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

Preischemic hyperglycemia induced by feeding or glucose infusion worsens the brain damage and the clinical outcome following ischemia of a given duration and density, and characteristically causes postischemic seizure activity. Light microscopy has previously showed that, in the rat, transient hyperglycemia ischemia induced by bilateral carotid occlusion in combination with arterial hypotension causes a uni- or bilateral lesion in the pars reticulata of the substantia nigra. Since this region has a central role in preventing seizure discharges the present study was carried out to determine the ultrastructural characteristics of this lesion. In rats with 10 min of transient hyperglycemic ischemia followed by recirculation for 1 to 18 h, the pars reticulata of the substantia nigra showed signs of status spongiosus, as well as extensive nerve cell alterations. These changes were observed after all recovery periods studied. The spongiotic appearance was mainly caused by swelling of dendrites and, to a lesser degree, by astrocytic swelling. The dendrites were expanded at all recovery times but the severity increased during the later periods of recirculation. These swollen dendrites contained severely expanded mitochondrias and endoplasmic reticulum. The cytoskeletal elements showed disordered lining of microtubules. Two major types of nerve cell alterations were present: a "pale" and a "dark" variety. The pale type was the most frequent cell alteration. It occurred in all experimental groups and at all time points. Redistribution of the nuclear chromatin and of cytoplasmic organelles as well as swelling of the same type as in the dendrites were the essential changes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Substantia nigra damage induced by ischemia in hyperglycemic rats. A light and electron microscopic study. 332 23

Total ischemia of rat liver tissue within 30 min caused distinct alterations in lipid component of endoplasmic reticulum membranes, which occurred within three weeks of the postischemic period. During this period the rate of microsomal lipids saturation was elevated due to an increase in the relative content of saturated fatty acids. Two-step alterations were observed in the patterns of fluorescent probe binding (I-amino naphthalene-8-sulfonate) as well as in sensitivity of cytochrome P-450 to the impairment in vitro after induction of lipid peroxidation in microsomal membranes. Within 1-3 days after the ischemia affinity of the fluorescent probe to microsomes was decreased, while stability of cytochrome P-450 to impairment during lipid peroxidation induction was increased. Within 7-14 days affinity of the fluorescent probe to membranes was markedly elevated and stability of cytochrome P-450 to the impairment in vitro was lowered in the reactions of lipid peroxidation.
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PMID:[Structural changes in the lipid component of membranes of endoplasmatic reticulum in early and late periods after liver ischemia]. 336 23

The authors studied ultrastructural and biochemical changes in spinal ganglia neurons of dogs after ischemia. Partial spinal cord ischemia was induced by occlusion of the abdominal aorta just below the renal arteries and the arterial blood pressure was registered above and below the occlusion. - In the course of 2-4 hours' ischemia the amount of free ribosomes increased. In some cases the formation of filamentous material or tubular structures inside the cisterns of endoplasmic reticulum was apparent. The proteosynthesis declined. Incorporation of 14C - leucine into the spinal ganglion was 50% as compared to the control animals. The morphological and biochemical changes were more pronounced after 4 h ischemia.
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PMID:The arrangement of endoplasmic reticulum and proteosynthesis in spinal ganglia neurons of dog after ischemia. 359 Dec 43

Nonsteroid antiinflammatory preparations, influencing biosynthesis of renal prostaglandins, are able to produce certain changes in hemodynamics of the organ with successive ischemia. Administration of these preparation (indomethacin and voltaren) to rats in doses corresponding to human therapeutic ones, produces dystrophic changes in the canalicular epithelium of the nephron and appearance of infiltrates in the interstitium and in the lamina propria of the renal calyxes mucous membrane. Intercellular edema and changes in configuration of the cells, decreasing electron density of hyaloplasm, swelled mitochondria, diluted cysterns of the Golgi complex and of the endoplasmic reticulum--are general regularities in ultrastructural reorganization of the cells in response to administration of the two preparations. These changes differ only in degree of their manifestation. As demonstrate the results, the pharmacologic depression of the prostaglandin synthesis causes decreased blood supply of the kidneys and successive depression of their functional state. This can be considered as risk factors of the renal complications under treatment with the nonsteroid antiinflammatory preparations.
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PMID:[Changes in the filtration and reabsorption barrier of the kidneys of the rat after administration of nonsteroidal anti-inflammatory preparations]. 371 53

