Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous studies using the isolated ex vivo perfused canine pancreatitis preparation showed that during a 4-hour perfusion pancreatitis (edema, weight gain, hyperamylasemia) can be induced by four different stimuli. The stimuli include the intra-arterial infusion of oleic acid (FFA), a 2-hour period of ischemia before perfusion (ISCH), partial obstruction of the pancreatic duct with secretin stimulation (POSS), and the intra-arterial infusion of cerulein at supramaximal doses (CER). In the present study, changes in high-energy phosphate metabolism, as determined by nuclear magnetic resonance spectroscopy, and changes in cellular structure, determined by light and electron microscopy, were documented for all four models of acute pancreatitis. The control preparations remained stable for the 4-hour perfusion period, with no decrease in adenosine triphosphate (ATP) levels. In the FFA preparations, ATP decreased to 36% of baseline levels during the 4-hour perfusion (p less than 0.001). In the ISCH preparations, ATP decreased to undetectable levels during the 2-hour period of ischemia, but recovered rapidly and remained at baseline levels during the perfusion. ATP levels remained stable in the remaining two models of pancreatitis (POSS, CER). Microscopy demonstrated that the initial injury was located chiefly in the capillaries (swollen endothelium, intravascular thrombi) in the FFA and ISCH preparations. In the POSS and CER preparations, capillary changes were minimal and the injury was located chiefly in the acinar cells (swollen endoplasmic reticulum, zymogen granule depletion, vacuolization). The POSS preparations also showed striking dilation of centroacinar lumens reflecting duct obstruction. In additional studies it was shown that the ATP decline in the FFA preparations could be significantly reduced by pretreatment with free radical scavengers. The morphologic changes could be reduced by free radical scavengers in the FFA and ISCH preparations. Any amelioration of morphologic injury in the POSS preparations was obscured by dilatation of centroacinar lumens in both treated and untreated groups. The morphologic changes in the CER preparations were reduced by treatment with a cholecystokinin inhibitor.
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PMID:Changes in high-energy phosphate metabolism and cell morphology in four models of acute experimental pancreatitis. 200 16

Ultrastructural damage leading to delayed neuronal death was investigated in the mid-CA1 region of the hippocampus from the stratum (str.) moleculare to oriens after transient bilateral forebrain ischemia in Mongolian gerbils. After ischemia for 5 min without recirculation, mild swelling of the peripheral part of the apical and basal dendrites was already apparent in the str. moleculare and str. oriens. Mitochondria in the dendrites were also swollen in the same area. During recirculation for 12 h to 3 days, swelling of the dendritic cytoplasm persisted with formation of microvacuoles, but swelling of mitochondria receded. Microvacuolation and loss of microtubules were also observed in the proximal part of the dendrites during this period, and swelling and disruption of internal cristae were observed in mitochondria after recirculation for 3 days. The dendrites became severely degenerated after recirculation for 4 days. In the pyramidal cell bodies, no abnormality was observed at the end of ischemia for 5 min, but disaggregation of polyribosomes and swelling of the endoplasmic reticulum were observed 12 h after recirculation. Proliferation of the endoplasmic reticulum in parallel arrays occurred after recirculation for 1 day and persisted. Severe degeneration of the pyramidal cell bodies was obvious after recirculation for 4 days. The findings observed in the present investigation suggested that the neuronal structure most vulnerable to ischemia was the peripheral part of the dendrites and postischemic neuronal damage occurred early in this part of the dendrites.
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PMID:Ultrastructural investigation of the CA1 region of the hippocampus after transient cerebral ischemia in gerbils. 225 5

The early lesions induced in the pancreas of dogs by the intraductal injection of bile-trypsin were studied. Histological, histochemical and electron microscopic techniques were used. The primary lesions analyzed thirty three minutes after the induction of pancreatitis consisted in cell alterations, blood stasis and oedema. At first, the affected acinar cells showed enlargement of the rough endoplasmic reticulum cisternae, later they were disrupted and then appeared vesicles with ribosomes adhering to the external surface. Mitochondria were swelled and showed cristae disrupted which finally appeared destroyed. The zymogen granules lost density, decreased in size and number and later disappeared, Ducts maintained the normal structure and their cells were still observed in areas where the tissue was greatly destroyed. the results obtained suggest that: 1) The experimental acute pancreatitis induced by bile-trypsin is characterized by primary and severe damage in the acinar cells, with secondary ischemia due to stasis and intravascular coagulation. 2) Cellular rests and probably endogenous enzymes invade the periacinar spaces, then would penetrate into the vascular system producing the generalization of lesions.
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PMID:[Acute pancreatitis induced by bile trypsin: structural and ultrastructural study]. 227 10

