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)

Unilateral degenerative atrophy of the optic nerve (ON) occurred in 6 of 80 male and 4 of 80 female Slc: Wistar rats. Two of these cases completely lost the intracranial portion of the unilateral ON and the remainder had the small ON. The optic disc and ON were located histologically in the posterior pole of the eyeball of 2 rats with no intracranial ON. ON lesions in all cases were characterized by a reduced number of axons with a small number of myelinated axons and marked astrogliosis. There were also swelling, fragmentation and spheroid formation of axons, as well as thickening of the connective tissue sheaths and vessel walls in the ON. One side of the optic chiasma and optic tract contralateral to the affected ON reduced in volume, became degenerated and were accompanied by gliosis. Focal or diffuse degeneration of the retina was observed in the eyeballs with affected ON. Retinal ganglion cells decreased in the number showing chromatolysis. These retinae became thin and developed degeneration of both inner and outer portions with sclerotic changes in the retinal vessels. The ophthalmic and ciliary arteries in the eyeballs with affected ON often developed proliferative or occlusive endoarteritis, suggesting that retinal lesions may have resulted not only from axonal degeneration in the ON but also from ischemia. Histologic lesions suggestive of transneuronal degeneration were found in the contralateral lateral geniculate body and rostral colliculus. Based on the data presented, it was presumed that a primary lesion may have been induced in the ON by a circulatory disturbance and followed by retrograde and anterograde degenerations in the visual pathways.
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PMID:Unilateral atrophy of the optic nerve associated with retrograde and anterograde degenerations in the visual pathways in Slc: Wistar rats. 750 41

Previous studies in gerbils have shown that cytoskeletal disruption and a loss of the dendritic microtubule-associated protein, MAP2, may occur after short periods of transient global ischemia. tau, a predominantly axonal microtubule-associated protein, has not been examined following ischemia. We compared neuronal damage with alterations in MAP2, tau, and 72-kD heat shock protein (HSP72) immunostaining at various reperfusion times following 20 min of ischemia in the rat four-vessel occlusion model. tau accumulated in neuronal cell bodies throughout the hippocampal formation 30 min to 2 h after the ischemic insult. Perikaryal tau immunostaining was transient in most regions, but persisted in polymorphic hilar neurons. This was accompanied by a loss of immunostaining in the target of many hilar neurons, the inner molecular layer of the dentate gyrus. The same neuronal populations that exhibited increased tau immunostaining of perikarya later displayed an induction of HSP72 immunoreactivity. In contrast, loss of MAP2 immunostaining was not consistently observed before neuronal death and did not correspond to HSP72 induction. The altered tau immunostaining is not the direct result of excitotoxic insult, as intrahippocampal injection of kainic acid did not cause the somal accumulation of tau, but did cause disruption of MAP2 immunostaining. Taken together, the results suggest that the somal accumulation of tau is an early, sensitive, and selective marker of ischemic insult.
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PMID:Alterations in tau immunostaining in the rat hippocampus following transient cerebral ischemia. 751 35

We describe 2 patients in whom juvenile dermatomyositis (DM) was associated with well defined clinical polyneuropathies, and review the clinical and serological data. Light and electron microscopy were used to study muscle and nerve tissues from one patient. Neuropathy in our patients was associated with ulcerative skin lesions and elevated serum levels of factor VIII related antigen. Light microscopic studies of muscle revealed perifascicular atrophy and microinfarcts consistent with juvenile DM. Light microscopy of the affected sural nerve showed axonal degeneration. Electron microscopy of the same nerve demonstrated capillary endothelial inclusions characteristic of those observed as manifestations of early endothelial injury in juvenile DM muscle tissue. Polyneuropathy in patients with juvenile DM is a rare complication and is likely due to ischemia secondary to endothelial damage.
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PMID:Polyneuropathy in juvenile dermatomyositis. 897 68

