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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Circulatory arrest to the lumbar spinal cord of adult cat was produced by occlusion of the descending aorta and concurrent arterial hypotension. Local hypothermia of the cord was induced by paraffin oil at 5 C, which was circulated over the exposed surface of the cord, using the laminectomy wound as a trough. Intramedullary temperature was 15 C at a depth of 5 mm. In 10 control animals oil at 37 or 5 C was circulated over the exposed cords (normal-normothermic and normal-hypothermic controls with 1 and 2 hours hypothermia). Three animals had circulatory arrest and recirculation in normothermia (ischemic-normothermic) and 3 in hypothermia (ischemic-simultaneous hypothermia). Three had circulatory arrest and 15 minutes of recirculation in normothermia followed by 1 hour of hypothermia (ischemic-delayed hypothermia). The medial and lateral portions of the anterior gray horns of the last lumbar spinal segment were studied in the light and electron microscopes. Ischemic-normothermic tissue showed 20% shrinkage in mean areas of neuronal perikarya and massive "watery" swelling of astrocytic cell bodies and processes. Within neuronal perikarya and dendrites, cytoplasm increased in electron density, ribosomes dispersed, Golgi apparatus swelled and mitochondria swelled with loss of matrix density and disruption of cristae. Axons and axon terminals did not increase in size, but mitochondria within these structures doubled in size without loss of matrix density or change in pattern of cristae. Synaptic vesicles were no longer uniform in size, and they were clumped away from the synaptic cleft and diminished in number. Lysosomes were unchanged in appearance and size. Mitochondria of astrocytes underwent approximately fourfold enlargement without loss of matrix density or pattern of cristae. Bundles of astrocytic microfilaments were fragmented, spread apart and diminished in quantity. Oligodendroglia and endothelial cells were unchanged. Normal-hypothermic animals were similar to normal-normothermic except for clefts in rough endoplasmic reticulum of neurons and dendrites. These clefts were formed by a separation of the cisternal membrane from the adjacent row of ribosomal rosettes. Ischemic-simultaneous hypothermia animals had findings identical to normal-hypothermic animals. Ischemic-delayed hypothermia animals were similar to ischemic-normothermic animals except for less swelling of astrocytic processes, greater swelling of astrocytic mitochondria and less alteration of microfilaments. The findings show that ischemia in normothermia brings about alterations in virtually every organelle of the neurronal perikaryon except the lysosome. Simultaneous hypothermia in ischemia prevents the protean alterations of ischemia, whereas hypothermia delayed until after the ischemic episode only slightly modifies the cellular lesions found in ischemic-normothermic animals.
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PMID:Electron microscopy of cat spinal cord subject to circulatory arrest and deep local hypothermia (15 C). 472 89

An accelerated degradation of phospholipid is the likely basis of irreversible cell injury in ischemia, and the membranes of the endoplasmic reticulum of the liver are a convenient system with which to study the effect of such a disturbance on the structure and function of cellular membranes. In the present report, electron spin resonance spectroscopy has been used to evaluate changes in the molecular ordering of microsomal membrane phospholipids in the attempt to relate the loss of lipid to alterations in membrane structure. The order parameter, S, was calculated from spectra reflecting the anisotropic motion of 12-doxyl stearic acid incorporated into normal and 3-h ischemic microsomal membranes. Over the temperature range 4-40 degrees C, the molecular order (S) of ischemic membranes was increased by 8-10%. This increase was reproduced in the ordering of the phospholipids in liposomes prepared from total lipid extracts of the same membranes. In contrast, after removal of the neutral lipids, liposomes prepared from phospholipids of ischemic and control membranes had the same molecular order. There were no differences in the phospholipid species of control and ischemic membranes or in the fatty acid composition of the phospholipids. In the neutral lipid fraction of ischemic membranes, however, triglycerides and cholesterol were increased compared to control preparations. There were no free fatty acids. The total cholesterol content of the liver was unchanged after 3 h of ischemia. The cholesterol-to-phospholipid ratio of ischemic membranes, however, was increased by 22% from 0.258 to 0.315 as a consequence of the loss of phospholipid. Addition of cholesterol to the control total lipid extracts to give a cholesterol-to-phospholipid ratio the same as in ischemic membranes resulted in liposomes with order parameters similar to those of liposomes prepared from ischemic total lipids. It is concluded that the degradation of the phospholipids of the microsomal membrane results in a relative increase in the cholesterol-to-phospholipid ratio. This is accompanied, in turn, by an increased molecular order of the residual membrane phospholipids.
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PMID:Liver ischemia increases the molecular order of microsomal membranes by increasing the cholesterol-to-phospholipid ratio. 609 67