By means of histochemical revealing of zinc and applying radioactive isotope 65Zn accumulation, absorption and distribution of cations of this metal in the mucous membrane of the iliac intestine have been studied in chicken, normal, at ischemia and at A-avitaminosis. An essential zinc-depositing ability is peculiar to coverings of mucus upon the intestine epithelium, and among intracellular components--to smooth endoplasmic reticulum. A-avitaminosis and especially ischemia result in increasing permeability of the apical part of the external membrane of epitheliocytes, in overloading of the latter with zinc cations, when they are introduced into the intestine, as well as in decreasing transepithelial transport of zinc. The changes mentioned are accompanied with certain disturbances in the barrier function of the intestinal epithelium.
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PMID:[Disorders of zinc transport through the ileal epithelium in vitamin A deficiency and ischemia]. 227 11

Acute brain ischemia was accomplished in 18 rhesus monkeys through bilateral occlusion of the vertebral and carotid arteries. The temporary blood volumes (TBV) of the corresponding areas of the ischemic brains were compared with those of the normal controls. At the time of brain ischemia the TBV in basilar ganglion and internal capsule decreased significantly (7.28%) and that in the temporal cortex decreased moderately (22.76%) while the TBV in the brain stem did not show significant changes. The amplitude of EEG was suppressed or became isoelectric immediately after 15 minutes of ischemia. The EEG slightly restored following a reperfusion of 120 minutes, but it became irreversible if ischemia lasted more than 30 minutes. The sodium and water content increased as ischemic was prolonged. This was more significant after recirculation. Ultrastructural findings showed that mitochondria, endoplasmic reticulum and astrocytic processes became swollen after 15 minutes of ischemia. When ischemia lasted more than 30 minutes, mitochondria became swollen more significantly with ruptured cresta. There were marked margination of nuclear clumping chromatins. According to these changes the neuron underwent irreversible injury. As ischemia lasted more than 60 minutes these changes became more apparent, i,e, the mitochondria contained amorphous matrix densities. The nuclear chromatin showed aggregated clumping. The cellular membranes were damaged and the blood vessels contained microemboli. After reperfusion it became much more serious.
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PMID:[An experimental study of acute brain ischemia followed by reperfusion in rhesus monkeys]. 234 76

A monoclonal antibody (mAb 4B4) was raised against purified sarcoplasmic reticulum vesicles from canine myocardium, and shown to inhibit Ca2+ uptake by microsomes isolated from cardiac, skeletal, and smooth muscle. The amount of mAb 4B4 needed to inhibit the Ca2+ uptake 50% at a given membrane concentration correlated with the amount of Ca2+ pump protein in the microsomal preparation. This is consistent with the observation the mAb 4B4 binds specifically to the sarcoplasmic/endoplasmic reticulum Ca2+ pump (Mr 100 kDa), but has no effect on the T-tubule Mg2+-ATPase. Changes in the binding of mAb 4B4 to crude microsomes isolated from dog heart after various durations of global ischemia showed that the decrease in microsomal Ca2+ transport during the first 15 min of ischemia correlated with a loss of active Ca2+ pump molecules. The monoclonal antibody mAb 4B4 may therefore serve as a specific marker for the sarcoplasmic/endoplasmic reticulum Ca2+ pump system in various cells, and can provide quantitative information about the loss of active Ca2+ pump proteins under pathological conditions.
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PMID:Monoclonal antibodies to dog heart sarcoplasmic reticulum as markers of endoplasmic reticulum. 254 29

