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1
Herrey, Annekatrin Synje. "Hibernating Myocardium". Thesis, Imperial College London, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.508720.
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2
Park, Jade. "Myocardial fibrosis and effect of AZT in myocardium of Y995CB mouse". Thesis, Boston University, 2012. https://hdl.handle.net/2144/12581.
Testo completoAbstract (sommario):
Thesis (M.A.)--Boston University
PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.Pyrimidine nucleoside reverse transcriptase inhibitors (NRTIs), one of the primary classes of HIV/AIDS antiretroviral drugs, are known to cause mitochondrial toxicity by inhibiting polymerase gamma during extending mitochondrial DNA replication. Extensive, prolonged use of NRTIs, such as zidovudine (3'-azido-2',3'-deoxythymidine; AZT), is associated with cardiovascular complications, such as dilated cardiomyopathy, the most common form of heart failure in which cardiac fibrosis is seen. Moreover, cardiac fibrosis is part of the pathological response of the heart during the progression of heart failure. Thus, we hypothesized that AZT treatment will contribute to the progression of cardiac fibrosis indirectly. Our study specifically focused on the effects of AZT and the development of cardiac fibrosis in the myocardium of wildtype (WT) and Y955CB transgenic mice (TG). Y955CB TG expresses a dominant negative cardiac specific mutant mitochondrial DNA polymerase gamma and were used to enhance the mtDNA toxic effect of AZT. To estimate fibrosis, myocardial collagen levels in each treatment group were assessed using both the hydroxyproline assay and histological image analysis. WT mice treated with AZT 0.22 mg/day for 35 days revealed no change in the level of hydroxyproline. However, a significant increase in hydroxyproline abundance correlated with histologically detectable fibrosis in vehicle-treated Y955CB TG mice. Interestingly, there was no additional increase in the abundance of collagen in AZT-treated Y955CB mice. Taken together, these data demonstrate that Y955CB TG displays an increase in the collagen level of the heart, concomitant with its documented cardiomyopathy. However AZT treatment was insufficient to increase the abundance of collagen in the heart.
3
White, Melanie Yvonne. "Proteomics of ischemia/reperfusion injury in rabbit myocardium". Thesis, The University of Sydney, 2006. https://hdl.handle.net/2123/27890.
Testo completoAbstract (sommario):
Myocardial stunning is best defined as the persistent, yet reversible, contractile dysfunction
that occurs with brief myocardial ischemia / reperfusion (I/R) injury. In contrast, prolonged
ischemia results in myocardial infarction that leads to cell death of necrosis of the tissue. The
causes of stunning are not fully elucidated, however two major hypotheses currently exist;
firstly changes to calcium handling resulting from lowered cellular pH by means of anaerobic
respiration, and altered Nair/H)r antiporter kinetics, and secondly, the generation oxygen free
radical (OFR) that may occur in a dramatic ‘surge’ at the onset of reperfusion. Treatment of
ischemic myocardium with calcium channel blockers and / or OFR scavengers has been
successfully shown to prevent stunning in various animal models. Whilst much is known
about the physiological and biochemical changes that occur in stunned myocardium, very
little is known about events at the molecular level. Since stunning occurs after only brief (15
minutes low-flow in the rabbit model) ischemia and subsequent reperfusion, we hypothesized
that these molecular events are not predominated by large changes in protein expression and
abundance, yet rather by subtle and / or transient changes to protein post-translational
modifications (PTM). Such changes at the protein level are best analysed using the
technologies encompassed under the term ‘proteomics’.
4
Shenje, Lincoln Takura. "Studies assessing cardiac myocyte renewal and myocardial repair in the adult mammalian myocardium". Thesis, University of Leicester, 2007. http://hdl.handle.net/2381/29896.
Testo completoAbstract (sommario):
The initial aims of this thesis were to investigate whether the myocardium contains resident progenitor cells that contribute to myocardial renewal and whether extra-cardiac bone marrow derived cells contribute to myocardial regeneration. I reveal that the myocardium has the capacity to produce humoral factors that enable extra-cardiac progenitors to survive in vitro though this was insufficient to induce cardiac differentiation. I have shown that the myocardium has the capacity to produce a heterogeneous population of cells in vitro, some of which express cardiac related markers but do not adopt a full cardiac phenotype. When these cells are transplanted into a normal or injured heart they integrate into the myocardium but fail to develop a full mature functional cardiac phenotype. I have set up the frame work for demonstrating and defining the qualitative histological structure of the myocardium using lineage tracing techniques and strengthening the criteria for defining various cell lineages in the heart and therefore demonstrated the deficiencies of seminal studies that claimed that adult stem cells had the capacity to differentiate into cardiomyocytes and secondly that cultured heart explants produce cardiac progenitors. From this work it is clear that more needs to be done to identify the various cell lineages and roles of endogenous cardiac cells. The identification of clusters of perivascular cells expressing cardiac markers using 3 dimensional confocal imaging by two photon molecular excitation provided a different approach for identifying putative cardiac progenitors. This in combination with lineage tracing techniques and cell isolation is now required to identify the role of these interesting perivascular cells in cardiac homeostasis.
5
Sheehy, Sean Paul. "Design Considerations for Engineered Myocardium". Thesis, Harvard University, 2014. http://dissertations.umi.com/gsas.harvard:11607.
Testo completoAbstract (sommario):
The fabrication of biomimetic heart muscle suitable for pharmaceutical compound evaluation and disease modeling is hindered by limitations in our understanding of how to guide and assess the maturity of engineered myocardium in vitro. We hypothesized that tissue architecture serves as an important cue for directing the maturation of engineered heart tissues and that reliable assessment of maturity could be performed using a multi-parametric rubric utilizing cardiomyocytes of known developmental state as a basis for comparison. Physical micro-environmental cues are recognized to play a fundamental role in normal heart development, therefore we used micro-patterned extracellular matrix to direct isolated cardiac myocytes to self-assemble into anisotropic sheets reminiscent of the architecture observed in the laminar musculature of the heart. Comparison of global sarcomere alignment, gene expression, and contractile stress in engineered anisotropic myocardium to isotropic monolayers, as well as, adult ventricular tissue revealed that anisotropic engineered myocardium more closely matched the characteristics of adult ventricular tissue, than isotropic cultures of randomly organized cardiomyocytes. These findings support the notion that tissue architecture is an important cue for building mature engineered myocardium. Next, we sought to develop a quality assessment strategy that utilizes a core set of 64 experimental measurements representative of 4 major categories (i.e. gene expression, myofibril structure, electrical activity, and contractility) to provide a numeric score of how closely stem cell-derived cardiac myocytes match the physiological characteristics of mature, post-natal cardiomyocytes. The efficacy of this rubric was assessed by comparing anisotropic engineered tissues fabricated from commercially-available murine ES- (mES) and iPS- (miPS) derived myocytes against neonatal mouse ventricular myocytes. The quality index scores calculated for these cells revealed that the miPS-derived myocytes more closely resembled the neonate ventricular myocytes than the mES-derived myocytes. Taken together, the results of these studies provide valuable insight into the fabrication and validation of engineered myocardium that faithfully recapitulate the characteristics of mature ventricular myocardium found in vivo. These engineered tissue design and quality validation strategies may prove useful in developing heart muscle analogs from human stem cell-derived myocytes that more accurately predict patient response than currently used animal models.Engineering and Applied Sciences
6
Löwbeer, Christian. "Cardiac troponin T in clinical and experimental studies /". Stockholm, 2007. http://diss.kib.ki.se/2007/978-91-7357-426-6/.
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7
Shum-Tim, Dominique. "The protection of the newborn myocardium". Thesis, McGill University, 1994. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=26146.
