300 resultados para BLOOD-FLOW RESISTANCE


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PURPOSE: The intraoperative quality assessment of the arteriovenous fistula for hemodialysis is an essential process to limit early failure due to technical problems or inadequate vascular quality. This step is not clearly defined in the literature with no recommendations. METHODS: We selected published articles related to the topic of intraoperative quality control of the vascular access for hemodialysis. RESULTS: The intraoperative blood flow measurement greater than 120 ml/min in autologous fistula and less than 320 ml/min in arteriovenous graft was described as predictive factors for early failure. CONCLUSIONS: The blood flow measurement should be performed after the confection of the anastomosis. When blood flow is limited, fistulography is an essential step to assess patency.

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A 46-year-old woman with a severe polyradiculoneuropathy treated with high-dose intravenous immunoglobulin (IVIg) presented an encephalopathy with increased blood flow velocities of the middle cerebral arteries (MCAs) detected by transcranial Doppler (TCD) studies. The similitude between this observation and another case recently reported of a patient suffering from Guillain-Barré syndrome (GBS) and cerebral blood flow abnormalities after IVIg treatment prompted us to investigate the responsibility of the IVIg therapy in the genesis of these blood flow alterations. We studied therefore by TCD 10 consecutive patients who underwent this treatment for different reasons. In 1 case we observed an asymptomatic, spontaneously reversible increase in the blood flow velocities of the MCAs consistent with a vasospasm and occurring 3-10 days after completion of the therapy. Stroke and ischemic encephalopathy have been reported as possible complications of IVIg treatment. In the case under discussion, clinical events appeared shortly after the administration of the IVIg therapy and responded favorably to a treatment with nimodipine. Other etiopathogenic mechanisms, in particular a CNS vasculopathic process related to the GBS itself, have to be considered as well. Further studies, with a larger number of patients, are therefore needed to evaluate the underlying mechanisms of blood flow abnormalities occurring sometimes in GBS patients after IVIg treatment.

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IMPLICATIONS: A new combined ear sensor was tested for accuracy in 20 critically ill children. It provides noninvasive and continuous monitoring of arterial oxygen saturation, arterial carbon dioxide tension, and pulse rate. The sensor proved to be clinically accurate in the tested range.

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Résumé Il a été démontré que l'exercice physique modifiait le contrôle de la thermorégulation cutané, ce qui se manifeste par une augmentation de la perfusion de la microcirculation de la peau. Pour une même augmentation de température, ce phénomène est plus important chez les sportifs d'endurance que chez les sujets sédentaires. Dans cette étude, nous posons l'hypothèse qu'une composante de cette adaptation peut provenir d'une plus haute capacité des vaisseaux sanguins à répondre à un stimulus vasodilatateur. Pour la tester, nous avons recruté des hommes sains, non fumeurs, soit entraînés (surtout sport d'endurance) ou sédentaires que nous avons partagé en deux classes d'âges (18-35 ans [jeunes] et >50 ans[âgés]). Le flux sanguin cutané était mesuré par un laser-Doppler au niveau de la peau de l'avant-bras. Nous avons alors mesuré la vasodilatation obtenue par les stimuli suivant : Iontophorèse à l'acétylcholine (ACh, un vasodilatateur dépendant de l'endothélium), iontophorèse au nitroprussiate de sodium (SNP, un donneur d'oxyde nitrique) et par libération d'une interruption momentanée du flux artériel huméral (hyperémie réactive). Chez les sujets entraînés, l'effet de l'hyperémie réactive et de l'ACh n'ont pas montré de différence. Par contre, l'augmentation de la perfusion, suivant la iontophorèse de SNP, exprimé en unité de perfusion (PU), était plus importante chez les sujets entraînés que chez les sujets sédentaires (jeunes: 398±54 vs 350±87, p<0.05; âgés: 339±72 vs 307±66, p<0.05). Pour conclure, l'entraînement d'endurance augmente l'effet vasodilatateur de l'oxyde nitrique de la microcirculation cutanée humaine, au moins au niveau de la peau de l'avant-bras. Ces observations ont un intérêt physiologique considérable au vu des résultats d'études récentes qui montrent que le NO sert d'intermédiaire dans la vasodilatation cutanée produite par un stress thermique. Donc, l'augmentation de la bioactivité du NO dans la microcirculation cutanée pourrait être un des mécanismes par lequel l'entraînement physique modifierait le contrôle de la thermorégulation du flux sanguin cutané. Abstract Endurance training modifies the thermoregulatory control of skin blood flow, as manifested by a greater augmentation of skin perfusion for the same increase in core temperature in athletes, in comparison with se-dentary subjects. In this study, we tested the hypothesis that a component of this adaptation might reside in a higher ability of cutaneous blood vessels to respond to vasodilatory stimuli. We recruited healthy nonsmoking males, either endurance trained or sedentary, in two different age ranges (18-35 y and >50 y). Skin blood flow was measured in the forearm skin, using a laser Doppler imager, allowing to record the vasodilatory responses to the following stimuli: iontophoresis of acetylcholine (an endothelium-dependent vasodilator), iontophoresis of sodium nitroprusside (a nitric oxide donor), and release of a temporary interruption of arterial inflow (reactive hyperemia). There was no effect of training on reactive hyperemia or the response to acetylcholine. In contrast, the increase in perfusion following the iontophoresis of sodium nitroprusside, ex-pressed in perfusion units, was larger in trained than in sedentary subjects (younger: 398±54 vs 350±87, p<0.05; older 339±72 vs 307±66, p<0.05). In conclusion, endurance training enhances the vasodilatory effects of nitric oxide in the human dermal microcirculation, at least in forearm skin. These observations have considerable physiologic interest in view of recent data indicating that nitric oxide mediates in part the cutaneous vasodilation induced by heat stress in humans. Therefore, the augmentation of nitric oxide bioactivity in the dermal microcirculation might be one mechanism whereby endurance training modifies the thermoregulatory control of skin blood flow.

