myocardial infarction/hypoxia

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

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

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

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

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

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

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

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

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

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.

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

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

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

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

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