Relevant bibliographies by topics / Microcirculatory dysfunction

Academic literature on the topic 'Microcirculatory dysfunction'

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Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Microcirculatory dysfunction"

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Kanoore Edul, Vanina, Gonzalo Ferrara, and Arnaldo Dubin. "Microcirculatory Dysfunction in Sepsis." Endocrine, Metabolic & Immune Disorders - Drug Targets 10, no. 3 (September 1, 2010): 235–46. http://dx.doi.org/10.2174/187153010791936847.

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Lundy, David J., and Stephen Trzeciak. "Microcirculatory Dysfunction in Sepsis." Critical Care Nursing Clinics of North America 23, no. 1 (March 2011): 67–77. http://dx.doi.org/10.1016/j.ccell.2010.12.004.

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Bansal, Arun, and Gopala Krishnan. "Microcirculatory dysfunction in sepsis." Journal of Pediatric Critical Care 6, no. 2 (2019): 29. http://dx.doi.org/10.21304/2019.0602.00486.

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Lundy, David J., and Stephen Trzeciak. "Microcirculatory Dysfunction in Sepsis." Critical Care Clinics 25, no. 4 (October 2009): 721–31. http://dx.doi.org/10.1016/j.ccc.2009.06.002.

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Vollmar, Brigitte, and Michael D. Menger. "Microcirculatory Dysfunction in Acute Pancreatitis." Pancreatology 3, no. 3 (January 2003): 181–90. http://dx.doi.org/10.1159/000070727.

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Khalid, Nauman, and Lovely Chhabra. "Takotsubo cardiomyopathy and microcirculatory dysfunction." Nature Reviews Cardiology 12, no. 8 (June 16, 2015): 497. http://dx.doi.org/10.1038/nrcardio.2015.88.

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Selthofer-Relatic, Kristina, Martina Mihalj, Aleksandar Kibel, Ana Stupin, Marko Stupin, Ivana Jukic, Akos Koller, and Ines Drenjancevic. "Coronary Microcirculatory Dysfunction in Human Cardiomyopathies." Cardiology in Review 25, no. 4 (2017): 165–78. http://dx.doi.org/10.1097/crd.0000000000000140.

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Ikonomidis, Ignatios, John Lekakis, Sotirios Tsiodras, John Palios, Garyfalia Poulakou, Periklis Panagopoulos, Periklis Panagopoulos, et al. "MICROCIRCULATORY DYSFUNCTION IN HIV INFECTED PATIENTS." Journal of the American College of Cardiology 55, no. 10 (March 2010): A159.E1495. http://dx.doi.org/10.1016/s0735-1097(10)61496-9.

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Boros, M. "Microcirculatory dysfunction during intestinal ischemia-reperfusion." Acta Physiologica Hungarica 90, no. 4 (December 2003): 263–79. http://dx.doi.org/10.1556/aphysiol.90.2003.4.1.

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LEHR, HANS-ANTON. "Microcirculatory Dysfunction Induced by Cigarette Smoking." Microcirculation 7, no. 6 (December 2000): 367–84. http://dx.doi.org/10.1111/j.1549-8719.2000.tb00135.x.

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Dissertations / Theses on the topic "Microcirculatory dysfunction"

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Singh, Suveer. "Microcirculatory dysfunction in experimental sepsis." Thesis, Imperial College London, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312340.

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Naumann, David Nathaniel. "Early microcirculatory dysfunction following traumatic haemorrhage." Thesis, University of Birmingham, 2018. http://etheses.bham.ac.uk//id/eprint/8351/.