The effects of cerebral ischemia on perineuronal glia were studied in the rat model of transient four-vessel occlusion. Striatum containing irreversibly injured neurons and paramedian cerebral cortex containing reversibly injured neurons were prepared for electron microscopy at intervals of 3 min up to 24 h following ischemia. Perineuronal astrocytes showed cytoplasmic swelling and configurational changes in and pleomorphism of mitochondria similar to those described previously in parenchymal astrocytes in this model. Dark oligodendroglia showed only transient swelling of cisterns of Golgi apparatus and endoplasmic reticulum. However, medium-light oligodendrocytes significantly increased in size and accumulated microtubules and tubovesicular profiles in the cytoplasm. Reactive glia with features of both oligodendrocytes and astrocytes appeared at 15 min. A sharp drop in the number of perineuronal medium-light oligodendrocytes occurred at 3 h after ischemia and was accompanied by increased numbers of astrocytes and intermediate glia. Cortical glia showed similar changes that were milder and reversible. These studies suggest that certain perineuronal glia are transformed into reactive astrocytes in areas of ischemic neuronal necrosis, although current data are insufficient to determine if the transforming cells are astrocytes, light oligodendrocytes, or intermediate glia. Possible stimuli for these glial reactions include loss of or changes in neuronal trophic factors upon CNS glia or alterations in the interstitial fluid composition.
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PMID:Transformation of postischemic perineuronal glial cells. I. Electron microscopic studies. 376 46

Progression of cerebral ischemia from 5 min to 3 h after occlusion of a common carotid artery was investigated in the subiculum-CA1 region of the hippocampus of the gerbil by transmission electron microscopic and immunoelectron microscopic technique. The earliest change was found after 5 min in the periphery of the apical dendrites in the stratum moleculare, where mitochondrial swelling and disintegration of microtubules were clearly seen inside swollen dendritic processes. After ischemia for 10 min, similar abnormalities were observed in the more proximal part of the apical dendrites, and the basal dendrites also became similarly affected. After ischemia for 30 min to 1 h, the pyramidal cell bodies showed mitochondrial swelling, distension of endoplasmic reticulum and disaggregation of polyribosomes. The immunoelectron microscopic procedure for tubulin revealed irregularity of reaction products associated with microtubules after ischemia for 5 min in the dendritic terminals in the stratum moleculare and in the stratum radiatum after ischemia for 10 min. Reaction products in the pyramidal cell bodies became sparse after ischemia for 30 min to 1 h. The present investigation revealed early onset of ischemic damage in the dendritic terminals and subsequent proximal extension, with disintegration of microtubules and mitochondrial swelling.
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PMID:Cerebral ischemia in the gerbil: transmission electron microscopic and immunoelectron microscopic investigation. 379 Sep 87

