value after 5 min of stimulation and to 54% after 10 min. Microspheres were used to determine blood flow distribution (BFD) to red (RM) and white muscle (WM) within the perfused myotome. Mass specific BFD ratio at rest was found to be 4.03 ± 0.49 (RM:WM). After 5 min of electrical stimulation the ratio did not change. Perfusion with saline containing the tetrazolium salt 3-(4,5-Dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) revealed significantly more mitochondrial activity in RM. Formazan production from MTT was directly proportional to time of perfusion in both red and WM. The mitochondrial activity ratio (RM:WM) did not change over 90 min of perfusion.

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 Light-load exercise training with blood flow restriction (BFR) increases muscle strength and size. However, the hemodynamics of BFR exercise appear elevated compared with non-BFR exercise. This questions the suitability of BFR in special/clinical populations. Nevertheless, hemodynamics of standard prescription protocols for BFR and traditional heavy-load exercise have not been compared. We investigated the hemodynamics of two common BFR exercise methods and two traditional resistance exercises. Twelve young males completed four unilateral elbow flexion exercise trials in a balanced, randomized crossover design: (a) heavy load [HL; 80% one-repetition maximum (1-RM)]; (b) light load (LL; 20% 1-RM); and two other light-load trials with BFR applied (c) continuously at 80% resting systolic blood pressure (BFR-C) or (d) intermittently at 130% resting systolic blood pressure (BFR-I). Hemodynamics were measured at baseline, during exercise, and for 60-min post-exercise. Exercising heart rate, blood pressure, cardiac output, and rate–pressure product were significantly greater for HL and BFR-I compared with LL. The magnitude of hemodynamic stress for BFR-C was between that of HL and LL. These data show reduced hemodynamics for continuous low-pressure BFR exercise compared with intermittent high-pressure BFR in young healthy populations. BFR remains a potentially viable method to improve muscle mass and strength in special/clinical populations.

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Atherosclerosis is a progressive disease, involving the build-up of lipid streaks in artery walls, leading to plaques. Understanding the development of atherosclerosis and plaque vulnerability is critically important since plaque rupture can result in heart attack or stroke. Plaques can be divided into two distinct types: those likely to rupture (vulnerable) or less likely to rupture (stable). In the last decade, researchers have been interested in studying the influence of the mechanical effects (blood shear stress, pressure forces and structural stress) on the plaque formation, progression and rupture processes but no general agreement has been found. The purpose of the present work is to include more realistic conditions for the numerical calculations of the blood flow by implementing real geometries with plaques in the numerical model. Hemodynamical parameters are studied in both diseased and healthy configurations. The healthy configuration is obtained by removing numerically the plaques from three dimensional geometries obtained by micro-computed tomography. A new hemodynamical parameter is also introduced to relate the location of plaques to the characteristics of the flow in the healthy configuration. © 2014 .