We present a patient with a clinical picture of multiple mononeuropathy in which muscle and sural nerve biopsy revealed the existence of vasculitis compatible with panarteritis nodosa. Along with classical axonal lesion signs, we observed multifocal conduction blocks (CB) in all the nerves explored electrophysiologically. Topographic evolution was atypical in that distal BC disappeared earlier, whereas proximal BC appeared later and in all cases persisted longer. Ischemia may play a pathogenic role in BC along with other more well-known factors such as compression and immunological processes. BC detection would probably be less exceptional if, when ischemic neuropathy is suspected, patients were subjected to early and follow-up electrophysiological exploration that included proximal nerve segments.
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PMID:[Ischemic neuropathy with conduction blocks]. 757 30

This paper describes early morphological changes following the placement of four loose ligatures round the rat sciatic nerve, a method used to produce altered pain-related behaviour. The ligatures were tied so as not to constrict the nerve, but there was compression of some epineurial blood vessels. This mild lesion caused behavioural changes and nerve fiber abnormalities within 8.5 h. The distribution of nerve fiber changes was patchy, and initially due to stagnant ischemia, with necrosis of Schwann cells and evidence of axonal stasis. By 48 h, endoneurial oedema increased leading to a compressive lesion and eventually to severe nerve fiber degeneration.
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PMID:A morphological study of experimental mononeuropathy in the rat: early ischemic changes. 770 73

Intracellular localization of amyloid protein precursor (APP) in the normal and postischemic gerbil brain was examined by immunoelectron microscopy. In the normal brain, APP immunoreactivity was localized to the multivesicular body, the nuclear membrane, Golgi apparatus and rough endoplasmic reticulum. After ischemia for 5 min and reperfusion for 24 h, some neurons became intensely immunoreactive for APP in the subiculum and CA3 region of the hippocampus and layers III and V/VI of the cerebral cortex. No intense labeling occurred in glial cells. Intensely labeled neurons were characterized by eccentric nuclei and accumulation of cellular organelles in the center of the neuronal perikarya, as well as a strongly immunoreactive nuclear membrane and cisternal structures, which were presumed to be dispersed Golgi apparatus and/or fragmented rough ER. APP immunoreactivity in the multivesicular body suggests re-internalization of APP and its degradation in the endosomal-lysosomal pathway. The ultrastructural features of neurons with intense APP immunoreactivity suggested mild neuronal damage, similar to those found in central chromatolysis. This indicates that accumulation of APP in these neurons is caused by disturbance of axonal transport, although the information does not allow us to exclude the possibility of an increase in APP production.
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PMID:Ultrastructural localization of amyloid protein precursor in the normal and postischemic gerbil brain. 774 41

Post traumatic ischemia appears to be largely involved for the extension of lesions in acute injury of the spinal cord. The present study evaluate the putative improvement of spinal cord blood flow (S.C.B.F.) by calcium channel blocker after acute spinal cord injury in baboons. S.C.B.F. measured by a scannographic technique with 133Xe were realised each thirty min for 4 hours and seven days later; somatosensory evoked potentials (S.E.P.) magnetic resonance imaging (M.R.I.) and histological study of the spine were realised at different time of the experimentation. Ten monkey were used. Acute trauma was achieved by compression of the cord at T1 by applying a 2.10(2) kPa (2 bar) pressure for 5 s with a balloon catheter inflated with Ringer's solution. Then, five monkeys received saline infusion for seven days and the other five received a nimodipine infusion (0.04 mg.kg-1.h-1) during the same time. Nimodipine improved significantly S.C.B.F. Two monkeys in the treated group showed improvement of axonal function as judged by S.E.P. Conversely no significant difference was noted by R.M.I. although the histological study showed smaller lesions in the treated group. Nimodipine could represent in the next years a new medical treatment in acute spinal cord injury in man.
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PMID:[Medical treatment of spinal cord injury during the acute phase. Effect of a calcium inhibitor]. 780 54