Cell injury proceeds through a predictable series of stages as it progresses from reversible to irreversible injury (or "point of no return") and ends eventually in cell death. Ion deregulation is strongly implicated in this process and, in particular, the deregulation of cytosolic Ca2+ ([Ca2+]i) which is thought by most to be a critical step in the transition from reversible to irreversible injury. [Ca2+]i is normally maintained at approximately 100 microM, a level 10,000 times lower than for extracellular Ca2+ [( Ca2+]e). Deregulation may affect any of three Ca2+ buffering systems: the plasma membrane, the mitochondria, and the endoplasmic reticulum. Perturbation of [Ca2+]i is intimately related to perturbation of other ions, including, H+, Na+, and K+. In normal cells, [Ca2+]i elevation is also linked to activation of oncogenes as well as cell division, initiation, wound repair, differentiation, and possibly tumor promotion. In all models of acute injury for which we have measured [Ca2+]i, including ischemia, HgCl2 and calcium inophores, [Ca2+]i always became elevated. This elevation results from influx of [Ca2+]e (ionomycin), redistribution from intracellular stores (NEM, KCN), or from both sources (HgCl2). The degree of [Ca2+]i elevation is correlated with the degree of injury (as determined by blebbing and morphological changes) and cell killing. More recently, much work has been focused on the role of [Ca2+]i in neoplasia. Many stimuli, including the promoter TPA and transforming growth factor beta have been shown to affect normal and transformed cells differently. Both cause differentiation in normal human bronchial epithelial cells but stimulate growth in transformed cells. We propose that deregulation of ions, especially [Ca2+]i, plays an important role, if not a key role, in the initiation of acute and chronic cell injury, including neoplasia. Increases in [Ca2+]i appear to accelerate degradative processes and, unless regulated, lead to cell death.
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PMID:The relationship between cellular ion deregulation and acute and chronic toxicity. 264 22

Unilateral transient cerebral ischemia was produced in Mongolian gerbils by clipping the left common carotid artery for 1 h. About 60% of the gerbils with neurological symptoms had post-ischemic seizures. The majority of those that had seizures died within a few days, and sections of their cerebral cortices contained many dark and shrunken neurons. However, the gerbils that did not have seizures survived without any severe complications. In the cerebral cortex of the latter, the neurons with diffuse or peripheral pallor of the perikarya were seen along with a small number of dark and shrunken neurons. Diffuse pallor occurred within a few hours following ischemia in layers III, V, and VI, and disappeared 1 or 2 days after recirculation. Electron microscopically, these neurons showed dispersion of ribosomes, simple and elongated profiles of rough endoplasmic reticulum (r-ER), clustered vacuoles, and mild to moderate mitochondrial swelling. Occasional net-like tubulomembranous structures, probably derived from r-ER, were observed. On the other hand, peripheral pallor became apparent after 5 days following ischemia, usually involving layer II first and gradually extending to the deeper layers. Concomitantly, the amount of neuropil decreased and the dendrites exhibited tortuosity and irregularity in layer II. Electron microscopically, these neurons showed marked swelling of peripheral perikarya and polyribosomes and organelles were located peripherally to the nuclei. In addition, numerous degenerated axon terminals and distended dendrites were observed around the neurons. These observations indicate that diffuse pallor represents damage directly induced by ischemia and subsequent recirculation, while peripheral pallor is the delayed and remote effect of ischemia, probably due to degeneration of neuronal processes.
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PMID:Morphological studies on cerebral cortical lesions induced by transient ischemia in Mongolian gerbil--diffuse and peripheral pallor of the neuronal perikarya. 273 84

This study has defined the nature and sequence of ultrastructural changes in the organ of Corti following severe, total cochlear ischemia. Afferent nerve endings of IHC became swollen within 15 min and eventually ruptured. Outer hair cells were swollen within 30 min and showed alterations to mitochondria, endoplasmic reticulum and the nucleus whereas IHC remained unchanged for up to 60 min. Both efferent and afferent nerve endings of OHC were unaltered until after 60 min ischemia. Regardless of the type, cells in the base of the cochlea developed abnormalities more rapidly than those in the apical turns. These results imply a differential susceptibility to ischemic damage both among the different cell types and along the organ of Corti.
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PMID:The nature and progression of injury in the organ of Corti during ischemia. 280 49

Hypoglycemia was induced by intracarotid insulin infusions in adult Lewis rats. Electron microscopy of the acoustic cortices in these animals revealed that hypoglycemia provoked marked morphological and morphometric alterations in the pre- and postsynaptic terminals present, as well as in the astrocytic processes seen. The number of the synaptic vesicles in the "active zone" of the synapses was dramatically decreased, with most of the vesicles loosely dispersed in the entire presynaptic profile. Some of the pre- and postsynaptic terminals were enlarged and contained dilated cisternae of smooth endoplasmic reticulum, as well as mitochondria exhibiting a marked internal disorganization. The synaptic clefts in a large number of synapses were dilated and contained fibrillary material. The most striking morphological alterations seen involved a membrane discontinuity of the postsynaptic terminal and was found mostly in the synapses of the superficial layer of the acoustic cortex. Most of the morphological alterations observed in the acoustic cortex following uncomplicated hypoglycemia are seen in sensitive areas of the brain after ischemia or hypoxia.
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PMID:Synaptic alterations in the acoustic cortex of the rat following insulin-induced hypoglycemia. 330 32


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