The aim of this work is to find a stable scheme which would solve the Stokes problem of the fluid flow, in which an elastic structure is immersed. Unlike most of the schemes solving fluid-structure interaction problems, in our scheme meshes of fluid and structure do not have to coincide. We have restricted ourselves to two-dimensional domain occupied by fluid with one-dimensional im- mersed structure. To describe a fluid-structure interaction, we have used an Immersed boundary method. At first we consider the strucure to be massless. We have modified an existing scheme and made it unconditionally stable, which was mathematically proven and numerically tested. Then we have proposed a modification where the structure is not massless and also proved the uncondi- tional stability in this case. The proposed schemes were implemented using the Freefem++ software and tested on aneurysm-like geometry. We have tested the behavior of our scheme in case when the qrowing aneurysm touches an obstacle, for example a bone (with no-slip condition on the bone boundary). Powered by TCPDF (www.tcpdf.org)

This study investigated whether acute myocardial ischemia of the anterior left ventricular wall induced an increase in cardiac sympathetic efferent nerve activity and thereby affected regional myocardial blood flow and contractile function.

No description available.

The Arterial Spin Labelling (ASL) method is a Magnetic Resonance technique used toquantify the cerebral perfusion. It has the big advantage to be non-invasive so doesn’tneed the injection of any contrast agent. But due to a relatively low Signal-to-NoiseRatio (SNR) of the signal acquired (only approximately 1% of the image intensity), ithas been hampered to be widely used in a clinical setting so far.The primary objective of this project is to make the method more robust by improvingthe quality of the images, the SNR, and by reducing the acquisition time. DifferentASL protocols with different sets of parameters have been investigated. The modificationsperformed on the protocol have been investigated by analyzing images acquired onhealthy volunteers. An optimized protocol leading to a good trade-off between the differentaspects of the method, has been suggested. It is characterized by a 3:43:44:0mm3with a two-segment acquisition.A more advanced ASL method implies the acquisition of images at different inversiontimes (TI), which is called the mutli-TI method. The influence of the range of TI used inthe method has been explored. An optimized TI range (from 410ms to 3860ms, sampledevery 150ms) has been suggested to make the ASL method as performant as possible.A numerical model and a fitting algorithm have been used to extract the informationon the perfusion from the images acquired. Different models have been investigated aswell as their influence on the reliability of the results.Finally, a criterion has been implemented to evaluate the reliability of the results sothat the clinician or the user of the method can figure out how much he can count onthe results provided by the method.

Unilateral ischemia-reperfusion (UIR) injury leads to progressive renal atrophy and tubulointerstitial fibrosis (TIF) and is commonly used to investigate the pathogenesis of the acute kidney injury-chronic kidney disease transition. Although it is well known that contralateral nephrectomy (CNX), even 2 wk post-UIR injury, can improve recovery, the physiological mechanisms and tubular signaling pathways mediating such improved recovery remain poorly defined. Here, we examined the renal hemodynamic and tubular signaling pathways associated with UIR injury and its reversal by CNX. Male Sprague-Dawley rats underwent left UIR or sham UIR and 2 wk later CNX or sham CNX. Blood pressure, left renal blood flow (RBF), and total glomerular filtration rate were assessed in conscious rats for 3 days before and over 2 wk after CNX or sham CNX. In the presence of a contralateral uninjured kidney, left RBF was lower (P < 0.05) from 2 to 4 wk following UIR (3.6 + 0.3 mL/min) versus sham UIR (9.6 + 0.3 mL/min). Without CNX, extensive renal atrophy, TIF, and tubule dedifferentiation, but minimal pimonidazole and hypoxia-inducible factor-1α positivity in tubules, were present at 4 wk post-UIR injury. Conversely, CNX led (P < 0.05) to sustained increases in left RBF (6.2 ∓ 0.6 mL/min) that preceded the increases in glomerular filtration rate. The CNX-induced improvement in renal function was associated with renal hypertrophy, more redifferentiated tubules, less TIF, and robust pimonidazole and hypoxia-inducible factor-1α staining in UIR injured kidneys. Thus, contrary to expectations, indexes of hypoxia are not observed with the extensive TIF at 4 wk post-UIR injury in the absence of CNX but are rather associated with the improved recovery of renal function and structure following CNX.