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OBJECTIVES: The goal was to test 2 hypotheses: first, that coronary endothelial function can be measured noninvasively and abnormal function detected using clinical 3.0-T magnetic resonance imaging (MRI); and second, that the extent of local coronary artery disease (CAD), in a given patient, is related to the degree of local abnormal coronary endothelial function. BACKGROUND: Abnormal endothelial function mediates the initiation and progression of atherosclerosis and predicts cardiovascular events. However, direct measures of coronary endothelial function have required invasive assessment. METHODS: The MRI was performed in 20 healthy adults and 17 patients with CAD. Cross-sectional coronary area and blood flow were quantified before and during isometric handgrip exercise, an endothelial-dependent stressor. In 10 severe, single-vessel CAD patients, paired endothelial function was measured in the artery with severe stenosis and the contralateral artery with minimal disease. RESULTS: In healthy adults, coronary arteries dilated and flow increased with stress. In CAD patients, coronary artery area and blood flow decreased with stress (both p </= 0.02). In the paired study, coronary artery area and blood flow failed to increase during exercise in the mildly diseased vessel, but both area (p = 0.01) and blood flow (p = 0.02) decreased significantly in the severely diseased, contralateral artery. CONCLUSIONS: Endothelial-dependent coronary artery dilation and increased blood flow in healthy subjects, and their absence in CAD patients, can now be directly visualized and quantified noninvasively. Local coronary endothelial function differs between severely and mildly diseased arteries in a given CAD patient. This novel, safe method may offer new insights regarding the importance of local coronary endothelial function and improved risk stratification in patients at risk for and with known CAD.

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Systemic lupus erythematosus (SLE) affects multiple organs and systems, severely involving the cardiovascular system. The aim of this study was to evaluate the presence of endothelial dysfunction with N-13-ammonia PET in asymptomatic SLE patients. Methods: We enrolled 16 women with SLE and 16 healthy women. Myocardial blood flow (MBF) was quantified in a 64-slice PET/CT scanner at rest, during a cold pressor test (CPT), and during stress. Endothelium-dependent vasodilation index, %Delta MBF, and myocardial flow reserve (MFR) were calculated. Results: There were 16 women in the SLE group (mean age +/- SD, 31.4 +/- 8.3 y) and 16 women in the healthy control group (31.5 +/- 11.1 y). Mean endothelium-dependent vasodilatation index and %Delta MBF were significantly lower in SLE patients (1.18 +/- 0.55 vs. 1.63 +/- 0.65, P = 0.04, and 18 +/- 55 vs. 63 +/- 65, P = 0.04, respectively). MFR was also lower in the SLE group (2.41 +/- 0.59 vs. 2.73 +/- 0.77, P = 0.20). Conclusion: SLE patients who are free of active disease present abnormal coronary flow and endothelial dysfunction. It is necessary to develop and intensify treatment strategies directed to CAD in SLE patients.

