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myocardial infarction/hypoxie
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iTRAQ analysis of a mouse acute myocardial infarction model reveals that vitamin D binding protein promotes cardiomyocyte apoptosis after hypoxia.
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The proteome profile changes after acute myocardial infarction (AMI) and the roles played by important protein species remain poorly understood. Here, we constructed a mouse AMI model by ligating the left coronary artery of male C57B/6J mice to investigate the molecular changes after AMI on the
Acute right to left shunt through patent foramen ovale presenting as hypoxemia after myocardial infarction: a case report.
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BACKGROUND
This is a report of a 56-year-old man who became hypoxic due to an acute right to left shunt after sustaining a myocardial infarction involving the right ventricle. This case provides the opportunity to review several key pathophysiologic concepts in the setting of acute right ventricular
Isoflurane preconditioning decreases myocardial infarction in rabbits via up-regulation of hypoxia inducible factor 1 that is mediated by mammalian target of rapamycin.
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BACKGROUND
Volatile anesthetics are known to protect the heart against ischemia-reperfusion injury. The authors tested whether anesthetic preconditioning with isoflurane is mediated via activation of the transcription factor hypoxia inducible factor 1 (HIF-1) and evaluated the role of mammalian
Chronic inhibition of hypoxia-inducible factor prolyl 4-hydroxylase improves ventricular performance, remodeling, and vascularity after myocardial infarction in the rat.
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BACKGROUND
Hypoxia inducible factors (HIFs) are transcription factors that are regulated by HIF-prolyl 4-hydroxylases (PHDs) in response to changes in oxygen tension. Once activated, HIFs play an important role in angiogenesis, erythropoiesis, proliferation, cell survival, inflammation, and energy
Stabilization of hypoxia inducible factor rather than modulation of collagen metabolism improves cardiac function after acute myocardial infarction in rats.
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Prolyl hydroxylase domain-containing enzymes (PHD) hydroxylate a proline residue that controls the degradation of hypoxia inducible factor (HIF). Hypoxia inhibits this hydroxylation thus increasing HIF levels. HIF is upregulated in ischemic tissues, growing tumors and in nonischemic, mechanically
Hypoxemia and lung water in acute myocardial infarction.
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Pulmonary extravascular volume or lung water (PEV), arterial blood gases, and cardiac hemodynamics were measured in 88 patients with acute myocardial infarction. A progressive increase in PEV and a decrease in arterial oxygen tension (PaO2) were observed from Class I (uncomplicated) patients to
miR-7a/b attenuates post-myocardial infarction remodeling and protects H9c2 cardiomyoblast against hypoxia-induced apoptosis involving Sp1 and PARP-1.
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miRs (microRNAs, miRNAs) intricately regulate physiological and pathological processes. Although miR-7a/b protects against cardiomyocyte injury in ischemia/reperfusion injury, the function of miR-7a/b in myocardial infarction (MI)-induced cardiac remodeling remains unclear. Here, we sought to
[Decrease in constrictor response and increase in dilator response of the resistant artery in experimental myocardial infarction: effect of adaptation to hypoxia on this phenomenon].
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After adaptation to hypoxia experimental myocardial infarction does not result in enhanced vasodilatory responses of isolated tail artery from rat to acetylcholine and isoproterenol. At the same time the vascular reactivity to norepinephrine and phenylephrine is enhanced. These data may explain the
Targeted gene deletion of prolyl hydroxylase domain protein 3 triggers angiogenesis and preserves cardiac function by stabilizing hypoxia inducible factor 1 alpha following myocardial infarction.
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The key oxygen sensing molecules, Prolyl-hydroxylase domain 1-3 enzymes (PHD1-3), regulate hypoxia-inducible factor (HIF) under hypoxia. In the settings of cardiomyopathy and ischemia-reperfusion injury, PHD3 expression is elevated, resulting in decreased HIF activation. The role of PHD3 in
[Myocardial infarction in relation to perinatal hypoxia].
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Six newborn infants with myocardial infarction are presented. All of them had a history of perinatal hypoxemia and their natal weights were below 2,500 g. All infants developed cardiogenic "shock" during and required assisted ventilation. Autopsy confirmed the diagnosis in five of the six infants.
Allogeneic Mesenchymal Stromal Cells Overexpressing Mutant Human Hypoxia-Inducible Factor 1-α (HIF1-α) in an Ovine Model of Acute Myocardial Infarction.
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Bone marrow mesenchymal stromal cells (BMMSCs) are cardioprotective in acute myocardial infarction (AMI) because of release of paracrine angiogenic and prosurvival factors. Hypoxia-inducible factor 1-α (HIF1-α), rapidly degraded during normoxia, is stabilized during ischemia and upregulates various
Clinical significance of hypoxemia without congestive heart failure in patients presenting with acute myocardial infarction.
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This study investigated the clinical significance of hypoxemia without apparent clinical congestive heart failure in patients with acute myocardial infarction (AMI). Sixty-two patients with AMI of the Killip group I and Forrester subset I state were stratified into a hypoxemia group and a normoxemia
Refractory hypoxemia in inferior myocardial infarction from right-to-left shunting through a patent foramen ovale: a case report and review of the literature.
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Right ventricular (RV) infarction is a well-recognized complication of some acute inferior myocardial infarctions. Recently, there have been numerous case reports of RV infarctions complicated by severe refractory hypoxemia secondary to right-to-left shunting through a patent foramen ovale. An
Basic Fibroblast Growth Factor Attenuates Injury in Myocardial Infarction by Enhancing Hypoxia-Inducible Factor-1 Alpha Accumulation
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Background: The combination of antiapoptotic and angiogenic actions may represent a pharmacotherapeutic strategy for the treatment of myocardial infarction. Fibroblast growth factor (FGF) is expressed in various cell types including
Studies of hypoxemia and pulmonary hemodynamics in acute myocardial infarction.
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On 55 patients with acute myocardial infarction blood gas changes and A-aDO2 while breathing room air were observed for a period of 5 weeks. PaO2 during the 35% O2 inhalation was measured on admission and 5 weeks later for comparisons with the PaO2 while breathing room air. Pulmonary circulatory
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