Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: HUMANGGP:036206 (endoplasmic reticulum)
 63,868 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adenohypophyses of adult male rats have been investigated by light microscopy, immunocytology and electron microscopy 30 minutes, 1, 2, 4, 6 and 24 hours following electrolyte destruction of the pituitary stalk. Light microscopy revealed massive ischemic infarction of the adenohypophysis. Immunoreactive growth hormone, prolactin, TSH, FSH and LH were demonstrated up to 24 hours after surgery in necrotic adenohypophysial cells by the immunoperoxidase technique. Fine structural abnormalities were already noticeable 30 minutes following stalk lesion. The changes rapidly progressed and within 2 hours unmistakable signs of cellular necrosis became evident. Mitochondria, especially those of growth hormone cells, seemed to be affected at an early stage, whereas alterations in rough-surfaced endoplasmic reticulum membranes developed later. Nuclear changes, formation of cytoplasmic vacuoles and disruption of cell membranes were conspicuous findings. No evidence, indicating the participation of lysosomes in the development of cellular damage, was obtained. Secretory granules were prominent and well preserved even in cells which showed advanced necrosis. The failure of discharge and degradation of secretory granules in the necrotic cells suggest that factors accounting for their intracellular migration and extrusion are very sensitive to ischemia and are paralyzed at an early phase.
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PMID:Adenohypophysial necrosis in rats following destruction of the pituitary stalk. A histologic, immunocytologic and fine structural study. 33 35

The pars convoluta of the proximal tubule of the rat kidney was studied by light and electron microscopy during the recovery phase from transient ischemia. The left kidney was made ischemic by clamping the aorta just above the left renal artery leaving the blood supply to the right kidney and the intestine intact. The pars convoluta (P1 and P2 segments) of the proximal tubule was examined both immediately after various periods of ischemia (15, 30, 60 and 120 min) and after the same ischemic periods followed by 3, 6, 12 and 24 h of blood reflow (= recovery phase). It was found that ischemia for periods up to 60 min were compatible with cell survival whereas 120 min of ischemia gave rise to irreversible cellular changes. Before regaining a normal conformation during the recovery phase, cells made ischemic for 15 min were characterized by slightly decreased cell height, dispersed nuclear chromatin, mitochondria in orthodox conformation and increased numbers of digestive vacuoles and of lipid droplets (stage A2). Most cells made ischemic for 15 min appeared normal when examined after 24 h of reflow. Cells made ischemic for 30 min were also characterized by stage A2 changes after 3 h of reflow and remained in this stage during all recovery periods studied. Cells made ischemic for 60 min first passed into a stage designated A1 and then later during the recovery phase into stage A2. Stage A1 cells were characterized by decreased height, condensed mitochondria, apparently increased numbers and sizes of secondary lysosomes and slightly dilated rough surfaced endoplasmic reticulum; 120 min of ischemia followed by reflow was not compatible with cell survival. Cells made ischemic for 120 min showed the following alterations denoted as stages C and D: shrunken with pyknotic nuclei, swollen mitochondria with large flocculent densities, and filled with different sized vesicles in the apical portion (stage C). Stage D included cells which had undergone necrosis, i.e., phasma membranes and organelles were fragmented and occurred as debris in the tubule lumens.
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PMID:Studies on cellular recovery from injury. II. Ultrastructural studies on the recovery of the pars convoluta of the proximal tubule of the rate kidney from temporary ischemia. 40 90