Testo completoAbstract (sommario):
Definitive repair of complex congenital cardiac defects in early life has become the recent trend in pediatric cardiac surgery. This early aggressive surgical approach is to avoid the detrimental effects on the heart of chronic cyanosis, hypertrophy and volume overload which are the consequences of unrepaired congenital malformations. Adequate protection of the heart, not only during the period of corrective surgery, but also certain pre-ischemic events remain of paramount importance to the success of these operations. Profound systemic hypothermia followed by total circulatory arrest is widely used for the correction of congenital cardiac defects in the newborn. It involves a period of cold systemic perfusion on cardiopulmonary bypass before circulatory arrest is established. Using an isolated perfused piglet heart model, the first study demonstrated that prolonged cold perfusion of the immature heart could be detrimental in itself. When followed by a period of ischemic arrest, it further potentiated the myocardial injury and induced severe irreversible contracture. Further extension of this study showed that verapamil administered prior to prearrest cold perfusion could indeed minimize the functional and ultrastructural damage of prolonged myocardial cooling. This shed some light to the pathophysiology of prolonged prearrest cooling contracture of the newborn myocardium.
8
Gray, Caroline Claudia. "Indogenous protection of the iscaemic myocardium". Thesis, Imperial College London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.252345.
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9
Ahmad, Maqsood. "Kinin peptides in the ischaemic myocardium". Thesis, University of Strathclyde, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248756.
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10
Al-Mohammad, Abdallah. "Hibernating myocardium : prevalence and surrogate markers". Thesis, University of Aberdeen, 2017. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=235453.
Testo completoAbstract (sommario):
The aims of this thesis are to determine: 1. The true prevalence of hibernating myocardium in patients with severely impaired left ventricular contraction. (Chapter 3) 2. The viability status of the left ventricular wall aneurysm as defined by positron emission tomography. (Chapter 4) 3. The relationship between the incidence of hibernating myocardium and the coronary artery flow grade determined angiographically. (Chapter 5) 4. The relationship between the presence of Q waves (with or without preserved R wave) on the surface electrocardiogram and the presence of scar in the myocardium as diagnosed by positron emission tomography. (Chapter 6) 5. The relationship between the incidence of hibernating myocardium and QT dispersion on the surface electrocardiogram. (Chapter 7) 6. Looking for other markers of hibernation by PET. (Chapters 8 and 9) I proposed to look at the relationship between continuing metabolic activity in 10 akinetic or severely hypokinetic segments as an alternative method and thus as a new definition of pre-operative determination of hibernating myocardium. This is the topic in Chapter 8. Following the completion of question number 3, and the observed role of collateral circulation, I proposed to look into the role of TIMI 0-1 and collaterals grade 2-3 in maintaining viability and their role as a marker of hibernating myocardium. This won support in the form of a research grant from the British Heart Foundation in 1998. This was the topic of my last project, which was added to the thesis after its initial completion on the 23rd of December 2000. This is the topic of Chapter 9. 7. Following the delayed submission of the Thesis in 2015, I was asked to add Chapter 11 which summarised both my contribution since the Thesis was concluded into the topic of Hibernating myocardium; and the knowledge progression into the detection of the phenomenon and its clinical usefulness to bring the Thesis up to date. Methods: The patients were those with coronary artery disease and impaired left ventricular contraction recruited into a series of studies of the presence of hibernating myocardium using positron emission tomography, as the method of choice to preoperatively detect this phenomenon. The patients were either recruited from the cardiac catheterization laboratory or from the cohort of patients presenting with myocardial infarction to the cardiology unit at Aberdeen Royal Infirmary. All the studies were approved by the Grampian Research Ethics Committee. In some of the studies, cardiac magnetic resonance imaging was used for simple assessment of the myocardial contraction and thickening in the study reported in Chapter 9. Results and Conclusions: 1. Hiberanting myocardium affects over 50% of the patients with severe left ventricular systolic impairment with coronary artery disease. (Chapter 3). 2. None of the aneurysmal segments are viable. (Chapter 4) 3. Compared to the areas supplied by arteries with Thrpmbolysis In Myocardial Infarction (TIMI) flow grades 2-3, the areas supplied by almost occluded coronary arteries (TIMI 0-1 flow grades) are significantly more likely to have both evidence of scarred myocardium (highly significantly statistical difference p < 0.0001) and evidence of hibernating myocardium, just reaching statistical significance (p < 0.05). (Chapter 5) 4. The specificity of Q waves on the electrocardiogram (ECG) as markers for 11 myocardial scarring is 79%, with a low sensitivity of 41%. (Chapter 6) 5. Maintaining R waves following a pathological Q wave on the ECG is not helpful for predicting the presence of hibernating myocardium. (Chapter 6) 6. The presence or absence of hibernating myocardium did not impact on native QT dispersion, rate corrected QTc dispersion or on the maximum adjacent QT dispersion on the ECG. (Chapter 7). 7. A new definition of hibernating myocardium is proposed, helping to detect it preoperatively through the demonstration of metabolism – mechanical mismatch defect using a single radio-pharmaceutical. (Chapter 8) 8. As a marker of the classical perfusion –metabolism mismatch defect, the new proposed metabolism-mechanical mismatch defect by PET is sensitive (92%) and specific (97%), with excellent positive and negative predictive accuracies (96% and 93%, respectively). (Chapter 8) 9. While collaterals grade 2-3 supplying territories with blocked arteries and flow grades TIMI 0-1 may be sensitive markers (83%) of hibernating myocardium; they lack specificity (20%), and the differences between the two small groups completing the study did not reach statistical significance. (Chapter 9).
11
Howells, Ruairidh. "T₂-weighted BOLD in human myocardium". Thesis, University of Oxford, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.589620.
Testo completoAbstract (sommario):
The principal aim of this work is to test the viability of Blood Oxygenation Level Dependent (BOLD) measurements in human myocardium, an experiment which has seen promising attempts in recent literature. A central challenge to the ~uccess of these experiments has been in the limited scale of the measured effect; this work therefore includes efforts to separate the BOLD effect from noise and confounding signals. BOLD is then measured by intensity in MR images produced using Steady State Free Precession (SSFP) acquisition, weighted by a T2 preparation module to introduce the target contrast. Two modelling sections are included: first, the changes in physiology which influence the signal intensity in the MR images via the T2 dependence; and secondly the factors upon which the preparation depends, which are not entirely limited to the T2 of the tissue. These models are investigated with the aim of increasing the BOLD contrast and removing any other dependencies. An empirical model is shown to be suitable for the relationship between oxygenation and T2, and improvements are suggested and explained by thorough simulation ofthe preparation module. Compensation for a further confounding effect is also investigated: that of the increase in heart rate which accompanies the adenosine infusion used in the BOLD experiment protocol to reveal differences in the response of ischaemic and healthy tissue. The compensation is shown to reduce temporal variance in SI measurements, and to increase the separation between distributions of SI in tissue classes. A process of registration and segmentation is refined for sampling BOLD information from the SS FP images, and tested to show a low failure rate. Finally, the BOLD process is then tested in a set of human subjects including healthy volunteers and patients with coronary artery disease, investigating the consequent difference in tissue oxygenation. A significant difference is shown in the responses to stress of BOLD SI three tissue classes in these subjects.
12
Jager, Tertia de. "Estrogen action in the myocardium modulation of myocardial gene expression and the influence on cardiac hypertrophy /". [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=964433621.
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13
Aghassibake, Kristina Diane. "Quantifying non-axial deformations in rat myocardium". Thesis, Texas A&M University, 2004. http://hdl.handle.net/1969.1/1340.
Testo completoAbstract (sommario):
While it is clear that myocardium responds to mechanical stimuli, it is unknown whether myocytes transduce stress or strain. It is also unknown whether myofibers maintain lateral connectivity or move freely over one another when myocardium is deformed. Due to the lack of information about the relationship between macroscopic and cellular deformations, we sought to develop an experimental method to examine myocyte deformations and to determine their degree of affinity. A set of protocols was established for specimen preparation, image acquisition, and analysis, and two experiments were performed according to these methods. Results indicate that myocyte deformations are non-affine; therefore, some cellular rearrangement must occur when myocardium is stretched.
