4 edition of The effect of postnatal myocardial development on the response to ischemic stress found in the catalog.
The effect of postnatal myocardial development on the response to ischemic stress
Michael Andrew Libin
by National Library of Canada = Bibliothèque nationale du Canada in Ottawa
Written in English
|Series||Canadian theses = Thèses canadiennes|
|The Physical Object|
|Pagination||2 microfiches : negative.|
Anti-ischemic Drug therApy Anti-ischemic drug therapy during anesthesia is indicated whenever evidence of myocardial ischemia exists. The treatment of ischemia during anesthesia is compli-cated by the ongoing stress of surgery, blood loss, concurrent organ ischemia, and the patient’s inability to interact with the anesthesiologist. Glucose Metabolism in the Heart. The heart is an omnivore, consuming fuel constantly and using any substrate available. 8 The high rates of ATP production and turnover are critical in maintaining cardiac contractility to deliver blood and oxygen to the other organs. Under normal conditions, cardiac ATP is mainly derived from fatty acid (FA) oxidation (FAO), with glucose metabolism contributing Cited by: 3.
The following are key points to remember from this article on the role of exercise testing in hypertrophic cardiomyopathy (HCM): Previously underutilized in HCM, exercise (stress) echocardiography has become incorporated into the standard clinical assessment and diagnostic armamentarium of HCM using upright or supine symptom-limited treadmill or bicycle modalities. Stage I: Stable angina, an intermittent and reversible process indicating regional myocardial ischemia (restriction in blood supply to the tissues) caused by physical exertion or psycho-emotional stress, and loss of regional myocardial contractility;.
This test is performed at rest and during stress (produced by exercise or dipyridamol or dobutamine) A perfusion defect present during stress but not all rest indicates reversible myocardial ischemia, whereas a persistent perfusion defect on scan during both phases (rest and stress) usually indicates previous myocardial infarction. Thallium. There are alarming increases in the incidence of obesity, insulin resistance, type II diabetes, and cardiovascular disease. The risk of these diseases is significantly reduced by appropriate lifestyle modifications such as increased physical activity. However, the exact mechanisms by which exercise influences the development and progression of cardiovascular disease are by:
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Moreover, decreasing tolerance to ischemia during early postnatal life is counteracted by the development of endogenous protection; preconditioning failed to improve ischemic tolerance. One of the priorities in the treatment of myocardial ischemia is the reestablishment of coronary circulation.
Early reperfusion has a great impact on short-term mortality after a myocardial ischemic event. Coronary revascularization by either coronary bypass surgery (CABG) or percutaneous coronary intervention (PCI) constitutes the primary option in the treatment of coronary Cited by: 1. Impaired myocardial angiogenesis and ischemic cardiomyopathy in mice lacking the vascular endothelial growth factor isoforms VEGF and VEGF Peter Carmeliet 1,Cited by: Jörg-Detlef Drenckhahn, Jette Strasen, Kirsten Heinecke, Patrick Langner, Kom Voy Yin, Friederike Skole, Maria Hennig, Bastian Spallek, Robert Fischer, Florian Blaschke, Arnd Heuser, Timothy C.
Cox, Mary Jane Black, Ludwig Thierfelder, Impaired myocardial development resulting in neonatal cardiac hypoplasia alters postnatal growth and stress response in the heart, Cardiovascular Cited by: Climate change, and thermal stress (i.e., heat and cold) in particular, is a key limiting factor to efficient animal production and negatively impacts health and development during postnatal life.
In addition, thermal stress (especially heat stress) during in utero development can permanently alter postnatal phenotypes and negatively affect Cited by: In this chapter, we summarize the characteristics of pathophysiological changes after ischemic stroke. Ischemic stroke is a rapid occurring and developing disease, which is caused by one or several cerebral artery occlusions.
The occlusion could be due to the thrombus or by: 1. Myocardial Hypertrophy and Regeneration. During postnatal development, a modest number of cycling cardiomyocytes persist in the heart and participate in cardiac renewal.
