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formaldehyde/infarci
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Commonalities of cardiac rupture (left ventricular free wall or ventricular septum or papillary muscle) during acute myocardial infarction secondary to atherosclerotic coronary artery disease.
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Although mortality rates during acute myocardial infarction (AMI) continue to drop, cardiac rupture (left ventricular free wall [LVFW] or ventricular septum [VS] or papillary muscle [PM] or combination) remains relatively common. The aim was to identify commonalities among patients with AMI
Photoacoustic tomography of ex vivo mouse hearts with myocardial infarction.
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In the present study, we evaluated the applicability of ex vivo photoacoustic imaging (PAI) on small animal organs. We used photoacoustic tomography (PAT) to visualize infarcted areas within murine hearts and compared these data to other imaging techniques [magnetic resonance imaging (MRI),
Postinfarction ventricular septal perforation repair with endoventricular circular patch plasty using double patches and gelatin-resorcinol-formaldehyde biological glue.
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We describe a technique for repairing the ventricular septal perforation 10 days post acute anteroseptal myocardial infarction using the modified infarction exclusion method. The repair involves endoventricular circular patch plasty and application of gelatin-resorcinol-formaldehyde biological glue
Effects of myocardial infarction on adrenergic nerves of the rat heart muscle, a histochemical study.
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The anterior branch of the left coronary artery of the rat heart was ligated and the effects of anoxia on adrenergic nerves were studied histochemically using formaldehyde-induced fluorescence for localization of norepinephrine. Greenish catecholamine fluorescence was associated in the normal or
Immunohistochemical detection of very recent myocardial infarctions in humans with antibodies against heart-type fatty acid-binding protein.
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Depletion of human heart-type fatty acid-binding protein (H-FABP) from cardiomyocytes in infarcted areas with varying postinfarction intervals was studied in 25 autopsy cases. In 23 autopsy cases myocardial infarction was the clinical diagnosis; 2 cases were noncardiac deaths and served as controls.
Pericardial hood repair of cardiac rupture secondary to extended myocardial infarction.
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A surgical technique for simple and safe repair of oozing-type postinfarction cardiac rupture secondary to extended myocardial infarction is described. A hood-shaped pericardium was glued with gelatin-resorcinol and formaldehyde glue to cover the extended oozing infarcted myocardium. This technique
[Climatic and ecological risk factors of myocardial infarction in the Far North].
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Basing on analysis of 1383 hospitalizations because of myocardial infarction during 5 years the following climatic events were found to be associated with development of the disease: rapid changes of atmospheric pressure, temperature or humidity, and magnetic storms. Technogenic ecological factors
[Coronary thrombosis in patients who have died of acute myocardial infarct. A clinico-anatomical study of 167 successive cases].
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OBJECTIVE
To determine the incidence of recent coronary thrombus in a population died of acute myocardial infarction (AMI) and to evaluate the relation between its presence and some clinical parameters (age, gender, time interval between the onset of symptoms and death and cause of
Ketamine decreases cerebral infarct volume and improves neurological outcome following experimental head trauma in rats.
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In brain injury, concentrations of extracellular excitatory amino acids are increased and stimulate glutamate receptors in general and the N-methyl-D-aspartate (NMDA)-preferring subtype in particular. That stimulation causes substantial calcium influx, which appears to initiate a cascade of events
Morphometrical evaluation of triflusal in brain infarction.
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MCA occlusion in animals is a common model for experimental stroke. In previous studies we have shown that one of the factors, which influence evolution of an infarct is microthrombosis in the area of infarction and in the surrounding brain tissue. The present study was undertaken for assessment of
Hyperinsulinemia induces myocardial infarctions and arteriolar medial hypertrophy in spontaneously hypertensive rats.
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To investigate the effects of hyperinsulinemia on the myocardial vessels, long acting insulin (mixtard, a combination of 30% regular human insulin and 70% NPH human insulin) was injected daily for 8 weeks, intraperitoneally, in two strains of rats, normotensive WKY and hypertensive SHR. There were
Immunohistochemical study of fibronectin in experimental myocardial infarction.
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Light microscopic immunohistochemical studies were performed to evaluate the distribution of fibronectin in paraffin sections of p-formaldehyde-fixed normal rat hearts and the hearts of rats that had undergone ligation of the left coronary artery. A peroxidase-labeled antibody technique was used,
Myeloperoxidase-generated oxidants modulate left ventricular remodeling but not infarct size after myocardial infarction.
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BACKGROUND
Inflammation after myocardial infarction (MI) heralds worse left ventricular (LV) function and clinical outcomes. However, whether inflammation affects LV function by extending myonecrosis and/or altering LV remodeling remains unknown. We hypothesized that cytotoxic aldehydes generated
Protein cross-linkage induced by formaldehyde derived from semicarbazide-sensitive amine oxidase-mediated deamination of methylamine.
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Semicarbazide-sensitive amine oxidase (SSAO) catalyzes the conversion of methylamine to formaldehyde. This enzyme is located on the surface of the cytoplasmic membrane and in the cytosol of vascular endothelial cells, smooth muscle cells, and adipocytes. Increased SSAO activity has been found in
Reduction of infarct size following acute coronary occlusion by augmenting collateral blood supply induced by infusion of tricyclic antidepressants.
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Previously, it has been shown that following occlusion of the left anterior descending artery (LAD) in cats, i.v. administration of tricyclic antidepressants (TCAD) significantly decreases the incidence of ventricular fibrillation (VF), which terminates spontaneously upon appearance. Furthermore,
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