Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
 ...
PMID:The ultrastructure of "brain death". II. Electron microscopy of feline cortex after complete ischemia. 41 53

The ultrastructural alterations in the rabbit cerebral and cerebellar cortex resulting from 30 minutes complete, permanent cerebral ischaemia were studied. The ischaemia was induced by raising the intracranial pressure (ICP) above the systolic arterial pressure (compression ischaemia). Immediately after releasing the ICP the brain was fixed by intravascular glutaraldehyde perfusion. Samples from the cerebral and cerebellar cortex were processed for electron microscopy. The ultrastructural changes were relatively minor; there was a generalised, slight intracellular oedema, most prominent in the subpial area; the nuclear chromatin was clumped, the endoplasmic reticulum and cisternae of the golgi apparatus became somewhat dilated, the inner matrix of the slightly swollen mitochondria showed increased electron lucency, and microtubules and ribosomes began to loose their compact structure. These changes, unaccompanied by any extensive volumetric change of any cellular compartment, agree well with the recently presented hypothesis of two different types of anoxic-ischaemic nerve cell injury. This cellular reaction to complete, permanent compression ischaemia represents the type of injury that is seen resulting from ischaemic insults during which no flow of fluid irrigates the ischaemically injured cells.
 ...
PMID:The early ultrastructural alterations in the rabbit cerebral and cerebellar cortex after compression ischaemia. 47 Nov 91

In a light microscopical study, we previously showed that more than 80% of somatostatin (SS) immunoreactive (-i) neurons in the hilus of the dorsal part of the rat dentate gyrus are lost 4 days after ischemia. In order to verify that the loss of SS immunostaining is due to an actual loss of the SS-i neurons and not merely a loss in expression of SS immunoreactivity, we have now performed an ultrastructural study of these neurons before and 40 h after 20 min of global cerebral ischaemia in adult rats. The normal SS-i neurons were multipolar and fusiform in shape. The SS-i product was associated with the endoplasmic reticulum and occasionally the Golgi apparatus. The cell nuclei had indentations of the nucleolemma and contained intranuclear rods. After ischaemia, many SS-i neurons in the dentate hilus showed increased electron density of both the cell nucleus and the cytoplasm. In addition the cytoplasm was heavily vacuolated with the SS-i associated with some of these vacuoles. Other SS-i neurons had, in addition to the vacuoles a more homogeneous, and abnormal electron lucent nucleus and cytoplasm. These ultrastructural changes correspond to previously reported irreversible, ischaemic cell changes of neurons. Based on this we conclude that the SS immunoreactivity in the dentate hilus of the dorsal hippocampus is lost after ischaemia because of neuronal necrosis. As a minor part of this study, we examined whether the ischaemia-susceptible SS-i neurons in dentate hilus had commissural axonal projections. This was done utilizing double fluorescence microscopy of retrograde axonal transport of the fluorescent dye, Fluoro-Gold, and the observation that vulnerable SS-i neurons display homogeneously dispersed immunostaining 40 h after ischaemia. Fluoro-Gold was injected unilaterally into the dorsal dentate gyrus 5 days prior to ischaemia. Then, 40 h after ischaemia, sections were stained for SS immunofluorescence, and examined, in the dentate hilus contralateral to the injection, for neuronal co-localization of both events. Cell counts revealed double-labelling of 13% of all neurons which displayed one of the events. This observation suggests that at least some of the ischaemia-susceptible SS-i neurons in dentate hilus do project commissurally. The pathophysiological significance of ischaemic loss of commissurally projecting SS-i neurons in dentate hilus remains to be determined.
 ...
PMID:Ultrastructure of neurons containing somatostatin in the dentate hilus of the rat hippocampus after cerebral ischaemia, and a note on their commissural connections. 135 89

The effect of RSM on ultrastructural alterations of the cortical, hippocampal and caudate neucleus areas brought about by forebrain ischemia in rats were studied. In both RSM-treated and saline-treated groups the ischemic damage was detected in nearly all animals three hours after bilateral common carotid artery ligation, while it was much more mild in RSM-treated animals. The ultrastructural changes consisted of swollen mitochondria, partial loss of cristae, dilatation of rough endoplasmic reticulum and Golgi's complex. In addition, some dark neurons were present, capillary endothelial cells and processes of astrocytes were swollen and active pinocytosis appeared in the endothelial cells. Their presence was most severe in the hippocampus region and the least in the caudate nuclear area. No ultrastructural changes exhibited in the sham-operated animals. The findings of the present experiment demonstrate that RSM can reduce ultrastructural abnormalities of cerebral ischemia and are also direct evidence of the protective effect of RSM on cerebral ischemia.
 ...
PMID:The effect of radix Salviae miltiorrhizae on the changes of ultrastructure in rat brain after cerebral ischemia. 145 56