Ultrastructural changes in the small intestine during the early phase following mechanical obstruction were compared with those after vascular ligation. In both experiments (the early phase of mechanical ileus and ischemia) intestinal epithelial cells at the tips of villi showed common features. One of the most significant changes was an alteration in microvilli, with fragmentation into vesicles, narrowing of apical microvilli and decrease in number. The other change was fatty degeneration of the epithelial cells, which was accompanied by vesiculation of smooth endoplasmic reticulum beneath the terminal webs, fat deposition and dilated Golgi complex containing fat. These observations suggest that in the early phase of mechanical ileus, ischemic damage plays an important role.
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PMID:Electron microscopic studies on the small intestinal mucosa of rats after mechanical intestinal obstruction and ischemia. 610 22

We have studied the localization of osmium reduction products to investigate the functional state of organelles as well as organelle interrelationships during cell injury. In normal hepatocytes osmium deposits of variable intensity are seen in nuclear envelope, endoplasmic reticulum. Golgi cisternae and vesicles and lysosomes. Buffering of osmium with s- collidine (pH 7.4) prevents the deposition of osmium. Reversible (30 min) and irreversible (60 min) ischemia without reflow causes no change in the pattern of osmium deposition. Irreversible ischemia followed by reflow causes decreased staining of endoplasmic reticulum (ER) and redistribution of the osmium deposits through the cytoplasm. Reversibly injured pancreatic acinar cells in cultured explants manifest a similar loss of osmium staining in the endoplasmic reticulum cisternae. The administration of antimicrotubule drugs induces an accentuation of osmium staining in localized cisternal elements of hepatocytes. These heavily stained cisternae appear to give rise to the bounding membranes of drug-induced autophagic vacuoles. Cytoplasmic organelles sequestered inside the autophagic vacuoles acquire intense staining when they begin to undergo degradation. In homogenized liver tissue all the subcellular organelles show osmium deposits. The deposits are preferentially localized along the organelle membranes. In particular the dense deposits in the ER lumen are not seen in the subcellular fractions. Phospholipase A2 (3 units/mg protein) enhances the deposition of osmium in the lumen of microsomal vesicles, whereas the presence of detergent has no such effect. Addition of EDTA to the homogenizing medium enhances the ultrastructural preservation of the subcellular fractions but has little effect on the deposition of osmium. OsO4 deposition occurs at acid pH and the intensity and pattern of the stain can be modified in vivo and in vitro. Osmium tetroxide deposition is induced at sites of membrane transformation (autophagic vacuoles) and degradation (lysosomes). Calcium influx and phospholipase activation (ischemia, tissue homogenization, phospholipase addition) enhance osmium deposition and/or influence the localization of the staining pattern.
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PMID:Unbuffered osmium staining of cell organelles: alterations induced by cell injury. 620 40

Polysomic profiles and ultrastructure of granulated endoplasmic reticulum of the dog spinal cord as well as incorporation of labelled amino acids to cytosol proteins during ischemia and recirculation are studied. Ischemia does not evoke serious changes of the studied parameters while several minutes after ligature removal there appear pronounced changes in the ribosome distribution confirmed by electron-microscopic examination. Complete restoration of the observed parameters after the induced ischemia requires two days.
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PMID:[Impairment of protein biosynthesis in the spinal cord in ischemia and recirculation]. 650 35

To investigate the true structural changes in retinal cotton wool spots, serial sections of several blocks of retinal corresponding to cotton wool spots obtained from two hypertensive cases were studied by light and electron microscopy. Occlusion of the feeder arteriole and capillaries, and numerous vacuoles of various sizes in the inner retinal layer were the constant histological features in cotton wool spots. Cytoid body was another change in these areas but it was not a constant feature. Increase of membranous structure resembling endoplasmic reticulum was thought to be incorporated in the formation of the pseudonucleus in the cytoid body. Phagocytosis by macrophages led to the disappearance of the cytoid body. It was concluded that the true feature of the cotton wool spot is nothing but vacuolation, an edematous change of the inner retinal layers due to ischemia following occlusion of the feeder arteriole, and that the cytoid body is only a nonspecific and transient alteration of nerve fibers in the early stage of the ischemic lesion in the retina.
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PMID:Morphological study of the pathogenesis of retinal cotton wool spot. 662 Jul 20