Permanent, complete global cerebral ischemia was induced in cats by filling the cardiovascular system with a plasma substitute (37 degrees C). At variable intervals and up to 120 min thereafter, these feline brains were perfused with aldehydes and processed for electron microscopy. The resulting cellular alterations were homogeneous and uniform throughout the entire brain; they included early chromatin clumping, gradually increasing electron lucency of the cell sap, distention of endoplasmic reticulum and Golgi cisternae, transient mitochondrial condensation followed by swelling and appearance of flocculent densities, and dispersion of ribosomal rosettes. The marked contrast between the structural alterations in permanent, complete ischemia and incomplete cerebral ischemia, suggest differences in their pathogenesis. A basic determinant factor of the structural changes appears to be the volume of flow (serum, plasma, other) which is available at the time of the injury. This analysis of global cerebral ischemia provides some insight on the nature of cellular changes occurring shortly after somatic death.
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PMID:The ultrastructure of "brain death". II. Electron microscopy of feline cortex after complete ischemia. 41 53

Unilateral (50 to 118 minutes) and bilateral (2 to 33 minutes) carotid artery occlusion in gerbils resulted in two distinct types of neuronal alteration: ischemic cell change (ICC) in selectively vulnerable brain regions, and selective chromatolysis (SC) confined to the deeper layers of the cortex, the Sommer sector of zone h-1, and the paramedian region (PM) of the hippocampus. In typical SC the nucleus was eccentric and the Nissl substance was lost in the central eosinophilic cytoplasm. In electron micrographs this area of cytoplasm showed disruption of smooth and rough endoplasmic reticulum with disaggregation of polyribosomes and accumulation of mitochrondria and various dense bodies. SC was identified at 2 to 3 hours and was still recognizable at five days. When bilateral carotid artery occlusion lasted 5 to 6 minutes, SC was seen in the hippocampal Sommer sector and cerebral cortex, while ICC was restricted to the endfolium (h3-5). Unlike ICC, the frequency of SC was not related to the duration of ischemia but probably to the epileptic seizures (overt and subclinical) initiated by ischemia in the gerbil. These changes must be considered when the gerbil is employed as a model of experimental stroke.
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PMID:Selective chromatolysis of neurons in the gerbil brain: a possible consequence of "epileptic" activity produced by common carotid artery occlusion. 42 76

Hamster tracheal epithelium survived 3 hours of total ischemia at 37 degrees C as demonstrated by its ability to be maintained in organ culture for 7 days subsequent to the ischemic episode. Epithelium ischemic for longer periods did not survive in culture. Human bronchial epithelium obtained from surgically resected lungs showed the acute effects of ischemia, i.e., the cells had dilated endoplasmic reticulum and swollen mitochondria. These cellular effects of ischemia were, however, reversed by placing the bronchus in explant culture. Bronchus obtained at autopsy, 2 to 3 hours following death, showed epithelial cells suffering severe ischemic cell injury, most of which did not survive in culture, but in some cases, a few basal cells survived to form a non-keratinizing squamous epithelium.
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PMID:Studies on the pathogenesis of ischemic cell injury XV. Reversal of ischemic cell injury in hamster trachea and human bronchus by explant culture. 59 98

The pars convoluta of the proximal tubules of the rat kidney was examined by means of light and electron microscopy after 15, 30, 60 and 120 min of complete ischemia produced by clamping of the aorta. The same ischemia periods were also examined after 24 hrs of blood reflow. It was found that the vast majority of the cells of pars convoluta survived 60 min of ischemia as seen after 24 hrs of reflow. The following pattern of changes were observed at time intervals up to 60 min: progressive clumping of chromatin, progressive distortion of microvilli with bleb formation, increasing dilatation and finally vesiculation of rough-surfaced endoplasmic reticulum and initially condensation and later high amplitude swelling of mitochondria. It is concluded that these subcellular changes are compatible with cell survival. Also tubule cells containing swollen mitochondria with small flocculent densities are potential candidates for survival. 120 min of ischemia was associated with marked mitochondrial swelling with large flocculent densities, severe cell damage and necrosis and was not compatible with cell survival. A working hypothesis is presented relative to the pathogenesis of acute renal failure caused by complete ischemia.
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PMID:Studies on the pathogenesis of ischemic cell injury. II. Morphological changes of the pars convoluta (P1 and P2) of the proximal tubule of the rat kidney made ischemic in vivo. 81 77