Prompt dendritic damage has been observed in the hippocampus of the gerbil brain after transient cerebral ischemia. In the present study, we studied the frontoparietal cortex of the gerbil brain electron microscopically after brief bilateral carotid occlusion to assess the vulnerability of dendritic processes. After ischemia for 5 min, there was swelling of the periphery of dendrites accompanied by swelling of mitochondria, cytoplasmic vacuolation and disintegration of microtubules in layer I, which spread to layer III after ischemia for 20 min. After reperfusion for 3-24 h following ischemia for 20 min, swelling in the periphery of dendrites and of mitochondria inside receded but vacuole formation and disintegration of microtubules propagated proximally. In neuronal perikarya, polyribosomal disaggregation was observed after ischemia for 20 min and persisted thereafter, while fragmentation of rough endoplasmic reticulum (ER) and microvacuolation occurred after reperfusion for 3 h. Electron-dense clumping of neuronal perikarya was observed after reperfusion for 6 h particularly in layers III and Vb, which increased in number for up to 72 h. The observed progressive damage in dendrites may be common to neurons vulnerable to cerebral ischemia and may significantly contribute to development of delayed neuronal death.
 ...
PMID:Electron microscopic investigation of the cerebral cortex after cerebral ischemia and reperfusion in the gerbil. 148 6

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.
 ...
PMID:Morphological studies on cerebral cortical lesions induced by transient ischemia in Mongolian gerbil--diffuse and peripheral pallor of the neuronal perikarya. 273 84

Cerebral ischemia leading to infarction was produced in rats by intravascular thrombosis induced by a photochemical reaction between systemically injected rose bengal and green light (560 nm) transmitted through the intact skull for a 2-min period. At 2 or 15 min following photochemical sensitization, animals were perfusion-fixed for scanning (SEM) and transmission (TEM) electron microscopic analyses of the cerebral vasculature. At 2 minutes, ultrastructural examination of cortical regions destined to undergo infarction revealed numerous platelet aggregates within both pial and intraparenchymal vessels. Platelets close to the endothelial walls were routinely degranulated with pseudopodia. Endothelial cells were frequently swollen and contained dilated mitochondria and granular endoplasmic reticulum. The endothelial luminal membrane structure was shown by high-power TEM to be focally damaged. If brain temperature was reduced by 4 degrees C during the photochemical sensitization period, the platelet response was inhibited without interfering with other ultrastructural changes. These results are consistent with the hypothesis that photochemically induced endothelial alterations stimulate platelet activation and implicate abnormal endothelial function as a primary event in the pathogenesis of photochemically induced cerebral infarction.
 ...
PMID:Photochemically induced cerebral infarction. I. Early microvascular alterations. 357 87

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.
 ...
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.
 ...
PMID:Cerebral ischemia in the gerbil: transmission electron microscopic and immunoelectron microscopic investigation. 379 Sep 87

The results of ultrastructural studies of the nucleus supraopticus (SON) and n. paraventricularis (PVN) of male mongolian gerbils subjected to experimental cerebral ischemia induced by 10 min bilateral occlusion of the common carotids are reported. Marked alterations concerned endocrine neurons, some neurosecretory axons and synaptic terminals as well as astroglia cells. Basing on the electron density of cytoplasmic ground, two varieties of endocrine neurons, that is 'light' and 'intermediate', were designated in both SON and PVN nuclei. These findings suggest that during cerebral ischemia the SON and PVN neurons become activated (Golgi complex and granular endoplasmic reticulum enlargement) and that they represent different phases of secretory cycle of a single cell type. However, in SON nucleus some neurons were probably damaged because they had the appearance of decidedly 'dark' cells. With respect to some neurosecretory axons, the finding of externally lying lamellar whorls indicates ischemic injury of the axons. Similar significance may be attributed to some synaptic terminals which showed an increased polymorphism of synaptic vesicles and vesicular aggregation. There was marked swelling of perivascular astroglia cells and change of their cytoplasm in both SON and PVN nuclei. Moreover, the swollen astroglia cells contacted those 'dark' neurons in SON nucleus. The present study indicates that SON and PVN nuclei are highly sensitive to application of cerebral ischemia. At the same time perivascular injury may suggest involvement of astroglia cells in the production of subsequent changes in the SON and PVN neuropil.
 ...
PMID:The effect of cerebral ischemia on the ultrastructure of the hypothalamo-neurohypophysial system of the mongolian gerbil. The supraoptic and paraventricular nuclei. 666 Nov 13


1 2 3 4 5 6 7 8 9 10 Next >>