An unusual, delayed neuronal death (DND) has been noticed in the hippocampus of the Mongolian gerbil following brief ischemia (Kirino 1982). On day 1 following 5--10 min of ischemia, light microscopy showed the CA1 pyramidal cells unchanged. On day 2, the cells showed massive growth of membranous cytoplasmic organelles instead of overt cellular disintegration. These neurons were destroyed extensively by day 4 after ischemic insult. Following longer ischemia (20--30 min), however, the changes in the CA1 pyramidal cells appeared faster and resembled the well-characterized ischemic cell change (ICC). To further clarify the differences between ICC and DND, gerbils were submitted to transient 5--30 min ischemia. They were perfusion-fixed following a given survival period and then processed for electron microscopy. Following transient ischemia, specimens showed slow cell changes with growth of cisterns of the endoplasmic reticulum (ER). In some CA1 neurons, the cytoplasm was shrunken and darkly stained, but they also displayed accumulation of ER cisterns. Occasionally, the CA1 cells demonstrated highly shrunken dark perikarya, no different than in ICC. These results indicate that DND seems to be the typical disease process of the CA1 sector and that a severer insult makes the change faster and more similar to ICC. ICC seems to occur when the CA1 pyramidal cells are damaged so severely that they cannot react with proliferous activity.
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PMID:Fine structural nature of delayed neuronal death following ischemia in the gerbil hippocampus. 669 55

If 60 min long ischemia of a liver tissue lobe occurred after feeding of rats with oil emulsion of alpha-tocopherol at a dose of 50 mg/kg within 12 hrs during 2 days, the "ischemic" decrease in metabolism of amidopyrine and aniline, in content of cytochrome P-450 and activity of initial and middle steps of NADPH-dependent redox chain as well as intensification of ascorbate-dependent peroxidation of membrane lipids were prevented in endoplasmic reticulum of hepatocytes. The protective effect of alpha-tocopherol on these xenobiotics metabolism is apparently related to an increase in catalytic activity of cytochrome P-450, to the enzyme antioxidant and membrane-stabilizing properties.
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PMID:[Effect of alpha-tocopherol on the hydroxylating system and lipid peroxidation in membranes of endoplasmic reticulum from ischemic rat liver]. 683 66

An electron microscopic investigation on reparative regeneration of the myocardium has been performed in dogs survived after clinical death resulted from loss of blood. Some regenerative processes already begin on the first hours after reanimation and they proceed on the background of certain distrophic and destructive changes. On the 3d-7th days of the restorative period, the intracellular regeneration of cardiomyocytes increases considerably; it is demonstrated by newly formed myofilaments in the foci of myofibrillar lysis, increasing content of small mitochondria, hyperplasia of the granular endoplasmic reticulum. Simultaneously, a great number of secondary lysosomes is forming; as a result, the cells are releasing themselves from the substances formed after decomposition and decay of some organelles. Myelin-like bodies are observed to be pushed out of the cardiomyocytes into the intercellular space. In fact, by the end of the second week after total ischemia the structure of the cardiac muscle is fully normalized. T-system of cardiomyocytes is the one which is the slowest to restore.
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PMID:[Morphologic changes in the myocardium following acute blood loss and subsequent resuscitation]. 706 12

In the CA1 subfield of the gerbil hippocampus, an unusual series of changes were noticed after ischemia. Mongolian gerbils were subjected to bilateral carotid occlusion for 5 min. Perfusion fixation was performed 3, 6 and 12 h or 1, 2, 4, 7 and 21 days afterwards. Specimens obtained from the dorsal hippocampus were processed for light and electron microscopy. Three different types of changes were observed in the CA4, CA2 and CA1 subfields. In CA4, the change was rapid and corresponded to ischemic cell change. The alteration in CA2 was relatively slow, and identical to what has been called reactive change. On the contrary, the change in the CA1 pyramidal cells was very slow, only becoming apparent by light microscopy 2 days following ischemia. The CA1 subfield was selected for electron microscopic observation. The lamellar alignment of proliferated cisterns of the endoplasmic reticulum was the most conspicuous finding in these cells. Four days following ischemia, almost all of the pyramidal cells in CA1 were destroyed. In the CA1 neuropil, numerous presynaptic terminals remained without being apposed to normal postsynaptic sites. These changes in CA1, called here 'delayed neuronal death', may differ from those thought to be typical of ischemic neuronal damage. It was unlikely that the disturbance of local blood vessels was the cause of these changes.
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PMID:Delayed neuronal death in the gerbil hippocampus following ischemia. 709 91


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