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Traumatic haemorrhagic shock (THS) is the most frequent cause of preventable death after severe injury. Shock is characterised by inadequate provision of oxygen and substrates to tissues in relation to their requirements, and it is within the microcirculation that this process is regulated. Investigation of the microcirculation is therefore key to understanding the pathological processes following THS. In Part I, some mechanisms of microcirculatory dysfunction following trauma are presented. Endotheliopathy of trauma is associated with poor microcirculatory flow, and occurs within minutes of injury. It is also associated with higher levels of circulating cell-free DNA (cfDNA), supporting the hypothesis that cfDNA is an aetiological factor in this pathological response. Both endotheliopathy and elevated cfDNA and are related to poor clinical outcomes. In Part II, clinical implications of microcirculatory monitoring are discussed for patients in the early phase following THS. It is safe and feasible to monitor the microcirculation following THS, and a novel point-of-care grading system has performed well, suggesting that targeted fluid resuscitation towards microcirculatory flow after THS may be possible. The optimal fluid strategy in this context is unknown, but physical properties (e.g. oncotic potential and viscosity) as well as endothelial restorative properties appear to be as important as oxygen-carrying capacity. Potential therapeutic interventions aimed at microcirculatory and endothelial resuscitation open intriguing possibilities for improving outcomes after THS.
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Adingupu, D. D. "Determinants and mechanisms of microcirculatory dysfunction." Thesis, Exeter and Plymouth Peninsula Medical School, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.700471.

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De, Silva Kalpa. "Microcirculatory and myocardial physiology in ischaemic left ventricualr dysfunction." Thesis, King's College London (University of London), 2014. https://kclpure.kcl.ac.uk/portal/en/theses/microcirculatory-and-myocardial-physiology-in-ischaemic-left-ventricualr-dysfunction(cac6998a-da73-49c4-8e7c-8669cb8bf34c).html.

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Introduction: Left ventricular (LV) dysfunction influences, and is affected by, changes in coronary flow. The integrity of the microvasculature is integral in myocardial perfusion and myocyte function, and remains incompletely understood in the context of impaired LV function. The main aim of this thesis was to examine the physiological alterations that occur to the microcirculation and myocardial function following myocardial infarction. Methods: Simultaneous intra-coronary pressure and Doppler flow assessment with wave intensity analysis performed to determine the energy flux in the coronary circulation was undertaken following percutaneous revascularization, in two distinct cohorts. Firstly, in a group with recent myocardial infarction and secondly in a group undergoing revascularization supported by intra-aortic balloon counterpulsation {IABP) therapy. In a separate group, the electrophysiological alterations occurring following acute myocardial infarction were assessed using a novel trans-coronary epicardial voltage mapping technique. Results: We demonstrated that the microcirculatory expansion wave in the infarct-related artery is predictive of both infarct size and regional ventricular recovery following revascularization, assessed by cardiac MRI. Intra-aortic balloon inflation was temporally associated with a unique acceleratory aortic-originating compression wave energy. The magnitude of this wave relates linearly to augmentation of coron y flow velocity during hyperaemic conditions, where autoregulation is 'switched-off'. During basal, 'switched-on' autoregulatory conditions, IABP therapy does not significantly augment flow, due to an increase in microvascular resistance and reduction in microcirculatory expansion wave energy. Trans-coronary electrogram mapping is technically feasible during percutaneous revascularization procedures, with encouraging results in regard to voltage-mapped parameters that may allow prediction of infarcted versus viable tissue. Conclusion: The microcirculation is integral in the functioning of the myocardium. Wave energy derivatives provide an integrated assessment of microvascular haemodynamics and regional myocardial function. Furthermore, the efficacy of intra-aortic balloon counterpulsation is likely to be dependent on the degree of microvascular dysfunction present, with those whose salient haemodynamics are beyond the autoregulatory range most likely to benefit from mechanical assist support devices. Trans-coronary epicardial voltage mapping may provide a technique for the assessment of myocardial viability following infarction, though further development is required to determine its utility and accuracy.
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Dalgleish, Lizanne. "Microcirculatory dysfunction and skin failure in critically ill patients: An exploration of the phenomenon." Thesis, Queensland University of Technology, 2021. https://eprints.qut.edu.au/212524/1/Lizanne_Dalgleish_Thesis.pdf.