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Postoperative neurosurgical patients are at risk of developing complications. Systemic and neuro-monitoring are used to identify patients who deteriorate in order to treat the underlying cause and minimize the impact on outcome. Hypotension and hypoxia are likely to be the most frequent insults and can be detected easily with blood pressure monitoring and pulse oximetry. Repeated clinical examination, however, is probably the most important monitor in the postoperative setting. Clinical scores such as the Glasgow Coma Score and the more recently introduced FOUR Score are important tools to standardize the clinical assessment. Intracranial pressure monitoring, cerebral blood flow monitoring, electroencephalography, and brain imaging are often used postoperatively. Despite the numerous publications on this topic only few studies address the impact of postoperative monitoring on outcome. Accordingly, in most patients the decision on which monitors are to be used must be based on the patient's presentation and clinical judgment.

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Recent studies at high magnetic fields using the phase of gradient-echo MR images have shown the ability to unveil cortical substructure in the human brain. To investigate the contrast mechanisms in phase imaging, this study extends, for the first time, phase imaging to the rodent brain. Using a 14.1 T horizontal bore animal MRI scanner for in vivo micro-imaging, images with an in-plane resolution of 33 microm were acquired. Phase images revealed, often more clearly than the corresponding magnitude images, hippocampal fields, cortical layers (e.g. layer 4), cerebellar layers (molecular and granule cell layers) and small white matter structures present in the striatum and septal nucleus. The contrast of the phase images depended in part on the orientation of anatomical structures relative to the magnetic field, consistent with bulk susceptibility variations between tissues. This was found not only for vessels, but also for white matter structures, such as the anterior commissure, and cortical layers in the cerebellum. Such susceptibility changes could result from variable blood volume. However, when the deoxyhemoglobin content was reduced by increasing cerebral blood flow (CBF) with a carbogen breathing challenge, contrast between white and gray matter and cortical layers was not affected, suggesting that tissue cerebral blood volume (and therefore deoxyhemoglobin) is not a major source of the tissue phase contrast. We conclude that phase variations in gradient-echo images are likely due to susceptibility shifts of non-vascular origin.

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PURPOSE OF REVIEW: To present the practical aspects of transcranial Doppler (TCD) and provide evidence supporting its use for the management of traumatic brain injury (TBI) patients. RECENT FINDINGS: TCD measures systolic, mean, and diastolic cerebral blood flow (CBF) velocities and calculates the pulsatility index from basal intracranial arteries. These variables reflect the brain circulation, provided there is control of potential confounding factors. TCD can be useful in patients with severe TBI to detect low CBF, for example, during intracranial hypertension, and to assess cerebral autoregulation. In the emergency room, TCD might complement brain computed tomography (CT) scan and clinical examination to screen patients at risk for further neurological deterioration after mild-to-moderate TBI. SUMMARY: The diagnostic value of TCD should be incorporated into other findings from multimodal brain monitoring and CT scan to optimize the bedside management of patients with TBI and help guide the choice of appropriate therapies.

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Subarachnoid haemorrhage (SAH) is a form of stroke that is associated with substantial morbidity, often as a result of cerebral ischaemia that occurs in the following days. These delayed deficits in blood flow have been traditionally attributed to cerebral vasospasm (the narrowing of large arteries), which can lead to cerebral infarction and poor neurological outcome. Data from recent studies, however, show that treatment of vasospasm in patients with SAH, using targeted medication, does not translate to better neurological outcomes, and argue against vasospasm being the sole cause of the delayed ischaemic complications. Cerebral autoregulation-a mechanism that maintains stability of cerebral blood flow in response to changes in cerebral perfusion pressure-has been reported to fail after SAH, often before vasospasm becomes apparent. Failure of autoregulation, therefore, has been implicated in development of delayed cerebral ischaemia. In this Review, we summarize current knowledge about the clinical effect of disturbed cerebral autoregulation following aneurysmal SAH, with emphasis on development of delayed cerebral ischaemia and clinical outcome, and provide a critical assessment of studies of cerebral autoregulation in SAH with respect to the method of blood-flow measurement. Better understanding of cerebral autoregulation following SAH could reveal mechanisms of blood-flow regulation that could be therapeutically targeted to improve patient outcome.

