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infarction/hypoxia
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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
[Severe tricuspid valve insufficiency due to papillary anterior muscle infarction of the right ventricle secondary to neonatal hypoxia].
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A fatal case of a stressed newborn baby who developed tricuspid insufficiency due to an anterior papillary muscle infarction of the right ventricle, related to perinatal anoxia is reported. The baby needed resuscitation management and had a systolic murmur soon after birth. The echocardiographic
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
In vivo remote delivery of DNA encoding for hypoxia-inducible factor 1 alpha reduces myocardial infarct size.
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We tested if remote gene delivery of hypoxia-inducible factor 1 alpha (HIF-1 alpha) protected hearts against induced ischemia, hypothesizing that gene delivery into skeletal muscle may lead to secretion of proteins with actions elsewhere. Murine quadriceps muscles were transfected with DNA encoding
Major role for hypoxia inducible factor-1 and the endothelin system in promoting myocardial infarction and hypertension in an animal model of obstructive sleep apnea.
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OBJECTIVE
Our aim was to investigate the involvement of the endothelin (ET) system in the cardiovascular consequences of intermittent hypoxia (IH).
BACKGROUND
Obstructive sleep apnea (OSA) syndrome is an important risk factor for cardiovascular morbidity. Chronic IH, a major component of OSA, is
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
Oxidative stress mediates cardiac infarction aggravation induced by intermittent hypoxia.
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We have previously shown that chronic intermittent hypoxia (IH), a component of the obstructive sleep apnea syndrome, increases heart sensitivity to infarction. We investigate here the deleterious mechanisms potentially involved in the IH-induced infarction aggravation, investigating the role of
Induction of collateral circulation by hypoxia-inducible factor 1alpha decreased cerebral infarction in the rat.
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BACKGROUND
We recently reported that hypoxia-inducible factor 1alpha (HIF-1alpha), HIF-2alpha and cyclooxygenase 2 naked DNA induced angiogenesis in a rat indirect bypass model. In this work, we investigated whether the collateral circulation induced by HIF-1alpha DNA affected the cerebral
[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
[Effect of adaptation to periodic hypoxia on post-infarction fall of blood pressure and hyperactivation of the endothelium].
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Acute stress concomitant to the experimental myocardial infarction has induced endothelial hyperactivation of the rat aorta exhibited in an increase of inhibition of norepinephrine-induced contractions of vascular smooth muscle, enhanced endothelium-dependent relaxation correlating with a fall of
Misidentification of infarct core by computed tomography perfusion (CTP) in a patient with acute ischemic stroke with hypoxia.
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The authors reported a case with acute right, middle cerebral artery infarct in which the early infarct area was detected by CTP recovery later after the treatment. The patient had hypoxia and tachypnea from pulmonary edema during acute ischemic stroke, which may have accentuated the ischemic change
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