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This research investigated the role cutaneous microcirculatory dysfunction plays in the development of acute skin failure by examining cell, tissue, and blood flow changes in critically unwell, intensive care patients. This first of its kind research has advanced the construct of skin failure as a phenomenon in the critical care setting and delivered valuable insights into the current understanding and aetiological development of this condition.
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Nehrkorn, Kathrin [Verfasser], and Nikolaus [Akademischer Betreuer] Plesnila. "The role of pericytes in microcirculatory dysfunction after subarachnoid hemorrhage / Kathrin Nehrkorn. Betreuer: Nikolaus Plesnila." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2016. http://d-nb.info/1104697963/34.

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Liu, Hanhan [Verfasser], and Nikolaus [Akademischer Betreuer] Plesnila. "The role of blood components in microcirculatory dysfunction after subarachnoid hemorrhage / Hanhan Liu ; Betreuer: Nikolaus Plesnila." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2018. http://d-nb.info/1176409662/34.

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Guerci, Philippe. "Current and new therapies for the critically injured microcirculation The macro- and microcirculation of the kidney Endothelial dysfunction of the kidney in sepsis. Section 15: Infectious Diseases and Sepsis, Chapter 89 Impact of fluid resuscitation with hypertonic-hydroxyethyl starch versus lactated ringer on hemorheology and microcirculation in hemorrhagic shock Glycocalyx Degradation Is Independent of Vascular Barrier Permeability Increase in Nontraumatic Hemorrhagic Shock in Rats Glycocalyx shedding during stepwise hemodilution and microvascular permeability A LED-based phosphorimeter for measurement of microcirculatory oxygen pressure The role of bicarbonate precursors in balanced fluids during haemorrhagic shock with and without compromised liver function Effects of N-acetylcysteine (NAC) supplementation in resuscitation fluids on renal microcirculatory oxygenation, inflammation, and function in a rat model of endotoxemia Effect of Polyethylene-glycolated Carboxyhemoglobin on Renal Microcirculation in a Rat Model of Hemorrhagic Shock Resuscitation with PEGylated carboxyhemoglobin preserves renal cortical oxygenation and improves skeletal muscle microcirculatory flow during endotoxemia." Thesis, Université de Lorraine, 2020. http://www.theses.fr/2020LORR0053.