14
Tones, Michael Anthony. "Reoxygenation induced calcium uptake in the myocardium". Thesis, Imperial College London, 1985. http://hdl.handle.net/10044/1/37879.
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15
Baik, Sonya A. "Catecholamines and basal metabolism in the myocardium". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ34085.pdf.
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16
Fisher, Simon George. "Signalling in the ischaemic and preconditioned myocardium". Thesis, King's College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.407235.
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17
Debney, Michael Thomas. "Enhancing gap junction coupling in reperfused myocardium". Thesis, Imperial College London, 2015. http://hdl.handle.net/10044/1/28124.
Testo completoAbstract (sommario):
The work in this thesis sought to examine the effects of enhancing cardiac gap junction coupling using the pharmacological agent Rotigaptide in clinically applicable models of acute myocardial infarction. Specifically, the studies in this thesis investigated the effect of Rotigaptide on ventricular arrhythmogenesis and structural remodelling of the reperfused substrate, with particular emphasis on the development, application and histological validation of diffusion tensor magnetic resonance imagine (DTI) as a novel imaging modality to describe and quantify structural remodelling post-infarction. An ex vivo rat model of acute regional ischaemia-reperfusion was characterised and used to study the effect of Rotigaptide on ventricular arrhythmogenesis during acute ischaemia and reperfusion. Arrhythmias occurred during ischaemia in a monomodal distribution with a peak incidence between 12-15 minutes after ischaemia. The incidence of reperfusion arrhythmias was dependent on the preceding duration of ischaemia with a progressive reduction as ischaemic time extended from 15 to 60 minutes. Rotigaptide pre-treatment afforded a significant reduction in ischaemia-induced arrhythmias compared to administration at the onset of ischaemia or at the time of reperfusion. An in vivo rat model of infarction-reperfusion, mimicking clinical reperfusion in the setting of acute MI was characterised and Rotigaptide administered prior to reperfusion and for a week post-MI. At four-weeks post-MI animals were studied with 6-lead ECG, ambulatory telemetry, programmed electrical simulation (PES), optical mapping, DTI and histology. Rotigaptide reduced the susceptibility to arrhythmias induced by PES and partially restored DTI-derived indices of tissue disruption in infarcted myocardium.
18
Fesenko, I. V., e D. M. Sheyan. "Modeling cryonecrosis of the myocardium in rats". Thesis, Sumy State University, 2017. http://essuir.sumdu.edu.ua/handle/123456789/54314.
Testo completoAbstract (sommario):
Relevance. Every year in our country there are nearly 50 thousand new cases myocardial infarction. Myocardial infarction (MI) is one of the forms of myocardial necrosis caused by a violation of inflow of blood through the affected artery. Improving ways to prevent and treat THEM can be based on new experimental models.
19
Emery, Jeffrey Lorne. "Load-history dependence of resting ventricular myocardium /". Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 1997. http://wwwlib.umi.com/cr/ucsd/fullcit?p9804506.
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20
Wee, Shirley Sheau Yan. "P2Purinoceptor-Dependent Cardioprotection in Ischaemic-Reperfused Myocardium". Thesis, Griffith University, 2012. http://hdl.handle.net/10072/365704.
Testo completoAbstract (sommario):
The P2 purinoceptor family are perhaps the earliest (or most 'primitive') group of
regulatory cell surface receptors, and have been studied intensely for several decades.
The P2 receptors are subdivided into two major families, P2X subtypes (P2X1, P2X2,
P2X3, P2X4, P2X5, P2X6 and P2X7,) and P2Y subtypes (P2Y1, P2Y2, P2Y4, P2Y6,
P2Y11, P2Y12, P2Y13, and P2Y14). In the cardiovascular system P2 purinoceptors have
been implicated both in vasoconstriction and vasodilatation, cardiac inotropy,
cardioprotection (including pre- and postconditioning responses), and diseasedependent
cardiac dysfunction. Furthermore, increasing evidence indicates that P2
purinoceptors form functional heteromeric assemblies under certain conditions,
adding to the complexity of purinoceptor functionality. Thus, full characterisation of
the regulatory function of these receptors is yet to be accomplished. This thesis
comprises a series of studies aimed at elucidating the roles of P2 purinoceptors
(primarily the P2Y2 subtype) in protecting the heart during ischaemia-reperfusion
(relevant to the injurious effects of acute myocardial infarction).Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Medical Science
Science, Environment, Engineering and Technology
Full Text
21
Bull, Sacha Colette. "Aortic stenosis : pathophysiological effects on the myocardium and predictors of clinical events : physiology of the myocardium in aortic stenosis". Thesis, University of Oxford, 2012. http://ora.ox.ac.uk/objects/uuid:a05f5eea-ae68-43a5-84b3-d9a0a1ee40ce.
Testo completoAbstract (sommario):
The management of the asymptomatic patients with severe aortic stenosis (AS) is challenging; clinicians have to balance the risks of early surgery against the risk that irreversible myocardial damage may occur with a conservative management strategy. It has become increasingly apparent that prognosis in asymptomatic AS depends not only on the degree of valvular stenosis, but also on the myocardial response to pressure overload and understanding the mechanisms of myocardial decompensation may help to guide management in the future. The degree of myocardial fibrosis, microvascular dysfunction, hypertrophy and left ventricular (LV) geometry may all play important roles. However, current guidelines for management of asymptomatic AS limit assessment of the myocardium to the measurement of ejection fraction with echocardiography. More advanced techniques may provide greater information that could be clinically useful. This thesis seeks to further our understanding of the mechanisms of the myocardial response to AS, using Cardiac Magnetic Resonance (CMR) in patients with moderate and severe AS. Myocardial perfusion in AS is examined in chapter 3. The results show that CMR first pass perfusion can be carried out safely and is well tolerated by AS patients. Microvascular dysfunction in these patients was associated with age, exercise time and markers of diastolic dysfunction. Myocardial strain is examined in chapter 4, utilizing a new software tool to look at strain throughout the left ventricle, and also to explore the relationship between strain and myocardial fibrosis. The results show that there are significant variations in circumferential strain measurements, depending on slice position in the LV, and also that there was no relationship found between strain and the degree of LV fibrosis. In chapter 5, the potential of CMR T1 mapping to identify fibrosis is examined using a new shortened non-contrast sequence (ShMOLLI - Shortened Modified Look-Locker Inversion) developed in our unit. CMR T1 values were validated against histological quantification of myocardial fibrosis in a large group of moderate and asymptomatic AS. A good correlation was found between ShMOLLI derived T1 values, with T1 values increasing with the severity of AS. The clinical value of measuring myocardial perfusion and LV global strain is examined in chapter 6 by linking these to prognosis. Measurement of circumferential strain could predict prognosis in asymptomatic AS, but myocardial perfusion showed poor ability to predict events. In conclusion, this thesis offers further insights into the changes that occur in the myocardium of patients with asymptomatic moderate and severe AS, using established and new CMR techniques. The clinical value of measuring these CMR parameters to aid risk stratification is shown, and the future potential for monitoring new therapies in these patients is discussed in the final chapter.
22
Tahiliani, Arunkumar Govindram. "Studies on diabetes-induced myocardial alterations in streptozotocin diabetic rats". Thesis, University of British Columbia, 1985. http://hdl.handle.net/2429/25979.