The pars recta of the proximal tubule of the rat kidney was examined by means of light and electron microscopy after 15, 30, 60 and 120 min of ischemia produced by clamping of the aorta. Also the effects of 24 hrs of blood reflow following the same ischemia periods were determined. The maximal changes occurring after ischemic periods of up to 60 min included: marked cell swelling, swelling of the inner compartments of the mitochondria, swelling of the endoplasmic reticulum and of microvilli, pronounced chromatin clumping in the nuclei and distortion of the Golgi apparatus. These cell changes were reported to be reversible in the previous paper of this series. After 24 hrs of blood reflow it was found that with increasing periods of primary ischemia, ranging from 15 to 120 min, an increasing number of pars recta tubules cells were undergoing necrosis. Theses findings indicate that some additional mechanism other than the initial ischemia per se must be responsible for the progressive cellular damage leading to the necrosis. This is in contrast to the pars convoluta of the proximal tubule, which does not undergo further degenerative changes after the primary ischemia has been ended. The "no reflow" phenomenon may satisfactorily explain the necrosis seen in the pars recta segments following various periods of ischemia after 24 hrs of arterial renal reflow.
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PMID:Studies on the pathogenesis of ischemic cell injury. III. Morphological changes of the proximal pars recta tubules (P3) of the rat kidney made ischemic in vivo. 81 78

Rat pancreatic slices were incubated at 37 degrees C in vitro, in order to determine if complete ischemia would reproduce the subcellular alterations seen in human pancreatic acinar cells following shock. The ultrastructural alterations observed were similar to those seen in humans and in animal models of hypovolemic shock. These changes ranged from dilated endoplasmic reticulum and swollen mitochondria (reversible changes) to mitochondrial flocculent densities and later stages (evidence of cell death). In this in vitro study the pancreas remained in an apparently reversible stage longer than liver, heart, kidney, and brain treated similarly. However, once the pancreatic cells died, necrotic breakdown occurred very rapidly, perhaps due to intracellular release of lysosomal and zymogen granule hydrolases.
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PMID:Cellular and subcellular effects of ischemia on the pancreatic acinar cell: in vitro studies of rat tissue. 81 79

The fetal mouse heart (FMH) in organ culture continues to beat for a period of weeks, but degenerative changes occur. Electron microscopy revealed formation of autophagic vacuoles containing damaged organelles in some cells after the first day, indicating focal cytoplasmic injury. This process was accelerated by transient deprivation of oxygen and glucose followed by resupply of oxygen and glucose. FMHs were maintained for up to four hours in glucose-free media in an atmosphere of 95% N/5% CO2 followed by resupply of O2 and glucose. Twenty-four hours later, many cells recovered without residual injury. Many others revealed autophagic vacuoles ranging from those in which organelles were readily identified to those characteristic of residual bodies. It appears that focal injury stimulates the endoplasmic reticulum to enclose the damaged components, permitting localized lysosomal digestion without causing injury to the entire cell. Autophagy has not been emphasized as an important mechanism in transient ischemia in adult myocytes, but it may play a role in repair of sublethal injury. The FMH organ culture provides an excellent model for studying the sequential autophagic changes in a system in which these events can be accelerated.
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PMID:Autophagy in cardiac myocytes. 103

Ultrastructural analysis of the epithelium of the proximal and the distal portions of the kidney nephron of albino rats in "survival" of the organ in the cadaver and in experimental ischemia showed a different reaction of the cells to these actions. An intracellular edema and characteristic changes in the ultrastructure of the mitochondria appear in the tubular epithelium during the organ autolysis in the animal cadaver. Under conditions of experimental ischemia, against the background of intracellular edema, there develop marked changes in the lysosomal apparatus of the cells, swelling of the mitochondria and also a marked dilatation of the cysternae of the endoplasmic reticulum and of the Golgi complex.
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PMID:[Ultrastructural changes in the nephron during ischemia and organ "survival"]. 112 2


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