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Au cours des 20 dernières années, la microcirculation a été considérée comme la pierre angulaire du développement de la défaillance d’organe chez les patients critiques. De toute évidence, la microcirculation est devenue une cible thérapeutique. En raison de la complexité de la microarchitecture de ce système fonctionnel, variant d'un organe à l'autre, une thérapie ne peut pas «convenir pour tout». Les altérations observées dans la microcirculation sevèrement endommagée sont de 3 ordres: (i) le contenant défini par les différentes couches de la paroi vasculaire, y compris les cellules endothéliales et un gel protecteur appelé glycocalyx répandu à la surface, où le contact avec le sang est établi, (ii) le contenu représentant le plasma qui coule avec les différents éléments figures du sang et (iii) les tissus extraluminaux environnants. La microcirculation peut être endommagée de diverses manières, avec différents niveaux de dommage à ces éléments constitutifs. Ainsi, pour réanimer de manière appropriée la microcirculation lésée, le choix de la thérapie optimale ou du faisceau de thérapies doit être rationalisé avec une analyse méticuleuse des dommages subis par la microcirculation. Ainsi, l'évaluation de la microcirculation doit être obligatoirement multivariée. Dans cette thèse, la recherche s'est principalement concentrée sur un organe, le rein. La première partie est consacrée à la revue des mécanismes structurels et fonctionnels de la microcirculation rénale en condition physiologique et également septique. La deuxième partie tente d'identifier les rôles respectifs de chacun des composants de la microcirculation dans des conditions critiques notamment le glycocalyx et la viscosité du plasma. La perméabilité de la barrière vasculaire a été étudiée dans les modèles de choc hémorragique et d'hémodilution chez les rongeurs. Les principaux résultats suggèrent qu'il existe une gradation du niveau de lésion de la barrière vasculaire. La dernière partie de la thèse a examiné comment les thérapies actuelles et anciennes peuvent moduler la microcirculation en termes d'oxygénation, d'inflammation et de flux microcirculatoire dans le rein. Parmi les thérapies étudiées, la N-acétylcystéine était efficace pour limiter l'inflammation et augmenter l'oxygénation dans le rein. Une nouvelle génération de transporteur d'oxygène à base d'hémoglobine a montré une certaine efficacité dans le modèle endotoxémique murin. Dans l'ensemble, ces différents résultats se rejoignent pour montrer l'importance d'avoir une analyse multivariée de la microcirculation, car chacune des thérapies agit sur un aspect spécifique de celle-ci. Nous espérons que les résultats de cette recherche ouvrent la voie à une médecine plus personnalisée pour les patients
For the past 20 years, the microcirculation has been regarded as cornerstone in the development of organ failure in critically ill patients. Eventually, the microcirculation became a therapeutic target. Due to the complexity of the microarchitecture of this functional system, varying across organs, one therapy cannot “fit all”. The alterations observed in the critically injured microcirculation involve: (i) the container defined by the different layers of the vascular wall including the endothelial cells and a protective gel called the glycocalyx spread on the surface, where contact with blood is made, (ii) the contents representing the flowing plasma and the different elements of blood and (iii) the extraluminal surrounding tissue. The microcirculation can be injured in various ways, with different levels of injury to these constitutive elements. Thus, to appropriately resuscitate the injured microcirculation, the choice of the optimal therapy or bundle of therapies should be rationalized with a meticulous analysis of the damages suffered by the microcirculation. The evaluation of the microcirculation should be multivariate. In this thesis, the research was mainly focused on the kidney. The first part is dedicated to the review of the structural and functional mechanisms of the renal microcirculation in both healthy and septic states. The second part tries to identify the respective roles of each of the components of the microcirculation in critical conditions especially the glycocalyx and plasma viscosity. The vascular barrier permeability was investigated in hemorrhagic shock and hemodilution models in rodents. The main findings suggest that a gradation in the level of injury to the vascular barrier permeability exist.The last part of the thesis investigated how current and older therapies can modulate microcirculation in terms of oxygenation, inflammation and microcirculatory flow within the kidney. Among therapies investigated, N-acetylcysteine was efficient at limiting inflammation and increasing oxygenation within the kidney. A new generation of hemoglobin-based oxygen carrier showed some efficacy in murine endotoxemic model. Overall, these different findings coalesce to show the importance of having a multivariate analysis of the microcirculation, as each of the therapies acts on a specific aspect of it. Hopefully, this research helped pave the way for a more personalized medicine for the patients
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Biermann, Tanja [Verfasser]. "Microcirculatory dysfunctions present in early stages of metabolic alterations in a diabetic mouse model in vivo / vorgelegt von Tanja Biermann." 2006. http://d-nb.info/981149847/34.

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Books on the topic "Microcirculatory dysfunction"

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Ortiz, Julian Arias, Raphaël Favory, and Jean-Louis Vincent. Infection, sepsis, and multiorgan dysfunction syndrome. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0072.

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Sepsis is the main cause of multiple organ failure and remains a concern because of the associated high morbidity and mortality. In recent years, important advances have been made in the understanding of the pathophysiology of sepsis. Sepsis and septic shock are the end result of complex interactions between infecting organisms and various elements of the host response. A key feature of the common sequence of organ failure is dysfunction of the cardiovascular system, including microcirculatory elements. Outcome improvement in sepsis is based on recognizing the process early and instituting effective therapies. The time window for intervention is relatively short, and treatment must promptly control the source of infection, restore haemodynamic homoeostasis, and support failing organ systems.
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Favory, Raphaël, and Jean-Louis Vincent. Infection, sepsis, and multiorgan dysfunction syndrome. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0072_update_001.