It has been difficult to produce a good animal model for cyclosporine nephrotoxicity. It has been suggested that by following 20 minutes of renal ischemia with four daily doses of cyclosporine 60 mg/kg intraperitoneally, one can create a model of reproducible renal failure. We observed excessive mortality (65%), due in part to cyclosporine's CNS effects, with these combined insults in the Munich Wistar rat. In contrast, cyclosporine alone in this dosage produced only 17% mortality and resulted in a similar degree of renal failure. Pair-fed and pair-watered vehicle and saline controls were used. The morphologic changes brought about by the castor oil vehicle of the parenteral cyclosporine solution were qualitatively similar to those brought about by cyclosporine by light microscopy, although the severity of the changes was considerably less in the vehicle-treated groups. However, by electron microscopy, pale lipid vacuoles were seen only in the cyclosporine-treated groups, whereas dense alterations in lysosomes and dilated endoplasmic reticulum also were seen in other groups. Urine sodium determined by flame photometry and urine chloride determined by Saltex reagent strips tended to be high in the initiation phase of cyclosporine-induced acute renal failure and low in the maintenance phase. In animals that developed acute renal failure following the combination of ischemia and cyclosporine, the initial urine sodium and chloride were significantly correlated with the eventual degree of renal failure. The use of Saltex urine chloride sticks in clinical urine samples showed that the readings correlated well with urine sodium and chloride determined by conventional methods, suggesting that these strips may be useful in making a quick diagnosis in the setting of acute renal failure.
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PMID:Renal morphology and function and urine electrolytes in experimental acute renal failure produced by cyclosporine and ischemia. 384 27

Carbon tetrachloride, chloroform, dimethylnitrosamine, thioacetamide or acetaminophen was each administered to rats in a single hepatotoxic dose. Nifedipine, verapamil or chlorpromazine was administered in association with the hepatotoxic agents to determine if calcium channel blocking agents would prevent an increase in liver cell calcium associated with hepatotoxicity and to determine if these agents would protect against the development of centrilobular necrosis. Following a latent period different for each toxic agent, a 4- to 18-fold increase in liver cell calcium content had occurred by 24 hr. The calcium increase and the centrilobular necrosis (mean histologic score) were correlated. A relatively high calcium to necrosis ratio was obtained with dimethylnitrosamine, thioacetamide and acetaminophen. A lesser calcium to necrosis ratio was obtained with chloroform and carbon tetrachloride, the two toxic agents that destroyed the intracellular calcium sequestration activity of the liver endoplasmic reticulum. Nifedipine or chlorpromazine, administered prior to and 7 hr after the toxic agent, completely prevented the centrilobular necrosis caused by thioacetamide, carbon tetrachloride and acetaminophen; almost completely prevented necrosis with dimethylnitrosamine; and provided partial protection against chloroform toxicity. Two doses of verapamil provided partial protection against necrosis when carbon tetrachloride was the toxic agent and provided almost complete protection with dimethylnitrosamine. A reduction in liver cell calcium was associated with the protective action of the three calcium channel blocking agents. These findings are compared with earlier studies of the protective effects of calcium channel blocking agents in cardiac ischemia.
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PMID:Effects of calcium channel blocking agents on calcium and centrilobular necrosis in the liver of rats treated with hepatotoxic agents. 394 99

The experiments on rats have shown that total hepatic ischemia reduces the content of microsomal cytochromes P-450 and b5 and causes amidopyrine and aniline disturbances over a 2-3-week post-ischemic period. The analysis of hepatocyte ultrastructure has revealed the interdependence of structural and functional changes in endoplasmic reticulum during recovery period. The damage of monooxygenase inducibility correlated with stable decline in the number of fixed ribosomes in post-ischemic period.
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PMID:[Structural-functional aspects of the postischemic recovery of the hepatocyte endoplasmic network in rats]. 395 8

Human pancreas tissue was studied electron microscopically during various stages of shock. The subcellular changes of exocrine pancreas affect in particular endoplasmic reticulum (ER), mitochondria, cytoplasm, and nuclei. Alterations correlate with duration and severity of shock, causing cell death in prolonged or severe manifestations of shock. This is obviously due to release of enzymes from zymogen granules; the ensuing damage cannot be distinguished from autodigestive pancreatitis. Lesions of exocrine pancreas cells are of multifactorial origin, arising from general shock-induced hypoxia, but also from local ischemia due to disturbed microcirculation provoking intravasal coagulation. Beyond these main causes, intracellular disorders of metabolism, obstruction of lymph drainage, and nervous factors may be of influence. As the cases surveyed in this paper had no fatal outcome - except for one patient - the changes described can be defined as non-lethal or as reversible.
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PMID:Ultrastructural changes of the human pancreas in acute shock. 402 38


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