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BACKGROUND: Vascular reconstructions are becoming challenging due to the comorbidity of the aging population and since the introduction of minimally invasive approaches. Many sutureless anastomosis devices have been designed to facilitate the cardiovascular surgeon's work and the vascular join (VJ) is one of these. We designed an animal study to assess its reliability and long-term efficacy. METHODS: VJ allows the construction of end-to-end and end-to-side anastomoses. It consists of two metallic crowns fixed to the extremity of the two conduits so that vessel edges are joined layer by layer. There is no foreign material exposed to blood. In adult sheep both carotid arteries were prepared and severed. End-to-end anastomoses were performed using the VJ device on one side and the classical running suture technique on the other side. Animals were followed-up with Duplex-scan every 3 months and sacrificed after 12 months. Histopathological analysis was carried out. RESULTS: In 20 animals all 22 sutureless anastomoses were successfully completed in less than 2 min versus 6 +/- 3 min for running suture. Duplex showed the occlusion of three controls and one sutureless anastomosis. Two controls and one sutureless had stenosis >50%. Histology showed very thin layer of myointimal hyperplasia (50 +/- 10 microm) in the sutureless group versus 300 +/- 27 microm in the control. No significant inflammatory reaction was detected. CONCLUSIONS: VJ provides edge-to-edge vascular repair that can be considered the most physiological way to restore vessel continuity. For the first time, in healthy sheep, an anastomotic device provided better results than suture technique.

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Since its introduction 16 years ago, the astrocyte-neuron lactate shuttle (ANLS) model has profoundly modified our understanding of neuroenergetics by bringing a cellular and molecular resolution. Praised or disputed, the concept has never ceased to attract attention, leading to critical advances and unexpected insights. Here, we summarize recent experimental evidence further supporting the main tenets of the model. Thus, evidence for distinct metabolic phenotypes between neurons (mainly oxidative) and astrocytes (mainly glycolytic) have been provided by genomics and classical metabolic approaches. Moreover, it has become clear that astrocytes act as a syncytium to distribute energy substrates such as lactate to active neurones. Glycogen, the main energy reserve located in astrocytes, is used as a lactate source to sustain glutamatergic neurotransmission and synaptic plasticity. Lactate is also emerging as a neuroprotective agent as well as a key signal to regulate blood flow. Characterization of monocarboxylate transporter regulation indicates a possible involvement in synaptic plasticity and memory. Finally, several modeling studies captured the implications of such findings for many brain functions. The ANLS model now represents a useful, experimentally based framework to better understand the coupling between neuronal activity and energetics as it relates to neuronal plasticity, neurodegeneration, and functional brain imaging.

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OBJECTIVE: To determine the usefulness of computed tomography (CT), magnetic resonance imaging (MRI), and Doppler ultrasonography (US) in providing specific images of gouty tophi. METHODS: Four male patients with chronic gout with tophi affecting the knee joints (three cases) or the olecranon processes of the elbows (one case) were assessed. Crystallographic analyses of the synovial fluid or tissue aspirates of the areas of interest were made with polarising light microscopy, alizarin red staining, and x ray diffraction. CT was performed with a GE scanner, MR imaging was obtained with a 1.5 T Magneton (Siemens), and ultrasonography with colour Doppler was carried out by standard technique. RESULTS: Crystallographic analyses showed monosodium urate (MSU) crystals in the specimens of the four patients; hydroxyapatite and calcium pyrophosphate dihydrate (CPPD) crystals were not found. A diffuse soft tissue thickening was seen on plain radiographs but no calcifications or ossifications of the tophi. CT disclosed lesions containing round and oval opacities, with a mean density of about 160 Hounsfield units (HU). With MRI, lesions were of low to intermediate signal intensity on T(1) and T(2) weighting. After contrast injection in two cases, enhancement of the tophus was seen in one. Colour Doppler US showed the tophi to be hypoechogenic with peripheral increase of the blood flow in three cases. CONCLUSION: The MR and colour Doppler US images showed the tophi as masses surrounded by a hypervascular area, which cannot be considered as specific for gout. But on CT images, masses of about 160 HU density were clearly seen, which correspond to MSU crystal deposits.

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The effect of circulating arginine vasopressin (AVP) on blood pressure, heart rate, and skin blood flow was assessed in normotensive subjects, mild hypertensive patients, and patients with congestive heart failure, utilizing the specific antagonist of AVP at the vascular receptor level, d(CH2)5Tyr(Me)AVP (5 micrograms/kg i.v.). The renin system of the normal volunteers treated with the AVP antagonist was either intact or acutely blocked with the angiotensin converting-enzyme inhibitor captopril (25 mg p.o.). In some volunteers, the cardiovascular effect of AVP released by Finnish sauna or cigarette smoking was studied. In patients with congestive heart failure, hemodynamic measurements (pressures and cardiac output) were obtained invasively. Acute blockade of AVP vascular receptors produced no cardiovascular effect unless plasma AVP levels were markedly elevated. In our experience, abnormally high circulating AVP appears to be responsible for the decrease in skin blood flow induced by cigarette smoking and to some extent for the maintenance of vascular tone in the rare patients with particularly severe congestive heart failure.