Testo completoAbstract (sommario):
Diabetes is known to result in a large number of alterations which affect various systems and organs. One of the more prominent disorders associated with diabetes is that of cardiac disease. Clinically, diabetics
suffer from morbidity and mortality of cardiac origin to a greater extent than the nondiabetic population. Various functional studies have also revealed that the efficiency of diabetic hearts to function as pumps is lower than that of normal hearts. Experimentally, myocardial function of either rats or dogs made diabetic with either streptozotocin (STZ) or alloxan has been studied and a depression clearly demonstrated in both the species. The abnormalities of cardiac function in experimental diabetes are accompanied by depression of various enzyme systems in the heart. These include the ability of the sarcoplasmic reticulum (SR) to take up calcium; the myosin and actomyosin ATPase activities; and the Na⁺, K⁺ ATPase activity. All these changes can be prevented and reversed by insulin treatment suggesting that the myocardial problems seen in STZ or alloxan diabetic animals are due to diabetes and not direct toxicities of the drugs.
It is not known whether the beneficial effects of in vivo insulin treatment are due to its direct myocardial effects or whether they are secondary to its effects mediated via normalisation of metabolism in diabetic animals. Thus, in the first part of the present investigation, we examined the direct effects of insulin on hearts from either control or diabetic rats using the isolated working heart preparation. Rats made diabetic with STZ (55 mg/kg) were sacrificed either 3 days or 6 weeks after induction of the disease and their hearts isolated and perfused in the working heart mode. Glucose concentrations varying from 5mM to 20mM were used in the perfusion medium, either in the presence or absence of insulin (5mU/mL). Left ventricular function was expressed as left ventricular developed pressure (LVDP) and the rates of contraction and relaxation (positive and negative dP/dt respectively) at various left atrial filling pressures. Three days after injecting STZ into rats, the animals exhibited hypoinsulinemia, hyperglycemia and their body weights although not significantly different from those of control animals, tended to be lower than the body weights of controls. Animals treated in this manner did not exhibit depression of cardiac function when compared with the myocardial function of control rats. Hearts from control rats exposed to regular insulin in the presence of 5mM glucose exhibited values of contractility which were significantly greater as compared with those obtained from control rat hearts not exposed to the hormone. When insulin was perfused along with a higher concentration of glucose (10mM), function of control rat hearts was affected to a significant extent. As opposed to the effects on control rat hearts, insulin failed to increase contractility in hearts from 3 day diabetic rats when either 5 or 10mM glucose was used in the perfusion medium.
The study was then repeated using animals which had been diabetic for six weeks. At the time of sacrifice, these animals were hypoinsulinemic, hyperglycemic and weighed significantly less than their age-matched controls. Analysis of cardiac function revealed a significant depression in diabetic rats as compared with controls. Increasing glucose concentrations from 5 to 20mM in the perfusion medium did not affect the function of either control or diabetic rat hearts. Perfusion with regular insulin increased contractility in control rat hearts; the increase in contractility was not affected by increasing the glucose concentration from 5 to 10mM. However, contractility of diabetic rat hearts was not affected by insulin perfusion when either 5 or 10mM glucose was used in the perfusion medium. In order to eliminate the possibility of involvement of glucagon (which may contaminate commercial insulin preparations) in the effects of insulin on control rat hearts, part of the study was repeated using glucagon - free insulin. While the glucagon - free insulin increased contractility in control rat hearts, diabetic rat hearts were not affected. These results are identical to those obtained with regular insulin, suggesting that the effects of insulin observed were due to insulin itself.
Although insulin treatment prevents and reverses diabetes - induced myocardial alterations in the rats, due to its widespread metabolic effects, it is not a good tool for investigating the specific factors which cause the cardiac abnormalities. In addition, a major problem with insulin treatment clinically is the fact that hypoglycemia can be associated with it, inadequate control occurs in some diabetics and secondary complications, such as myocardial problems, occur despite insulin treatment. It is thus desirable to have treatments which selectively affect certain aspects of diabetes so that the suspected underlying causes can be corrected specifically and their significance in causing the myocardial problems assessed. It would also be useful to have drug treatments which could either substitute for insulin or could be used in addition to the peptide. We have thus studied the effectiveness of certain treatments in preventing diabetes - induced myocardial alterations. The first one used was methyl palmoxirate, a fatty acid analog which is reported to reduce blood glucose levels in diabetic rats and dogs. The glucose - lowering effect is mediated via inhibition of fatty acid metabolism due to inhibition of carnitine acyl transferase resulting in inhibition of acyl carnitine formation and eventually inhibition of fatty acid transport across the mitochondrial membrane. Rats were treated with the drug (25mg/kg/day p.o.) three days after they were injected with either STZ or buffer. The treatment was carried out for 6 weeks and cardiac performance was then assesed. Untreated and treated diabetic rats were hypoinsulinemic, hyperglycemic and hyperlipedemic at the time of sacrifice. Cardiac function, which was depressed in diabetic animals, was still depressed despite the methyl palmoxirate treatment. However, the ability of the myocardial sarcoplasmic reticulum (SR) to take up calcium, which was depressed in diabetic rats, was normal in treated diabetic rats. Also, the levels of long chain acyl carnitines (LCAC) in the myocardial SR were normalised by methyl palmoxirate treatment in diabetic rats.
In an effort to normalise diabetes - induced myocardial alterations in rats, we then attempted a combination of either methyl palmoxirate or carnitine (as both can prevent the depression of SR calcium uptake) with thyroid hormone treatment (as it can normalise myosin ATPase depression in diabetic rat hearts). The treatment protocol was identical to that described above (30µg/kg/day s.c. T₃ was used). Although the general features of both control and diabetic animals were not affected by either of the combination treatments, cardiac dysfunction in diabetic rats was prevented by methyl palmoxirate and T₃ treatment. Carnitine and T₃ treatment, on the other hand, affected the function of diabetic rat hearts only at the lower left atrial filling pressures. These results suggest that the combination treatment of methyl palmoxirate and T₃ affect parameters besides SR calcium uptake and myosin ATPase. This is because the combination of carnitine and T₃, which also supposedly affects same parameters as the other combination, could not prevent the myocardial alterations. One of the possible reasons for the effectiveness of the combination of methyl palmoxirate and T₃ could be that animals treated with methyl palmoxirate derived at least part of their metabolic energy (especially at higher left atrial filling pressures) from glucose and thus reduced the oxygen demand at higher filling pressures as opposed to the untreated diabetic rat hearts which depended completely on fatty acids for their metabolic energy demands.Pharmaceutical Sciences, Faculty of
Graduate
23
Dhillon, Paramdeep Singh. "The relationship between changes in myocardial resistivity, conduction velocity and gap-junction topology in diseased human myocardium". Thesis, Imperial College London, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.516811.
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24
Gude, Natalie A. "Notch activated protective signaling in damaged mammalian myocardium". Diss., [La Jolla] : [san Diego] : University of California, San Diego : San Diego State University, 2010. http://wwwlib.umi.com/cr/ucsd/fullcit?p3407860.
Testo completoAbstract (sommario):
Thesis (Ph. D.)--University of California, San Diego, and San Diego State University, 2010.Title from first page of PDF file (viewed June 17, 2010). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references (leaves 135-149).
25
Vandenberg, Jamie Ian. "Intracellular pH and reperfusion of the ischaemic myocardium". Thesis, University of Cambridge, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.282156.
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26
McGill, Laura-Ann. "Novel cardiovascular magnetic resonance phenotyping of the myocardium". Thesis, Imperial College London, 2016. http://hdl.handle.net/10044/1/49247.
