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

Transient cerebral ischemia in rats was produced by permanent occlusion of the vertebral arteries and 30-minute occlusion of the common carotid arteries. This model produces ischemic necrosis of neurons in the corpus striatum, cerebral cortex, and hippocampus; infarcts, with necrosis of neuropil, astrocytes, and blood vessels, are rare. Changes in striatal astrocytes at 40 minutes and 3 hours of reperfusion were evaluated by electron microscopy, and quantitative estimates of increases in cytoplasmic and mitochondrial area were performed. In areas of corpus striatum with moderate ischemic cell change, the percentage of astrocytic nuclei increased from 10.79% in controls to 17.76% at 40 minutes after ischemia (p less than 0.01) and 19.86% at 3 hours (p less than 0.01). Astrocytic cytoplasm was expanded and contained increased numbers of mitochondria, many of which were pleomorphic and had dilated intracristal spaces and condensed matrix. Rough endoplasmic reticulum was increased. Total mitochondrial area and number of mitochondrial profiles rose significantly in the astrocytic perikarya and foot processes at 3 hours postischemia. The greater number of astrocytes, the increases in mitochondria and rough endoplasmic reticulum and the configurational changes in the mitochondria suggest increased metabolic activity of astrocytes in postischemic, noninfarcted brain.
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PMID:Early proliferative changes in astrocytes in postischemic noninfarcted rat brain. 710 27

Forty-minute lobular ischemia of the rat liver produces no considerable changes in the activity of the enzymes of the hydroxylation system of the hepatocyte endoplasmic reticulum. After resumption of circulation in the microsomes of ischemized and intact lobes of the liver the activity of hydroxylases appreciably decreases, reaching the minimum level by the 72nd hour of the postischemic period. During this time lipid peroxidation increases.
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PMID:[Enzyme activity of microsomal oxidation in ischemic and intact lobes of the rat liver after resumption of the liver blood circulation]. 712 87

Status epilepticus was induced in rats by the GABA receptor blocking agent, bicuculline, during artificial ventilation and with closely monitored physiologic parameters. After 1 or 2 h of status epilepticus the brains were fixed by perfusion with glutaraldehyde and processed for light and electron microscopy. In the cerebral cortex two different types of changes were present, i.e., nerve cell injuries and status spongiosus. Type 1 injured neurons, mainly in the areas of most marked sponginess (layer 3), displayed progressive condensation of both karyo-and cytoplasm. In the most advanced stages the nucleus could no longer be distinguished from the cytoplasm in the light microscope, and vacuoles of apparent Golgi cisterna origin appeared in the darkly stained cytoplasm. This type of injured neurons comprised 41 and 56% of the cortical neurons after 1 or 2 h of status epilepticus, respectively. Seven to 9% of the neurons showed another type of injury (type 2). They were mainly located in the deeper cortical layers, and showed slit-formed cytoplasmic vacuoles chiefly due to swelling of the endoplasmic reticulum including the nuclear envelope. Marked sponginess of the cortex developed principally in layer 3 and it spread into deeper layers with longer duration of status epilepticus, but the outermost layers retained a compact structure. As judged by electron microscopy, the sponginess resulted mainly from swelling of astrocytes and their processes causing both perivascular and perineuronal vacuolation. The structural changes observed are considered to be caused by astrocytic and to a lesser extent intraneuronal edema related to the seizure activity. Although the exact pathogenetic mechanisms are not known, our findings indicate that hypoxia-ischemia is not a major determinant of the tissue damage observed.
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PMID:Pathogenesis of brain lesions caused by experimental epilepsy. Light- and electron-microscopic changes in the rat cerebral cortex following bicuculline-induced status epilepticus. 725 31