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Sepsis is the main cause of multiple organ failure and remains a concern because of the associated high morbidity and mortality. In recent years, important advances have been made in the understanding of the pathophysiology of sepsis. Sepsis and septic shock are the end result of complex interactions between infecting organisms and various elements of the host response. A key feature of the common sequence of organ failure is dysfunction of the cardiovascular system, including microcirculatory elements. Outcome improvement in sepsis is based on recognizing the process early and instituting effective therapies. The time window for intervention is relatively short, and treatment must promptly control the source of infection, restore haemodynamic homoeostasis, and support failing organ systems.
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Favory, Raphaël, and Jean-Louis Vincent. Infection, sepsis, and multiorgan dysfunction syndrome. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0072_update_002.

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Sepsis is the main cause of multiple organ failure and remains a concern because of the associated high morbidity and mortality. In recent years, important advances have been made in the understanding of the pathophysiology of sepsis. Sepsis and septic shock are the end result of complex interactions between infecting organisms and various elements of the host response. A key feature of the common sequence of organ failure is dysfunction of the cardiovascular system, including microcirculatory elements. Outcome improvement in sepsis is based on recognizing the process early and instituting effective therapies. The time window for intervention is relatively short, and treatment must promptly control the source of infection, restore haemodynamic homoeostasis, and support failing organ systems.
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Favory, Raphaël, and Jean-Louis Vincent. Infection, sepsis, and multiorgan dysfunction syndrome. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0072_update_003.

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Sepsis is the main cause of multiple organ failure and remains a concern because of the associated high morbidity and mortality. In recent years, important advances have been made in the understanding of the pathophysiology of sepsis. Sepsis and septic shock are the end result of complex interactions between infecting organisms and various elements of the host response. A key feature of the common sequence of organ failure is dysfunction of the cardiovascular system, including microcirculatory elements. Outcome improvement in sepsis is based on recognizing the process early and instituting effective therapies. The time window for intervention is relatively short, and treatment must promptly control the source of infection, restore haemodynamic homoeostasis, and support failing organ systems.
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Magalhaes, Eric, Angelo Polito, Andréa Polito, and Tarek Sharshar. Sepsis-Associated Encephalopathy. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0032.

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Brain dysfunction is a major complication of sepsis and is characterized by alteration of consciousness, ranging from delirium to coma and marked electroencephalographic changes. It reflects a constellation of dynamic biological mechanisms, including neurotransmitter imbalance, macro- and microcirculatory dysfunction resulting in ischaemia, endothelial activation, alteration of the blood-brain barrier impairment with passage of neurotoxic mediators, activation of microglial cells within the central nervous system, cumulatively resulting in a neuroinflammatory state. Sepsis-associated brain dysfunction is associated with increased mortality and long-term cognitive decline, whose mechanisms might include microglial activation, axonopathy, or cerebral microinfarction. There is no specific treatment, other than the management of the underlying septic source, correction of physiological and metabolic abnormalities, and limiting the use of medications with neurotoxic effects.
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Waldmann, Carl, Neil Soni, and Andrew Rhodes. Shock. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199229581.003.0026.

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Shock: definition and diagnosis 446Hypovolaemic shock 450Cardiogenic shock 452Anaphylactic shock 456Septic shock: pathogenesis 458Shock, or acute circulatory failure, defines a state in which the delivery of oxygen and nutrients to the tissue is insufficient to meet basal metabolic needs, leading to tissue hypoxia, and, if persistent, to MOF and death. Shock results from tissue hypoperfusion and microcirculatory dysfunction, and should thus not be restricted to hypotension. Although frequent, hypotension is not mandatory for the diagnosis of shock. In the absence of hypotension, increased lactate levels may indicate tissue hypoper-fusion and can be used to diagnose shock (at least at its initiation)....
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Bhopal, Raj S. Epidemic of Cardiovascular Disease and Diabetes. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198833246.001.0001.