Indiana University-Purdue University Indianapolis (IUPUI) / Coronary microvascular function is markedly impaired by the onset of the metabolic syndrome and may be an important contributor to the increased cardiovascular events associated with this mutlifactorial disorder. Despite increasing appreciation for the role of coronary K+ channels in regulation of coronary microvascular function, the contribution of K+ channels to the deleterious influence of metabolic syndrome has not been determined. Accordingly, the overall goal of this investigation was to delineate the mechanistic contribution of K+ channels to coronary microvascular dysfunction in metabolic syndrome. Experiments were performed on Ossabaw miniature swine fed a normal maintenance diet or an excess calorie atherogenic diet that induces the classical clinical features of metabolic syndrome including obesity, insulin resistance, impaired glucose tolerance, dyslipidemia, hyperleptinemia, and atherosclerosis. Experiments involved in vivo studies of coronary blood flow in open-chest anesthetized swine as well as conscious, chronically instrumented swine and in vitro studies in isolated coronary arteries, arterioles, and vascular smooth muscle cells. We found that coronary microvascular dysfunction in the metabolic syndrome significantly impairs coronary vasodilation in response to metabolic as well as ischemic stimuli. This impairment was directly related to decreased membrane trafficking and functional expression of BKCa channels in vascular smooth muscle cells that was accompanied by augmented L-type Ca2+ channel activity and increased intracellular Ca2+ concentration. In addition, we discovered that impairment of coronary vasodilation in the metabolic syndrome is mediated by reductions in the functional contribution of voltage-dependent K+ channels to the dilator response. Taken together, findings from this investigation demonstrate that the metabolic syndrome markedly attenuates coronary microvascular function via the diminished contribution of K+ channels to the overall control of coronary blood flow. Our data implicate impaired functional expression of coronary K+ channels as a critical mechanism underlying the increased incidence of cardiac arrhythmias, infarction and sudden cardiac death in obese patients with the metabolic syndrome.

No description available.

The study applies in vivo technique for profiling hemodynamics and wall shear stress (WSS) distribution in human coronary arteries. The methodology involves fusion of 2D Intra Vascular Ultra Sound and Bi-plane angiograms to reproduce the 3D arterial geometry. This geometry is then used in a Computational Fluid Dynamics (CFD) module for flow modeling. The Walburn and Schneck constitutive relation was used to represent the non-Newtonian blood rheology. The methodology is applied to study the relationship between WSS and Neointimal Hyperplasia (NIH) in two groups of diabetic patients after being treated separately with bare metal stents (BMS) and Sirolimus Eluting Stents (SES). The stent assignments were blinded until the end of the study. The study was repeated for the patients after 9 months. The predicted WSS ranged from (0.1- 8 N/m2) and was categorized into five classes: low ( < 1 N/m2); low-normal (1-2 N/m2); normal (2-3 N/m2); high-normal (3-4 N/m2); high ( > 4 N/m2). The results indicate NIH in 5 of the patients treated with BMS and none in SES cases. These results correlate with our predicted WSS distribution.

Purpose The vascular endothelium is an influential contributor to vasodilation at rest, yet its role during peak exercise is relatively unknown. The purpose of this study is to determine if exercise leg blood flow during dynamic submaximal and maximal exercise is related to resting vascular endothelial function. Methods Nineteen subjects (aged 23 ± 0.57 yr) completed multiple assessments of vascular endothelial function including passive leg movement (PLM), rapid onset vasodilation, (ROV) and flow-mediated dilation (FMD). Peak muscle blood flow was assessed during single leg knee extension (KE) exercise. Doppler ultrasound of the femoral artery was utilized to assess muscle blood flow. Results Peak exercise blood flow was linearly related with microvascular endothelial function determined by PLM (P < 0.001) and ROV (P < 0.001). Normalizing muscle blood flow for quadriceps mass did not change this significant association. Individuals with high vascular endothelial function had greater muscle blood flow during KE compared to those with low endothelial function (P = 0.05). Post hoc analysis indicated a significant difference in blood flow between high and low endothelial function groups at 20 W, 30 W, and peak flow (P = 0.042, 0.048, 0.001, respectively). Conclusion Peak muscle blood flow during dynamic exercise is correlated with vascular endothelial function, as measured by PLM and ROV, accounting for between 30 to 50% of the variance in this relationship. These data support the hypothesis that endothelial function significantly contributes to the peak blood flow response during dynamic exercise.

Patients who are treated in an intensive care unit need continuous monitoring in orderfor clinicians to be prepared to intervene should a secondary event occur. For patientstreated at the neurointensive care unit (NICU) who have suffered a subarachnoid hemorrhage (SAH) this secondary event could be ischemia, resulting in a lack of blood flow.Blood flow can be measured using magnetic resonance imaging (MRI). The process is facilitated with a software called NOVA. Repeated measurements can therefore be performedas a way to monitor the patients, which in this context would be referred to as longitudinalmeasurements. As more data can be collected ways of analyzing and visualizing the datain a comprehensible way is needed. The aim of this thesis was therefore to develop and implement a method for analyzing and visualizing the longitudinal MR measurement data.With this aim in mind two research questions were relevant. The first one was how NOVAflow longitudinal measurements can be visualized to simplify interpretation by cliniciansand the second one was in what ways the longitudinal data can be analyzed. A graphicaluser interface (GUI) was created to present the developed analysis and visualization tool.Development of the tool progressed using feedback from supervisors and neurosurgeons.Visualization and analysis was done through plots of blood velocity and blood flow as themain component as well as a 2D vessel map. The final implementation showed multipleexamples of how the longitudinal data could be both visualized and analyzed. The resultstherefore provided a tool to analyze and visualize NOVA flow longitudinal measurementsin a way which was easily interpreted. Further improvements of the tool is possible andan area of improvement could involve increasing the adaptability of the tool.