The results of the study have shown that the changes occurring in ischemia are reversible. These changes are: perivascular edema of the astrocytes, dilation of the pericaryon and the cisterns of the endoplasmic reticulum, various forms of chromatolysis, and some changes of the capillary endothelium. An increase of the number of direct contacts between the basal membrane of the capillaries and the astrocytes, oligodendrocytes, neurons and their axons was observed. Complexes characterized by direct contact of all the constituents of the neuron-glia-capillary system were encountered. Such complexes were most typical for the median layers of the cortex. The types of the neuroglia-capillary interrelations described can be regarded as evidences of increased activity of the transport through the hematoencephalic barrier after post-ischemic restoration of the circulation. The direct contacts between the neurons. The glia, and the capillaries point to a possibility of direct exchange between the microcirculatory system and the neurons during the post-ischemic restoration of the circulation.
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PMID:[Effect of post-ischemic restoration of blood flow on neuron-glia-capillary interrelations]. 729 7

During short-term (3.7 and 15 min) circulatory hypoxia (ischemia) pronounced ultrastructural changes, having an obvious focal character, were observed in the rabbit cerebral cortex. In some regions, the extracellular space was widened; in the neurons, changes are seen both in the nucleus (appearance of polymorphic vacuoles and deep invaginations of nuclear envelope, aggregation of chromatin) and cytoplasmic organelles (mitochondrial swelling, swelling of profiles of endoplasmic reticulum, dislocation of ribosomes). Most striking reactions were observable in synapses - the number of synaptic vesicles was sharply reduced, its location in the axon terminal changed, the dense material associated with pre- and postsynaptic membranes was enlarged, mitochondria were swollen. The degree of the above alterations was proportional to the duration of ischemia.
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PMID:[Ultrastruct characteristics of neurons and synapses in the central cortex during circulatory hypoxia]. 738 56

The influence of prolonged postischemic hyperventilation was studied in the model of global brain ischemia produced by 15 min cardiac arrest in dogs with 8 h recirculation. Histopathological examination of neuronal damage using silver impregnation showed the presence of numerous heavy argyrophylic neurons in the striatum and CA2 hippocampal subfield after 8 h of normoxic reperfusion. In dogs with prolonged 8 h postischemic hyperventilation a reduction in the occurrence of argyrophylic neurons in the striatum and their significant decrease in the hippocampal area were found. Electron microscopic study was performed to characterize the effect of respiratory alkalosis on the ultrastructural changes in neurons and correlate them with the results of silver impregnation. Ultrastructural analysis after the cardiac arrest without recirculation did not reveal the presence of dark neurons within the striatal and hippocampal areas. Neuronal alterations included a decrease in endoplasmic reticulum, mitochondrial swelling and a mild chromatin clumping. After 8 h of normoxic reperfusion many dark, shrinked neurons containing perinuclear clusters of clear vesicles were found. In hyperventilated animals the occurrence of dark neurons with extensive perineuronal edema was substantially reduced in the CA2 subfield. The effect of hyperventilation on postischemic calcium overload is discussed.
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PMID:Effect of prolonged hyperventilation on ischemic injury of neurons after global brain ischemia in the dog. 756 Sep 2