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Coronary heart disease (CHD) and stroke, collectively cardiovascular disease (CVD), are caused by narrowing and blockage of the arteries supplying the heart and brain, respectively. In type 2 diabetes (DM2) insulin is insufficient to maintain normal blood glucose. South Asians have high susceptibility to these diseases. Drawing upon the scientific literature and discussions with 22 internationally recognized scholars, this book focuses on causal explanations and their implications for prevention and research. Genetically based hypotheses are considered together with the developmental origins of health and disease (DOHAD) family of hypotheses. The book then considers how CHD, stroke, and DM2 are closely linked to rising affluence and the accompanying changes in life-expectancy and lifestyles. The established causal factors are shown to be insufficient, though necessary, parts of a convincing explanation for the excess of DM2 and CVD in South Asians. In identifying new explanations, this book emphasizes glycation of tissues, possibly leading to arterial stiffness and microcirculatory damage. In addition to endothelial pathways to atherosclerosis an external (adventitial) one is proposed, i.e. microcirculatory damage to the network of arterioles that nourish the coronary arteries. In addition to the ectopic fat in their liver and pancreas as the cause of beta cell dysfunction leading to DM2, additional ideas are proposed, i.e. microcirculatory damage. The high risk of CVD and DM2 in urbanizing South Asians is not inevitable, innate or genetic, or acquired in early life and programmed in a fixed way. Rather, exposure to risk factors in childhood, adolescence, and most particularly in adulthood is the key. The challenge to produce focused, low cost, effective actions, underpinned by clear, simple, and accurate explanations of the causes of the phenomenon is addressed.
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Dangayach, Neha S., Charles L. Francoeur, Stephan A. Mayer, and Tarek Sharshar. Neuroprotection in Sepsis and Acute Respiratory Distress Syndrome. Edited by David L. Reich, Stephan Mayer, and Suzan Uysal. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190280253.003.0013.

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Diffuse cerebral dysfunction in sepsis and acute respiratory distress syndrome (ARDS) patients is highly prevalent. Delirium and alterations in level of consciousness in septic patients are symptoms that constitute sepsis-associated encephalopathy (SAE), which is distinct from hypoxic encephalopathy. SAE is associated with substantial mortality and long-term cognitive impairment. The underlying pathophysiology of SAE is complex and poorly understood. The pathophysiology of SAE includes neuroinflammation, microglial activation, microcirculatory failure, autoregulation impairment, blood–brain barrier disruption, apoptosis, and development of microinfarcts and microhemorrhages. Apart from standard resuscitation techniques targeted at maintaining adequate cerebral perfusion and oxygenation, specific neuroprotective interventions are not currently available. Given the vast unmet need for improving functional outcome among survivors of SAE, it is a priority for the critical care community to better define, understand, and prevent this common and devastating form of neurological injury.
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Book chapters on the topic "Microcirculatory dysfunction"

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van der Hoeven, Nina W., Hernán Mejía-Rentería, Maurits R. Hollander, Niels van Royen, and Javier Escaned. "Microcirculatory Dysfunction." In Physiological Assessment of Coronary Stenoses and the Microcirculation, 39–53. London: Springer London, 2017. http://dx.doi.org/10.1007/978-1-4471-5245-3_3.

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Altura, Burton M. "Microcirculatory Regulation and Dysfunction." In The Reticuloendothelial System, 355–95. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2353-2_15.

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Chioncel, Ovidiu, and Alexandre Mebazaa. "Microcirculatory Dysfunction in Acute Heart Failure." In Microcirculation, 193–221. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-28199-1_13.

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Dorobantu, Maria, and Lucian Calmac. "Coronary Microcirculatory Dysfunction Evaluation in Chronic Angina." In Microcirculation, 141–59. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-28199-1_9.