Testo completoAbstract (sommario):
INTRODUCTION: Left ventricular (LV) microstructure is unique, composed of a winding helical pattern of myocytes and rotating aggregations of myocytes called sheetlets. Hypertrophic cardiomyopathy (HCM) is a cardiovascular disease characterised by left ventricular hypertrophy (LVH), however the link between LVH and underlying microstructural aberration is poorly understood. In vivo cardiovascular diffusion tensor imaging (cDTI) is a novel cardiovascular MRI (CMR) technique, capable of characterising LV microstructural dynamics non-invasively. In vivo cDTI may therefore improve our understanding microstructural-functional relationships in health and disease. METHODS AND RESULTS: The monopolar diffusion weighted stimulated echo acquisition mode (DW-STEAM) sequence was evaluated for in vivo cDTI acquisitions at 3Tesla, in healthy volunteers (HV), patients with hypertensive LVH, and HCM patients. Results were contextualised in relation to extensively explored technical limitations. cDTI parameters demonstrated good intra-centre reproducibility in HCM, and good inter-centre reproducibility in HV. In all subjects, cDTI was able to depict the winding helical pattern of myocyte orientation known from histology, and the transmural rate of change in myocyte orientation was dependent on LV size and thickness. In HV, comparison of cDTI parameters between systole and diastole revealed an increase in transmural gradient, combined with a significant re-orientation of sheetlet angle. In contrast, in HCM, myocyte gradient increased between phases, however sheetlet angulation retained a systolic-like orientation in both phases. Combined analysis with hypertensive patients revealed a proportional decrease in sheetlet mobility with increasing LVH. CONCLUSION: In vivo DW-STEAM cDTI can characterise LV microstructural dynamics non-invasively. The transmural rate of change in myocyte angulation is dependent on LV size and wall thickness, however inter phase changes in myocyte orientation are unaffected by LVH. In contrast, sheetlet dynamics demonstrate increasing dysfunction, in proportion to the degree of LVH. Resolving technical limitations is key to advancing this technique, and improving the understanding of the role of microstructural abnormalities in cardiovascular disease expression.
27
Kellar, Robert Shawn. "Tissue-engineered polymers stimulate angiogenesis in infarcted myocardium". Diss., The University of Arizona, 2001. http://hdl.handle.net/10150/279837.
Testo completoAbstract (sommario):
The development and maintenance of a vascular network is critical to the growth and survival of a tissue and ultimately an organism. An understanding of the mechanisms which regulate angiogenesis within and surrounding currently used polymeric devices would contribute to the success of these implants by establishing methods to enhance tissue in-growth and new vessel development. Furthermore, tissue-engineering currently used polymers such as expanded polytetrafluoroethylene (ePTFE) may create an angiogenic material that can be used to induce new microvessel formation in infarcted myocardium. Myocardial infarcts represent a pathology that affects a large percentage of the patient population who suffer from coronary heart disease. Disease of the coronary vasculature can lead to narrowing of the coronary vasculature and result in regions of ischemia which can progress to infarction. Studies in this dissertation evaluate two different tissue-engineered polymer constructs for their ability to stimulate a new collateral network in infarcted myocardium. The results from these studies indicate that the tissue site of implantation is an important factor in influencing the healing response. Therefore, it is important to evaluate future polymer devices in tissues where the device will ultimately reside. Additionally, the physical and chemical characteristics of polymers were found to have a significant influence on the healing response. Furthermore, tissue-engineered polymer constructs stimulated a significant angiogenic response within infarcted myocardium. Tissue-engineered constructs that secreted soluble angiogenic agents were found to have the greatest depth of angiogenic effect into infarcted myocardium leading to the formation of arterioles, capillaries, and venules. Additionally, hearts treated with these devices demonstrated significantly greater left ventricular function in comparison to infarct-only hearts. Based on this work, it is apparent that tissue-engineered polymer constructs may have a future role as cardiac patches and thus provide the patient population with an additional therapy to revascularize infarcted cardiac tissues.
28
Taylor, David Glenn. "Roles of sarcoplasmic reticular ca2+ -atpase 2a and action potential duration in rat normal and hypertrophied myocardium". [Gainesville, Fla.] : University of Florida, 2004. http://purl.fcla.edu/fcla/etd/UFE0006643.
Testo completoAbstract (sommario):
Thesis (Ph.D.)--University of Florida, 2004.Typescript. Title from title page of source document. Document formatted into pages; contains 133 pages. Includes Vita. Includes bibliographical references.
29
Kotlyar, Eugene St Vincents Hospital Clinical School UNSW. "The role of aldosterone in myocardial remodelling". Awarded by:University of New South Wales. St Vincents Hospital Clinical School, 2006. http://handle.unsw.edu.au/1959.4/27011.
Testo completoAbstract (sommario):
The pathophysiology of cardiac failure involves activation of the renin-angiotensinaldosterone system that contributes to adverse left ventricular remodelling. This is a complex pathologic process that has been shown to be stimulated by haemodynamic and humoral factors including aldosterone. The precise mechanisms by which aldosterone contributes to this process are not known. In a mouse animal model of pressure overload induced cardiac hypertrophy and failure, the treatment with selective mineralocorticoid receptor, eplerenone, was shown to attenuate adverse left ventricular remodelling. This was associated with decreases in myocardial apoptosis, collagen turnover, oxidative stress and inflammation, in the absence of a significant blood pressure change. Furthermore, we administered aldosterone infusion and high salt diet to uninephrectomised mice deficient in the gp91phox subunit of NADPH oxidase and to the wild type strain. It was demonstrated that the increase in the blood pressure did not occur in the gp91phox deficient mice and that both wild-type and knock-out strains developed cardiac hypertrophy, but not interstitial fibrosis. Additionally, patients with chronic stable heart failure were also studied. We found that plasma aldosterone level was independently associated with levels of markers for oxidative stress (of 8- isoprostaglandin F2??), inflammation (soluble intercellular adhesion molecule-1) and matrix turnover (tissue inhibitor of metalloproteinase-1). High plasma osteopontin levels were also noted. Our experiments suggest that myocardial apoptosis, collagen turnover, oxidative stress and inflammation may be involved in mediating the adverse effects of mineralocorticoid receptor activation in pressure overload. In addition, the development of cardiac hypertrophy may be a haemodynamically independent process, but gp91phox subunit deficiency did not attenuate the hypertrophic response to aldosterone infusion when administered in conjunction with high salt diet, suggesting that there may be another mechanism that mediates aldosterone-induced hypertrophy. The state of increased oxidative stress and inflammation, seen in animal models, may also play an important role in chronic heart failure subjects. The importance of local factors in the regulation of myocardial tissue remodelling has become increasingly evident, but future investigations are required to clarify the role of aldosterone, oxidative stress and inflammation in heart failure.
30
Zhang, Heye. "An inverse framework for estimating cardiac electrophysiological activity from medical image sequence /". View abstract or full-text, 2007. http://library.ust.hk/cgi/db/thesis.pl?ECED%202007%20ZHANGHY.
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Varghese, Jamie J. "A study of factors determining the crossbridge kinetics, work and power of cardiac muscle analysed with sinusoidal oscillation and other techniques". Thesis, University of Glasgow, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.274283.
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Wong, Chun Lok. "Cardiac motion estimation with finite deformation and composite material models /". View abstract or full-text, 2004. http://library.ust.hk/cgi/db/thesis.pl?ELEC%202004%20WONGCL.
Testo completoAbstract (sommario):
Thesis (M. Phil.)--Hong Kong University of Science and Technology, 2004.Includes bibliographical references (leaves 84-87). Also available in electronic version. Access restricted to campus users.
33
Ko, Robert K. M. "Molecular aspects of myocardial ischemia/reperfusion injury and the protective effects of allopurinol". Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/30699.
Testo completoAbstract (sommario):
A growing body of evidence has now accumulated supporting the involvement of oxygen-derived free radicals in the development of myocardial ischemia/reperfusion (I/R) injury. We have, therefore, undertaken the present study to examine (1) I/R-related alterations in myocardial antioxidant capacity in pentobarbital anesthetized open-chest rabbits subjected to left circumflex coronary artery ligation followed by reperfusion; (2) the protective effects of pretreatrnent with allopurinol or the 21-aminosteroid U74006F; (3) alternative mechanisms to xanthine oxidase inhibition for allopurinol protection against I/R injury; and (4) the effect of allopurinol treatment on the antioxidant capacity of erythrocytes in pigs used in a heart-lung transplantation study.
