Electron Microscopic Alterations Research Articles

Epinephrine-induced biochemical and electron microscopic alterations in generalized glycogen storage disease

Epinephrine-induced biochemical and electron microscopic alterations in generalized glycogen storage disease

Isoproterenol-induced myocardial necrosis. A histochemical and electron microscopic study

Electron microscopic and histochemical alterations in heart muscle after the administration of isoproterenol are described in detail. Isoproterenol-induced myocardial necrosis develops more slowly than that resulting from coronary artery occlusion. The first prominent electron microscopic changes are: thickening of the Z lines, swelling of mitochondria, and enlargement of the vesicles of the endoplasmic reticulum. Little depletion of glycogen was observed in the early stages. Fat droplets in various stages of formation were observed within the vesicles of the endoplasmic reticulum. No fatty degeneration of the mitochondria was seen. Histochemical studies demonstrated an early rise in the succinic dehydrogenase activity, followed by a fall. No early rise was seen with the cytochrome oxidase reaction. The accumulation of fat droplets in myocardium was studied by a sensitive fluorescence microscopy technique. The significance of these observations and the relationship of fatty change in the myocardium to cellular injury are discussed.

ELECTRON MICROSCOPIC ALTERATIONS IN THE RAT HYPOPHYSIS AFTER SCALDING.

ELECTRON MICROSCOPIC ALTERATIONS IN THE RAT HYPOPHYSIS AFTER SCALDING.

Effects of specific antibodies on tissue cells.

Cells can be altered or damaged by immunological reactions in many ways. Some of these are indirect because the antibody reaction is not di­ rected against the tissue cell or its components. These reactions include acute anaphylaxis (1), the Arthus (2) and the Auer (3) reactions, delayed hypersensitivity (4), and serum sickness (5). In general, each of these im­ munopathological processes involves a response of blood and lymph vessels as well as inflammatory cells; and in some instances, at least, they are brought about by the release of inflammatory materials, including esterases as well as histamine and other stored perivascular chemicals (1). Distinct from these indirect mechanisms by which cell injury is pro­ duced immunologically are the effects which have as their basis the direct interaction of specific antibodies with tissue cells and their components. The purpose of this paper is to review the current state of our knowledge concerning these specific antibodies and their actions. Means of evaluating cell damage .-There are various ways of evaluat­ ing the effects of these cell-specific antibodies. The term cytotoxic is best applied to the in vivo or in vitro alterations visible with light microscopy in the antibody-treated cells. This term does not ade­ quately describe the subtle changes which may occur when specific anti­ bodies interact with such widely studied tissue components as renal glom­ erular basement membrane, thyroglobulin, coHagen, ground substance, and platelets. In a sense, these reactions also may be considered to be cyto­ toxic but their evaluation is often more difficult and the changes are usually described in other terms. Electron-microscopic alterations in chemical components as shown by histochemistry and cytochemistry, as well as changes in function, are all useful in evaluating the damage produced by specific antibody. A correla­ tion of new knowledge of ceHular structure, composition, and function fol­ lowing antibody action appears to be a particularly promising way to gain understanding. For example, correlation of proteinuria, electron-microscopic changes in the glomerulus, and in vivo labeling of the glomerular compo­ nents offers a new dimension to our study of the effects of nephrotoxic se­ rum (6). Similar correlative studies are proving to be particularly helpful in

THE EFFECTS OF A CARDIAC GLYCOSIDE ON SUBCELLULAR STRUCTURES WITHIN NERVE CELLS AND THEIR PROCESSES IN SYMPATHETIC GANGLIA AND SKELETAL MUSCLE

Nerve cells and their processes in cat sympathetic ganglia and frog skeletal muscle have shown on electron microscopic examination alterations in subcellular morphology as a result of treatment with digoxin. Non-nervous cells were unaffected by the drug. These changes included, in ganglia, swelling of the affected cells, shrinkage of mitochondria with pronounced increase in internal density, swelling of Nissl substance in nerve cell bodies, and loss of structural detail in nerve processes. At the myoneural junction the motor nerve endings were swollen, mitochondria were altered, and the synaptic vesicles were reduced in numbers, those that remained being swollen. These changes were accompanied by invagination of the axon surface by Schwann cell processes.Cell swelling, but not the subcellular changes, was prevented by substitution of sulphate for chloride ions in the extracellular space. When the extracellular sodium ion concentration was reduced to 20 meq/l. the cells were completely protected against digoxin. It is concluded that swelling is caused by net uptake of sodium and chloride as a result of the known inhibitory action of digoxin on sodium extrusion by nerve cells. The possibility that these structural changes in subcellular organelles may be caused by a raised concentration of intracellular sodium ions, such as might occur during activity of excitable cells, is discussed.

THE EFFECTS OF A CARDIAC GLYCOSIDE ON SUBCELLULAR STRUCTURES WITHIN NERVE CELLS AND THEIR PROCESSES IN SYMPATHETIC GANGLIA AND SKELETAL MUSCLE

Nerve cells and their processes in cat sympathetic ganglia and frog skeletal muscle have shown on electron microscopic examination alterations in subcellular morphology as a result of treatment with digoxin. Non-nervous cells were unaffected by the drug. These changes included, in ganglia, swelling of the affected cells, shrinkage of mitochondria with pronounced increase in internal density, swelling of Nissl substance in nerve cell bodies, and loss of structural detail in nerve processes. At the myoneural junction the motor nerve endings were swollen, mitochondria were altered, and the synaptic vesicles were reduced in numbers, those that remained being swollen. These changes were accompanied by invagination of the axon surface by Schwann cell processes.Cell swelling, but not the subcellular changes, was prevented by substitution of sulphate for chloride ions in the extracellular space. When the extracellular sodium ion concentration was reduced to 20 meq/l. the cells were completely protected against digoxin. It is concluded that swelling is caused by net uptake of sodium and chloride as a result of the known inhibitory action of digoxin on sodium extrusion by nerve cells. The possibility that these structural changes in subcellular organelles may be caused by a raised concentration of intracellular sodium ions, such as might occur during activity of excitable cells, is discussed.