Hyperbaric oxygenation is effective in augmenting the delivery of oxygen to tissue, but also causes oxidative stress. As part of our focus on improving peripheral nerve salvage from ischemic fiber degeneration, we evaluated whether hyperbaric oxygenation rescues peripheral nerve, rendered ischemic by microembolization, from ischemic fiber degeneration. The supplying arteries of rat sciatic nerve were embolized with microspheres of 14 microns diameter at moderate (2 x 10(6)) and high (5.6 x 10(6)) doses. Rats were randomized to receive hyperbaric oxygenation treatment (2.5 atm 100% oxygen for 2 hours/day for 7 days beginning within 30 minutes of ischemia), or room air. End points for the embolized limb were (1) behavioral scores (0-11 in increasing levels of limb function), (2) nerve action potential of sciatic-tibial nerve, (3) nerve blood flow, and (4) histological grade as percentage of fibers undergoing ischemic fiber degeneration (0 = < 5%; 1 = 5-25%; 2 = 26-50%; 3 = 51-75%; 4 = > 76%). Nerve blood flow and nerve action potential were uniformly absent and more than 90% of fibers had degenerated in both control and treatment groups receiving high doses. Control and treatment groups receiving moderate doses were well matched by level of ischemia (8.5 +/- 0.3 [N = 18] vs 7.7 +/- 0.4 ml/100 gm/min [N = 18], p > 0.05) but were significantly different by behavior score (5.6 +/- 0.7 vs 9.2 +/- 0.5 [N = 19], p < 0.001), nerve action potential (1.4 +/- 1.0 vs 3.9 +/- 0.5 [N = 6], p < 0.05), and histology (2.4 +/- 0.4 [N = 5] vs 0.8 +/- 0.5 [N = 4], p < 0.05). On single teased fiber evaluation, the predominant abnormality was E (axonal degeneration). We conclude that hyperbaric oxygenation will effectively rescue fibers from ischemic fiber degeneration, providing the ischemia is not extreme.
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PMID:Experimental ischemic neuropathy: salvage with hyperbaric oxygenation. 781 63

Our purpose was to use whole brain echo planar magnetic resonance imaging (MRI) to identify and characterize diffusion abnormalities in acute cerebral ischemia. We studied 40 patients as early as 3 hours after onset of signs and symptoms of cerebral ischemia. Diffusion-weighted imaging (DWI) of the entire brain could be completed in 3 seconds or, using seven different diffusion sensitivities (maximum b = 1,271 sec/mm2), in 48 seconds. Measurements and synthetic maps were made of apparent diffusion coefficients (ADC), a physiological parameter that characterizes the self-diffusion of water in tissue. Early ischemic lesions were identified with DWI as hyperintense regions of decreased ADC in all patients who subsequently developed infarction, before changes were evident on conventional MRI in cases studied earlier than 6 hours after onset of ischemic symptoms. Lesions as small as 4 mm in diameter were identified. The extent of lesions within white matter was best defined by controlling for the anisotropic effect of axonal orientation. The mean ADC (+/- SD) for control regions in the 36 patients was 9.15 (+/- 2.91) x 10(-4) mm2/sec. Mean ADC of ischemic regions was 56% of control values at 6 hours or less and stayed significantly reduced for 3 to 4 days after onset of ischemia. The relative ADC increased progressively over time to be pseudonormalized at 5 to 10 days and elevated in the chronic state, making the distinction of acute lesions adjacent to chronic infarcts readily apparent. DWI with echo planar imaging measures a unique physiological parameter that is sensitive to ischemic changes before conventional MRI. Its potential role in the quantitative study of human stroke pathophysiology and therapeutics is the subject of further investigation.
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PMID:Acute human stroke studied by whole brain echo planar diffusion-weighted magnetic resonance imaging. 784 64

The neonatal cat model of kaolin-induced hydrocephalus is associated with progressive and severe ventriculomegaly. In this experiment we studied the evolution of the histopathological changes in hydrocephalic (n = 23) cats from 5-168 days after the induction of hydrocephalus along with age-matched controls (n = 10). In the periventricular white matter, extracellular edema and axonal damage were present within days of the onset of hydrocephalus. This was followed by reactive gliosis, white matter atrophy, and in some animals gross cavitation of the white matter. Even in the chronic, apparently compensated state there was ongoing glial cell death. Six cats were shunted an average of 23.6 +/- 6.5 days after the induction of hydrocephalus because they were no longer able to feed independently. In spite of clinical improvement the white matter changes persisted. Overt cortical changes were minimal except where areas of white matter destruction encroached upon the deep layers. The white matter changes are very similar to those seen in periventricular leukomalacia and suggest that ischemia plays a role in neonatal brain injury caused by hydrocephalus.
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PMID:Acute and chronic cerebral white matter damage in neonatal hydrocephalus. 787 13


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