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Colloidal lanthanum as a marker for impaired plasma membrane permeability in ischemic dog myocardium.
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Colloidal lanthanum salts have an average particle size of 40 degrees A; consequently, this electron-opaque marker remains extracellular and does not cross the intact plasma membrane. The affinity of lanthanum for calcium-binding sites on mitochondrial membranes makes it possible to demonstrate loss
[Ultrastructure of the sinus and atrioventricular nodes in experimental myocardial infarct].
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The ultrastructure of sinus and atrioventricular nodes was studied in white rats with experimental myocardial infarction. 24 hours after the induction of the disease mitochondrial enlargement characterized by the increase in their area, decrease in the number of cristae and the decline in the rate
[Changes in the biochemical and morphological indices of structural disturbance in the peri-infarct area of the myocardium as affected by opioid peptides in an experiment].
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The effect of opiate peptides (leu-enkephalin, met-enkephalin and beta-endorphin) as well as of enkephalin synthetic analogs (two tetrapeptides and dalargin hexapeptide) on the activity of blood enzymes CPK and LDG1, the scope of myocardial infarction and ultrastructure of periinfarction
[Ultrastructure of cardiomyocytes in the peri-infarct zone during the treatment of experimental myocardial infarct in rats using the hexapeptide dalargin].
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The experiments on white rats with induced myocardial infarction have studied the influence of dalargin on the infarction size and peri-infarction zone ultrastructure. 24 hours later the decrease in the infarction zone size was detected in rats who had received dalargin in a dose of 50 and 100
[Ultrastructure of the subendocardiac cardiomyocytes of the dog heart in acute experimental myocardial infarct].
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Experimental myocardial infarction was reproduced in large random-bred dogs by ligation of the left descending coronary artery. After 24 hours of ischemia, subendocardial Purkinje cells showed accumulations of lipid drops, development of foci of myofibril overcontraction with simultaneous
Lysosomes in myocardial infarction: studies by means of cytochemistry and subcellular fractionation, with observations on the effects of methylprednisolone.
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To evaluate lysosomal involvement in myocardial infarction, coronary artery thrombosis was induced by ligation in 16 dogs. Biopsies of infarcted and normal left ventricles were studied by ultrastructural cytochemistry and subcellular fractionation (0.25 M sucrose) from 30 min to 96 hrs post injury.
Protection of ischemic myocardium by exogenous phosphocreatine (neoton): pharmacokinetics of phosphocreatine, reduction of infarct size, stabilization of sarcolemma of ischemic cardiomyocytes, and antithrombotic action.
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The effect of exogenous phosphocreatine on ischemic myocardium was studied in experimental infarction in rabbits and in total ischemia of pig heart tissue (in vitro). It is shown that single dose administration of phosphocreatine is followed by its rapid clearance from blood plasma (with a half
Assessment of myocardial infarction and postinfarction scar remodeling with an elastin-specific magnetic resonance agent.
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BACKGROUND
To prospectively evaluate an elastin-specific MR contrast agent (ESMA) for in vivo targeting of elastic fibers in myocardial infarction (MI) and postinfarction scar remodeling.
RESULTS
MI was induced in C57BL/6J mice (n=40) by permanent ligation of the left anterior descending coronary
[Condition of the sarcolemma of subendocardial Purkinje cells in the late stages of experimental myocardial infarction in the dog].
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The ultrastructure of subendocardial Purkinje fibers of the dogs left heart ventricle was studied 24 hours after ligation of the descending left coronary artery. The structure of the collagen layer and glycocalyx of the sarcolemma were studied by staining with ruthenium red and the structure of the
[Comparative study using colloidal lanthanum of defects in cardiomyocyte membrane permeability in deep ischemia and in isoproterenol exposure].
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A comparative study of defects in permeability of contractile heart cell membranes in "calcium" necroses of the myocardium and "calcium-free" necroses developing in a focus of deep ischemia in experimental myocardial infarction was carried out. "Calcium" necroses of the myocardium were reproduced by
Morphological changes in acute cerebral ischemia after occlusion and reperfusion in the rat.
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Blood-brain barrier permeability was investigated in acute focal ischemia after MCA occlusion and reperfusion. Four kind of tracers were used: sodium fluorescein and ionic lanthanum as a small molecular tracer, and Evans blue and HRP as a macromolecular tracer. BBB permeability to the tracers was
[Role of the sarcolemma in the morphogenesis of acute heart failure].
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Acute heart insufficiency was simulated in dogs, rabbits and rats with experimental myocardial infarction, hypothyrosis, thyrotoxicosis, autoimmune cardiomyopathy, myocardium hypertrophy by exerting additional mechanical load on the heart (graded aortic stricture, swimming, running in a tread-ban).
[Changes in the ultrastructure of the myocardium after fibrillation and in the process of autolysis].
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Ultrastructure of the myocardium in the experiment was studied just after the heart ventricular fibrillation and 3 h after the animal death; the results were compared to those obtained by studying ultrastructure of human myocardium in patients dying from myocardial infarction complicated by
[Mitochondrial contacts of cardiomyocytes].
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The myocardium of the left and right ventricles in mature rabbits has been studied electron microscopically. The material is fixed by means of vital perfusion and/or by immersion in 2.5% glutaraldehyde with cacodylate buffer 0.05-0.1 M, pH 7.4 and treated in 1% OsO4 with the same buffer. For
Phosphate binders for preventing and treating chronic kidney disease-mineral and bone disorder (CKD-MBD).
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Phosphate binders are used to reduce positive phosphate balance and to lower serum phosphate levels for people with chronic kidney disease (CKD) with the aim to prevent progression of chronic kidney disease-mineral and bone disorder (CKD-MBD). This is an update of a review first published in
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