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Granger, D. Neil. "Risk Factors for Cardiovascular Disease Amplify Reperfusion-Induced Inflammation and Microvascular Dysfunction." In Molecular Basis for Microcirculatory Disorders, 333–42. Paris: Springer Paris, 2003. http://dx.doi.org/10.1007/978-2-8178-0761-4_17.

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Yen, Michael. "Microcirculatory Dysfunction in Acute Myocardial Infarction." In Acute Coronary Syndromes, Third Edition, 615–33. CRC Press, 2004. http://dx.doi.org/10.3109/9780203025673-28.

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Vincent, Jean-Louis. "Infection, sepsis, and multiorgan dysfunction syndrome." In The ESC Textbook of Intensive and Acute Cardiovascular Care, edited by Marco Tubaro, Pascal Vranckx, Eric Bonnefoy-Cudraz, Susanna Price, and Christiaan Vrints, 945–55. Oxford University Press, 2021. http://dx.doi.org/10.1093/med/9780198849346.003.0071.

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Sepsis is the main cause of multiple organ failure and remains a concern because of the associated high morbidity and mortality. In recent years, important advances have been made in the understanding of the pathophysiology of sepsis. Sepsis and septic shock are the end result of complex interactions between infecting organisms and various elements of the host response. A key feature of the common sequence of organ failure is dysfunction of the cardiovascular system, including microcirculatory elements. Outcome improvement in sepsis is based on recognizing the process early and instituting effective therapies. The time window for intervention is relatively short, and treatment must promptly control the source of infection, restore haemodynamic homoeostasis, and support failing organ systems.
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Bhopal, Raj S. "A causal synthesis and models." In Epidemic of Cardiovascular Disease and Diabetes, 198–220. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780198833246.003.0009.

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This chapter synthesizes explanations that are relevant to each of diabetes, CHD, and stroke, and all three collectively. This synthesis emphasizes glycation of tissues, possibly leading to arterial stiffness and microcirculatory damage. In addition to endothelial pathways to atherosclerosis an external (adventitial) one is proposed, i.e. microcirculatory damage to the vasa vasorum, the network of arterioles that supplies nutrients to the larger arteries themselves. DM2 plays into this pathway through glycosylation and dyslipidaemia. The cause of the high prevalence of DM2 in South Asians may lie in protective factors in Europeans not just detrimental ones in South Asians. The high glucose level is considered as an allostatic mechanism controlled by the brain. In addition to the ectopic fat in their liver and pancreas as the cause of beta cell dysfunction, two additional ideas are proposed, i.e. firstly, microcirculatory damage and secondly, glycation, possibly compounded by dietary factors including neoformed contaminants, e.g. AGEs.
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"Microcirculatory Dysfunction in the Pathophysiology of Skeletal Muscle Ischemia." In Vascular Surgery, 437–50. CRC Press, 2003. http://dx.doi.org/10.1201/9780203912904-32.

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Durán, Walter, Mauricio Bori_, Peter Pappas, and Robert HobsonII. "Microcirculatory Dysfunction in the Pathophysiology of Skeletal Muscle Ischemia." In Vascular Surgery. CRC Press, 2003. http://dx.doi.org/10.1201/9780203912904.ch28.

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Conference papers on the topic "Microcirculatory dysfunction"

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Liu, A., R. Wijesurendra, J. Liu, J. Langrish, A. Lucking, R. Choudhury, A. Banning, et al. "10 A high index of microcirculatory resistance in non-obstructed vessels is associated with ischaemia and lv dysfunction." In British Cardiovascular Intervention Society, Young Investigator Award Shortlisted Presentations, Royal College of Physicians of London, November 30 2017. BMJ Publishing Group Ltd and British Cardiovascular Society, 2018. http://dx.doi.org/10.1136/heartjnl-2018-bcis.10.

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