In response to Author: Angelino Calderone. Adverse ventricular remodeling after myocardial infarction (MI) is a process of regional and global structural and functional changes in the heart as a consequence of loss of viable myocardium, exuberant inflammatory response, increased wall stress in the border zone and remote myocardium, and neurohormonal activation (Figure 1).
myocardial infarction -ischemic necrosis of an area of the cardiac muscle that results in cell death due to partial or complete obstruction of one or more of the coronary arteries -necrotic area is nonfunctional (decreased contractility) and unable to conduct impulses, which. Myocardial infarction ("heart attack") is the irreversible damage of myocardial tissue caused by prolonged ischemia and hypoxia.
This most commonly occurs when a coronary artery becomes occluded following the rupture of an atherosclerotic plaque, which then leads to the formation of a blood clot (coronary thrombosis). Sonic hedgehog (Shh) is a crucial regulator of organ development during embryogenesis.
We investigated whether intramyocardial gene transfer of naked DNA encoding human Shh (phShh) could promote a Cited by: Therefore, the present study was designed to evaluate the effect of tyrosol treatment (5mg/kg/day for 30 days) on myocardial ischemic stress in rat in vivo model of Myocardial Infarction (MI) and to identify key molecular targets involved in this mechanism.
MI was induced by Left Anterior Descending (LAD) coronary artery by: Titin architecture and binding partners. (A) Layout of cardiac titin-isoforms, N2B and N2BA, in the red lines indicate differentially spliced segments in I-band titin. (B) Domain structure of human cardiac titin and binding sites of known titin-ligands (listed in parentheses behind the ligand name).For full names of titin-ligands, see legend to Figure by: Recently, Hippo signaling was also reported to play crucial roles in the regulation of fetal cardiac development and postnatal CM proliferation.
Hippo signaling pathway regulates diverse aspects of cell proliferation, apoptosis, and stemness in response to a wide range of. We recently identified a brief time period during postnatal development when the mammalian heart retains significant regenerative potential after amputation of the ventricular apex.
However, one major unresolved question is whether the neonatal mouse heart can also regenerate in response to myocardial ischemia, the most common antecedent of heart failure in humans. Here, we induced ischemic Cited by: mTORC2 also seems to limit ischemic injury.
Völkers et al 20 previously demonstrated that cardiac rictor gene knockdown accelerates cardiac dysfunction and remodeling in response to chronic myocardial infarction, suggesting that mTORC2 exerts important antiremodeling effects in response to myocardial infarction.
The cardioprotective effects of Cited by: DM is one of the co-morbidities that potentially modify myocardial response to protective interventions, including PC and PostC.
A number of studies have been carried out to determine the efficacy of ischemic PC and PostC for protecting the myocardium in animal models of DM (Tables 3 and 4) and diabetic patients (Table 5).The majority of those studies showed that DM interferes with Cited by: Oxidative stress and inflammation play major roles in the pathogenesis of coronary heart disease including myocardial infarction (MI).
The pathological progression following MI is very complex and involves a number of cell populations including cells localized within the heart, as well as cells recruited from the circulation and other tissues that participate in inflammatory and reparative Cited by: -prolonged myocardial ischemia 2) subendocardial: involves the innermost one-third to one-half (maximally) layer of the myocardial muscle; most poorly perfused region of the myocardial wall These tissues are the most susceptible to ischemia.
Acute myocardial infarction (AMI) always hits the left ventricle. Myocardial infarction is virtually synonymous with left ventricular infarction. All myocardial infarctions affect the left ventricle. Right ventricular infarction is uncommon but may occur if there is 5/5(1). Ischemic heart disease is a leading cause of mortality worldwide (Benjamin et al., ).Although significant advances in treatment have improved early survival after myocardial infarction (MI), such as bypass surgery, percutaneous coronary intervention, and thrombolytic therapy, the high prevalence of post-MI-associated heart failure (HF) remains (Sanchis-Gomar et al., ).Mental stress and the induction of myocardial ischemia in Brown et al Stress: Neurobiology and Neuroendocrinology Marcel Dekker (NY) the risk of ischemic stroke and transient ischemic attack Stroke 7 •) The inverted U – immune The effect of stress on the suppression of erroneous competing responses Anxiety, Stress & Coping: An File Size: 98KB.ISCHEMIC HEART DISEASE.
The underlying cause of ischemic heart disease is usually atherosclerosis of the coronary arteries The most common cause of acute coronary syndromes (unstable angina or acute myocardial infarction) is a sudden increase in luminal narrowing .