In the rabbit myocardium, a marked impairment in myocardial antioxidant capacity developed in association with the onset of irreversible injury, as reflected in the enhancement in glutathione (GSH) depletion and formation of thiobarbituric acid-reactive substances (TBARS) following in vitro incubation of tissue homogenate with tert-butylhydroperoxide (TBHP). During the course of post-ischemic reperfusion, the protracted time-course of
alterations in antioxidant capacity dissociated them from the early burst of radical formation known to occur at the onset of post-ischemic reperfusion of the myocardium. When
the time-dependent changes in functional indices of antioxidant status (TBHP-induced GSH depletion and formation of TBARS) were analysed in relation to activities of antioxidant enzymes, evidence suggestive of functionally relevant impairments in Cu,Zn-superoxide dismutase (Cu,Zn-SOD) and glutathione reductase (GRD) activities was found. These results and our demonstration of significant decreases in the activity of GSH-dependent antioxidant enzymes under acidotic conditions suggest that a transient impairment in the functioning of antioxidant enzymes may be involved in triggering irreversible myocardial I/R injury.
Repetitive brief episodes of I/R produced a
progressive decrease in myocardial ATP levels, which was not associated with any detectable changes in myocardial antioxidant capacity. Ischemic preconditioning produced by brief episodes of I/R did not affect the severity of subsequently induced I/R injury. These results suggest that brief episodes of myocardial ischemia do not produce oxidative tissue damage and the ischemia-induced depletion in myocardial ATP level is at least partially dissociable from the I/R-related impairment in tissue antioxidant capacity.
Isolated Langendorff-perfused rabbit hearts subjected to I/R did not show any changes in antioxidant capacity. However, when intact hearts were subjected to ischemia in vivo and a subsequent reperfusion in vitro, an impairment in myocardial antioxidant capacity became apparent. These
results suggest that blood elements, possibly activated neutrophils, may be a crucial factor involved in the development of I/R-induced oxidant injury.
Chronic allopurinol pretreatment (1 mg/ml in drinking water or approximately 75 mg/kg/day) for 7 days prior to ischemia provided significant protection against I/R-induced alterations in myocardial antioxidant capacity, but not the decrease in tissue ATP levels. This chronic allopurinol regimen was found to enhance myocardial GRD activity in nonischemic
tissue. In addition, both allopurinol and oxypurinol inhibited the transition metal ion-catalysed ascorbate oxidation and lipid peroxidation in vitro, likely as a consequence of their metal chelating properties. Similarly, myoglobin-TBHP-catalysed oxidation of uric acid and lipid peroxidation were also suppressed by allopurinol. All these suggest that allopurinol may favorably alter myocardial antioxidant capacity directly by virtue of its transition metal chelating properties and its antioxidant actions in myoglobin-mediated oxidative processes.
The acute administration of 21-aminosteroid U74006F (3 mg/kg, i.v) under conditions comparable to those known to protect against trauma-induced damage in the central nervous system failed to reduce manifestations of oxidative injury in rabbit hearts subjected to ischemia and reperfusion. Although reactive oxy-radicals have been implicated in both types of tissue damage, the observed difference in susceptibility to protection by this steroidal antioxidant
suggests that the molecular mechanisms involved are not identical.
In the heart-lung transplantation study, erythrocytes from allopurinol-treated pigs (given repeatedly at an oral dose of 50 mg/kg) showed a time/dose-dependent increase in antioxidant capacity as reflected in the decrease in malondialdehyde production following in vitro oxidative challenge. The extent of red cell protection in both donor and recipient animals correlated significantly with the functional viability of the transplanted lung tissue, as assessed by tissue water content. These results suggest that the measurement of erythrocyte antioxidant capacity may provide an useful assessment of generalized alterations in tissue antioxidant status produced by pharmacological interventions.Medicine, Faculty of
Anesthesiology, Pharmacology and Therapeutics, Department of
Graduate
34
Moreno-Gonzalez, Alicia. "Mechanical properties of myocardium following cardiomyocyte transplantation into infarcted hearts and investigations of the role of troponin C Ca2+ binding kinetics in skeletal muscle contraction /". Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/8053.
Testo completo
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Al, Kindi Adil Hashim 1976. "Cellular cardiomyoplasty : optimizing cellular dosage and retention by microencapsulation". Thesis, McGill University, 2008. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111585.
Testo completoAbstract (sommario):
Cellular Cardiomyoplasty (cell therapy for myocardial regeneration) targets the basic pathophysiology of heart failure and represents a novel technique for augmenting the function of the failing heart. Previous studies have demonstrated massive mechanical losses in the first few minutes. Thus, efforts to reduce mechanical losses may prove more beneficial than those directed against biological losses alone. We believe that "Wash-out" into the disrupted blood vessels is responsible for these early losses.In the first part of this study we hypothesized that by increasing the size of the injectate, the amount of immediate losses can be reduced achieving better retention. Using Alginate-poly-L-lysine-Alginate (APA) miscrocapsules of two different sizes (200mum&400mum) and comparing retention with bare microspheres (10mum) of similar size to MSCs, we demonstrated that immediate retention rate increased by four folds. The retention rate for group 1 (microspheres only) was 4.28+/-3.46% which was significantly lower than that for groups 2 (microspheres in 200mum microcapsules) at 16.45+/-12.66% and group 3 (microspheres in 400mum microcapsules) at 12.93+/-6.28% for Group (p<0.05). There was no difference between group 2 and 3.
In the second part, we investigated the potential of gradually increasing the cell load on functional improvement and engraftment using conventional intramuscular delivery. Five groups of rats received escalating doses of MSCs after surgically induced ischemia (gp1 no cells, gp2 0.5x 10 6, gp3 1.5x106, gp4 3x106,gp5 5x106 MSCs). At 7 weeks, we observed significant improvement in cardiac function in groups 3 to 5 compared to post-infarction baseline. This was not observed in groups 1 & 2. However, in groups 3 to 5, we observed no functional advantage for increasing the cell load beyond a minimal therapeutic dose. This is consistent with our hypothesis that small cells are washed out into the circulation.
We also showed the ability of Alginate-Poly-l-lysine-Alginate (APA) microcapsules to sustain the viability of encapsulated MSCs in-vitro. Finally, the ability of encapsulated MSCs to improve the function of the heart in-vivo was tested.
36
Nussbaum, Jeannette. "Embryonic stem cells for myocardial infarct repair /". Thesis, Connect to this title online; UW restricted, 2004. http://hdl.handle.net/1773/6312.
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Arís, Sánchez Ruth. "Electromechanical large scale computational models of the ventricular myocardium". Doctoral thesis, Universitat Politècnica de Catalunya, 2014. http://hdl.handle.net/10803/284398.
Testo completoAbstract (sommario):
Els models computacionals del cor són una eina important que pot donar als investigadors biomèdics una font addicional d’informació per entendre el funcionament del miocardi. Els models numèrics poden ajudar a interpretar dades experimentals i proporcionar informació complementària sobre mecanismes cardíacs que no poden ser determinats amb precisió mitjançant dispositius clínics clàssics. En aquesta tesi, s’apliquen tècniques de computació a gran escala per construir una eina computacional capaç d’executar-se en paral•lel en milers de processadors, permetent simulacions
d’alta fidelitat en malles fines. Per simular el bombeig del cor, s’utilitza un esquema d’acoblament explícit entre les equacions electrofisiològiques en tres dimensions i la formulació en mecànica de sòlids. Per trobar la solució numèrica, s’utilitza el mètode d’elements finits. A més, s’implementen tècniques en assimilació de dades per a l’estimació efectiva dels paràmetres electrofisiològics i mecànics rellevants que apareixen a les equacions, la qual cosa ´es un pas crucial cap a un model cardíac sensible a cada pacient. El codi computacional s’aplica per simular problemes físics reals. S’estudia la propagació electromecànica en una geometria de conill, on es prova la sensibilitat del model a les variacions d’entrada. En particular, l’eina de càlcul s’utilitza per avaluar la influència del camp de fibres cardíaques en la contracció del teixit.