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

To evaluate the pathogenesis of lipid peroxidation in skin-flap necrosis and to select a novel herbal antioxidant to suppress lipid peroxidation and salvage the flaps, in vitro and in vivo experiments were instituted. In vitro studies revealed (1) the potentiality of the cutaneous microsomal system (vesicular fragment of endoplasmic reticulum) to generate oxyradicals by FeCl3 (oxidative agent), since NADPH-dependent lipid peroxidation was elevated time-dependently, (2) suppression of microsomal lipid peroxidation by herbal antioxidants (dose- and time-dependently), further supporting the theory of oxyradical-induced lipid peroxidation in the skin, and (3) that ellagic acid showed the strongest response, with curcumin, chlorogenic acid, and alpha-tocopherol (tocopherol) being moderate, and ferulic acid and gallic acid remaining weakest. Thus ellagic acid, curcumin, chlorogenic acid, and tocopherol at doses of 10, 60, 80 and 100 microM (twice I50, the dose which could inhibit lipid peroxidation by 50 percent) were chosen for in vivo assessments, respectively. In vivo studies were performed using rat back skin random flaps (70 x 15 mm and based anteriorly) and circular island flaps (20 mm in diameter and raised on superficial epigastric vessels). Control flaps were painted with a Tris-ethanol solution, and test flaps were painted with either ellagic acid, curcumin, chlorogenic acid, or tocopherol (above-mentioned doses per 250 microliters of Tris-ethanol per 300 mm2 of flap surface 1 hour before the operation and once a day for 3 postoperative days). Doses, frequency, and period of drug application were based on in vitro and in vivo pilot experiments. The results were as follows: (1) a direct and time-dependent relation was noticed between lipid peroxide levels and the rate of necrosis in both types of flap; (2) time-dependent elevation of lipid peroxide levels of skin, subcutaneous fat, and exudate of island flaps during ischemia and those of skin and subdermal fat after reperfusion indicated pre- and post-reflow states of lipid peroxidation rather than the original conception of merely reperfusion state; and (3) in good agreement with the results of in vitro experiments, ellagic acid exerted the strongest effect to suppress lipid peroxide levels of skin and to augment the viability of random flaps more than that of island flaps.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Involvement of lipid peroxidation in necrosis of skin flaps and its suppression by ellagic acid. 797 56

The effects of selenium on experimental ischemia, anoxia and ischemia plus anoxia myocardial injuries of hearts in organ culture in vitro were studied. The survival and spontaneous beating of cultured hearts with experimental ischemia, anoxia and ischemia plus anoxia were prolonged by selenium. The lanthanum probe technique and ACPase technique demonstrated that the permeability function of cell membrane, mitochondria membrane, lysosome membrane and Golgi membrane could be protected by selenium. The transition electron microscopy showed that selenium may to some extent maintain membrane system integrity of cultured hearts with experimental ischemia, anoxia and ischemia plus anoxia and postpone the occurrence of irreversible injuries. The obvious difference in amount of intracellular ribosome, polyribosome and short rough surfaced endoplasmic reticulum indicated that selenium may play an important role in synthesis of protein and promoting cell repair.
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PMID:[Effects of selenium on experimental ischemic myocardial injuries of heart in organ culture]. 812 11

Morphological changes in the neurons of the gerbil hippocampus following 5 min of forebrain ischemia were examined using light and electron microscopy. Although non-pyramidal neurons in the CA1 region of the hippocampus survived through the full length of the observation period, up to six weeks after ischemia, they consistently demonstrated degenerative changes distinct from those of the well-known "delayed neuronal death" of CA1 pyramidal cells. When examined with the light microscope, CA1 non-pyramidal neurons were found to be shrunken and their nuclei and cytoplasm were hyperchromatic between seven days and six weeks after ischemia. When examined with the electron microscope, postischemic non-pyramidal neurons were found to have markedly electron-dense profiles; their cytoplasm contained numerous free ribosomes and heterogeneous smaller granular substances, the latter also filling the nuclei. However, there was no loss of ribosomes from the rough endoplasmic reticulum, and mitochondrial cristae were preserved, suggesting that these neurons were viable. CA1 non-pyramidal neurons were studied immunohistochemically using three types of monoclonal antibodies, one each against parvalbumin, a nonphosphorylated epitope on the 168,000 mol. wt and 200,000 mol. wt subunits of neurofilament proteins, and microtubule-associated protein 2. CA1 non-pyramidal neurons lost immunoreactivity to these neuron-specific substances six weeks after ischemia, suggesting that these degenerating cells lacked certain types of normal neuronal activity. We conclude that non-pyramidal neurons in the hippocampal CA1 region survive transient ischemia but undergo degenerative changes following complete loss of CA1 pyramidal cells. These changes may be due to depletion of presumptive target-derived trophic factors within the non-pyramidal neurons.
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PMID:Persistent degenerative state of non-pyramidal neurons in the CA1 region of the gerbil hippocampus following transient forebrain ischemia. 846 9


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