Per desenvolupar una simulació cardíaca útil per a fins clínics, el model requereix la integració i combinació de la mecànica computacional i les tècniques de processament d’imatge més recents. El model resultant pot ser la base d’estudis teòrics sobre mecanismes de patologies, oferint als investigadors i cardiòlegs pistes addicionals per comprendre el funcionament del cor. Pot ajudar a la planificació de cirurgia i modelització, com és la predicció dels efectes de compostos farmacològics en el ritme cardíac o l’estudi de l’efecte de medicaments. Aquest projecte només és possible en un equip multidisciplinar, on grups especialitzats uneixen les seves forces en les respectives disciplines: cardiòlegs, investigadors imatge, bioenginyers i científics de la computació. El present model computacional del cor és un pas més cap a la creació d’un laboratori cardíac virtual.A cardiac computational model is a relevant tool that can give biomedical researchers an additional source of information to understand how the heart works. Numerical models can help to interpret experimental data and provide information about cardiac mechanisms that can not be determined accurately by classical clinical devices. In this thesis, High Performance Computing (HPC) techniques are used to build a cardiac computational tool, which is capable of running in parallel in thousands of processors, bioengineers and computational scientists. The present cardiac computational model is one further step towards the creation of a virtual lab, allowing high fidelity simulations on fine meshes. To simulate the pumping heart, an explicit coupling scheme between the three-dimensional electrophysiological equations and the solid mechanics formulation is used, solving the governing equations with finite element methods. Also, data assimilation techniques are implemented for the effective estimation of some relevant electrophysiological parameters, which is a crucial step towards the patient-sensitive cardiac model. The data assimilation techniques are assessed on synthetic data generated by the model. Finally, the computational code is applied to simulate real physical problems. The electromechanical propagation in a rabbit geometry is studied to test the sensitivity of the framework to input variations. Particularly, the computational tool is used to evaluate the influence of the fiber field in the contraction of the tissue. To develop a cardiac simulation useful for clinical purposes, the integrative model requires combining computational mechanics and image processing techniques via data assimilation methods. Coupled with the most advanced image processing analysis, the framework can be the base of theoretical studies into the mechanisms of cardiac pathologies. It can help surgery planning and cardiac modeling, such as the prediction of the impact of pharmacological compounds on the heart’s rhythm or to improve the knowledge of drug study, giving medical researchers additional hints to understand the heart. This realization is only possible in a multidisciplinary team, where specialized groups join forces in their respective disciplines: cardiologists, image researchers, bioengineers and computational scientists. The present cardiac computational model is one further step towards the creation of a virtual lab
38
Murtuza, Bari. "Interactions between skeletal muscle precursor cells and adult myocardium". Thesis, Imperial College London, 2004. http://hdl.handle.net/10044/1/8427.
Testo completo
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Blais, Angeline. "Monopole antennas for microwave catheter ablation of the myocardium". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/mq20903.pdf.
Testo completo
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Ausma, Jantje. "Structural changes in chronic hibernating myocardium: aspects of dedifferentiation". Maastricht : Maastricht : Universiteit Maastricht ; University Library, Maastricht University [Host], 1997. http://arno.unimaas.nl/show.cgi?fid=5811.
Testo completo
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Rees, P. S. C. "Pharmacological cardioprotection of the human myocardium in diseased states". Thesis, University College London (University of London), 2011. http://discovery.ucl.ac.uk/1336879/.
Testo completoAbstract (sommario):
Background: Coronary artery disease is the leading worldwide cause of death. Even despite restoration of blood flow following acute myocardial infarction, further myocardial damage is seen during the reperfusion phase. Pharmacological strategies to induce resistance to ischaemia reperfusion injury have been shown to share common pathways. The most important common signalling pathway involved is the Reperfusion Injury Salvage Kinase pathway, and in animal models this can be pharmacologically activated, resulting in inhibition of the opening of the mitochondrial permeability transition pore, with a resultant cardioprotective effect. Atorvastatin has been shown to act in this way in animal models of ischaemia-reperfusion injury, although this has not been demonstrated in humans. This thesis examines (a) the role of atorvastatin in acute protection from ischaemia-reperfusion injury in human myocardium, (b) the ability of high-dose atorvastatin to recapture cardioprotection in human myocardium in the setting of chronic statin therapy, and (c) the functionality of the mitochondrial permeability transition pore in human hypertrophic cardiomyopathy, and the role of atorvastatin in inhibiting pore opening following oxidative stress. Methods and Results: Using human models to simulate ischaemia-reperfusion injury we have demonstrated: (1) Human atrial myocardium can be protected from simulated ischaemia-reperfusion injury by treatment with atorvastatin at the time of reperfusion; (2) Cardioprotection against simulated ischaemia-reperfusion injury can be recaptured with high-dose atorvastatin; (3) The mitochondrial permeability transition pore is a critical determinant in cell death in hypertrophic cardiomyopathy, and its inhibition can be achieved using atorvastatin. Conclusion: The key aim of emergency reperfusion therapy in the setting of myocardial infarction is salvage of myocardium and preservation of cardiac function. These studies contribute to the field by exploring the cardioprotective effects of atorvastatin in human myocardium and delineating protective cascades involved. They offer a key translational step in our understanding of statin cardioprotection, and an insight into cardioprotection in hypertrophic cardiomyopathy.
42
Yusupova, A. F. "Morphological changes of myocardium in conditions of simulated osteoporosis". Thesis, Sumy State University, 2017. http://essuir.sumdu.edu.ua/handle/123456789/53918.
Testo completoAbstract (sommario):
Relevance. Various forms and stages of osteoporosis are characterized by changes in the concentration of Calcium in blood. Calcium is one of the foundational elements which influences myocardial contractile function. Aim. The aim of the study is to investigate pathological changes of myocardium in conditions of modelled osteoporosis.
43
Arnal, Pastor María Pilar. "New scaffolding materials for the regeneration of infarcted myocardium". Doctoral thesis, Editorial Universitat Politècnica de València, 2015. http://hdl.handle.net/10251/46129.
Testo completoAbstract (sommario):
There is growing interest in the development of biomimetic matrices that are simultaneously
cell-friendly, allow rapid vascularization, exhibit enough mechanical integrity to be comfortably
handled and resist mechanical stresses when implanted in the site of interest. Meeting all these
requirements with a single component material has proved to be very challenging.
The hypothesis underlying this work was that hybrid materials obtained by combining scaffolds
with bioactive hydrogels would result in a synergy of their best properties: a construct with
good mechanical properties, easily handled and stable thanks to the scaffold; but also, because
of the gel, cell-friendly and with enhanced oxygen and nutrients diffusion, and promoter of cell
colonization. Moreover, such a composite material would also be useful as a controlled release
system because of the gel’s incorporation.
Poly (ethyl acrylate) (PEA) scaffolds prepared with two different morphologies were envisaged
to provide the mechanical integrity to the system. Both types of scaffolds were physicochemically
characterized and the effect of the scaffolds production process on the PEA
properties was examined. The scaffolds preparation methods affected the PEA properties;
nevertheless, the modifications induced were not detrimental for the PEA biological
performance.
Two different bioactive gels were studied as fillers of the scaffolds’ pores: hyaluronan (HA),
which is a natural polysaccharide, and a synthetic self-assembling peptide, RAD16-I. HA is
ubiquitously present in the body and its degradation products have been reported to be
angiogenic. RAD16-I is a synthetic polypeptide that mimics the extracellular matrix providing a
favourable substrate for cell growth and proliferation.
Given the hydrophobic nature of poly(ethyl acrylate), the combination of PEA scaffolds with
aqueous gels raised a number of problems regarding the methods to combine such different
elements, the ways to gel them inside the pores, and the procedures to seed cells in the new
composite materials. Different alternatives to solve these questions were thoroughly studied and
yielded protocols to reliably obtain these complex structures and their biohybrids.
An extensive physico-chemical characterization of the components’ interaction and the
combined systems was undertaken. As these materials were intended for cardiac tissue
engineering applications, the mechanical properties and the effect of the fatigue on them were studied. The different composite systems here developed were homogeneously filled or coated
with the hydrogels, were easy to manipulate, and displayed appropriate mechanical properties.
Interestingly, these materials exhibited a very good performance under fatigue.
The use of the composite systems as a controlled release device was based on the possibility of
incorporating active soluble molecules in the hydrogel within the pores. A release study of
bovine serum albumin (BSA), intended as a model protein, was performed, which served as a
proof of concept.
The biological performance of the hybrid scaffolds was first evaluated with fibroblasts to discard
the materials cytotoxicity and to optimize the cell seeding procedure. Subsequently, human
umbilical vein endothelial cells (HUVECs) cultures were performed for their interest in
angiogenic and vascularization processes. Finally, co-cultures of HUVECs with adipose-tissue
derived mesenchymal cells (MSCs) were carried out. These last cells are believed to play an
important role for clinical regenerative medicine, and their cross-talk with the endothelial cells
enhances the viability and phenotypic development of HUVECs. Through the different
experiments undertaken, hybrid scaffolds exceeded the outcome achieved by bare PEA scaffolds.Arnal Pastor, MP. (2014). New scaffolding materials for the regeneration of infarcted myocardium [Tesis doctoral]. Editorial Universitat Politècnica de València. https://doi.org/10.4995/Thesis/10251/46129
Alfresco
Premiado
44
Firoozan, Soroosh. "Quantification of myocardial blood flow and function : an experimental study". Thesis, University of Southampton, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.274665.
Testo completo
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Станишевская, Н. В., М. В. Золотаревская e Д. А. Абросина. "Морфологические изменения миокарда при моделировании некоронарогенного некроза после введения алкилселенонафтиридина". Thesis, Сумский государственный университет, 2013. http://essuir.sumdu.edu.ua/handle/123456789/32059.
Testo completoAbstract (sommario):
Сердечно-сосудистая патология является одной из актуальных проблем современной медицины. При неблагоприятных условиях стресс, гипоксия могут явиться причиной развития некоронарогенного некроза миокарда (НМ).
При цитировании документа, используйте ссылку http://essuir.sumdu.edu.ua/handle/123456789/32059
46
Adix, Longlet Nancy J. "Chronic Ventricular Sympathectomy : Effects on Myocardial Metabolism". Thesis, University of North Texas, 1993. https://digital.library.unt.edu/ark:/67531/metadc278768/.
Testo completoAbstract (sommario):
Chronic ventricular sympathectomy elicits changes in the coronary circulation, myocardial oxygen consumption and size of infarction resulting fromcoronary occlusion. These changes indicate a change occurring in the basic metabolism of the heart in response to the removal of its sympathetic nervous input. This hypothesis was tested using two groups of dogs, a shamoperated control and a ventricular sympathectomized group. The sympathectomy procedure was an intrapericardial surgical technique which selectively removes ventricular sympathetic input. Four weeks after surgery, left ventricular tissue samples were obtained and rapidly frozen to -80°C. Selected metabolic variables were then compared between the two groups.
47
Labonté, Sylvain. "A theoretical study of radio frequency ablation of the myocardium". Thesis, University of Ottawa (Canada), 1992. http://hdl.handle.net/10393/7559.
Testo completoAbstract (sommario):
Theoretical modeling of the lesion formation process during radio-frequency ablation of the myocardium is presented. The model is axisymmetric and consists of a catheter electrode coming in contact at right angle with the heart tissue. The electric power dissipated in the tissue is calculated and from it the temperature distribution and the resulting lesion are evaluated as a function of time. The cooling effect of the blood flow and the temperature dependence of the electrical conductivity are included in the model, making it non-linear. The finite-element method is used to discretize the spatial domain and a finite-difference algorithm resolves the time dependence. The numerical simulator is validated with a series of experiments performed on a tissue-equivalent material. Both the measured temperature distribution in the tissue sample and the electrode resistance as a function of time agree well with the theoretical predictions. The model is used to study the effect of the electrode geometry and the electrical excitation on the resulting lesion. Theoretical predictions for the time evolution of the lesion size and the electrode resistance are presented for the first time. Recommendations for the improvement of the RF ablation procedure are formulated.
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Wallace, Alison Fiona. "Endothelin system expression and function in failing and nonfailing myocardium". Thesis, University of Edinburgh, 2004. http://hdl.handle.net/1842/27599.
Testo completoAbstract (sommario):
The aims of this thesis were to investigate the endothelin system in failing and nonfailing myocardium and to evaluate the role of ET receptor function in relation to contractility in vivo and in vitro. In addition, transmural differences in gene expression were explored in human failing myocardium to establish whether genes associated with stiffness, hypertrophy and the ET system correlate to wall stress. Rats underwent myocardial infarction (MI) and developed left ventricular (LV) dysfunction at 15 weeks post-MI, as evidenced by an increase in LV end-diastolic pressure (LVEDP, 3 ± 0.2mmHg to 12 ± 2mmHg, P<0.01) and an increase in expression of atrial natriuretic peptide mRNA. A reduction in the basal contractile response of papillary muscles from failing hearts was also consistent with dysfunction. However, responses to ET-1 were inconsistent and prevented conclusions about the role of individual receptors. Investigation of ET receptor expression by RT-PCR failed to show a selective increase in ETB receptors and prepro ET-1 mRNA remained unchanged at 15 weeks post-MI. Subsequently, experiments were designed to investigate the influence of ET on myocardial contractility using ET receptor antagonists in papillary muscles from control animals. Results suggested that both ET receptors contribute to contractility in rat myocardium, corresponding with the presence of both receptor subtypes, found using RT-PCR. Furthermore, the data showed that expression of ET receptors in the heart undergo seasonal variation, which corresponds with the contribution of receptors to regulation of contractility. LV function was evaluated in vivo using a novel technique developed in our laboratory. Echocardiography in conjunction with associated LV pressure data demonstrated a reduced shortening fraction (SF, 18.7 ± 1.9% to 13.6 ± 1.3%, P<0.05) and ejection fraction (EF, 31.1 ± 2.6% to 22.4 ± 1.2%, P<0.01) in rats 12 weeks post-MI indicating LV dysfunction, also evidenced by elevated LVEDP (5.7 ±1.0mmHg to 15.6 ±1.5mmHg P<0.001). Subsequently, the technique was used on control animals following chronic (7 day) administration of Bosentan, a dual ET receptor antagonist (100mg/kg/day). However, antagonist treatment failed to influence haemodynamics, SF or EF, suggesting that unlike in vitro, the ET system does not play a central role in regulating cardiac function in vivo. In the human heart, wall stress is highest in the endocardial layer. Different types of heart failure alter myocardial contractility and wall stress in different ways. Semi-quantitative RT-PCR identified that genes linked to hypertrophic remodelling were consistently increased in the endo relative to epicardium. Interestingly, expression of the ETA receptor and the cytoskeletal elastic protein, titin, in particular the N2B isoform linked to increased myocardial stiffness showed 2 distinct patterns of expression across the LV wall, depending on the type of heart failure. ETB expression was uniform across the wall. In conclusion, the ET system is expressed in the normal myocardium and both receptors can regulate contractility in vitro, however the system is not essential for normal heart function in vivo.
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Diaz, Roberto Jose. "Ischemic preconditioning of the myocardium, role of angiotensin II receptors". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0006/MQ28785.pdf.
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Ford, Meredith Katherine. "Ischemic preconditioning of the myocardium, role of protein tyrosine kinases". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape10/PQDD_0022/MQ40863.pdf.
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