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

In the present study we investigated the relative vulnerability of neuronal subsets in the striatum to ischemia that was induced by bilateral transient ligation of the common carotid arteries in gerbils. After 4 days of survival, brains were evaluated using histochemical methods (NADPH-diaphorase and silver degeneration procedures) and neurochemical methods with radioimmunoassays for somatostatin-, neuropeptide Y-, and substance P-like immunoreactivity and measurements of amino acids using high-pressure liquid chromatography with electrochemical detection. NADPH-diaphorase-positive neurons were strikingly preserved in the ischemic dorsolateral portion of the striatum, in which there was severe neuronal loss. There was no significant depletion of NADPH-diaphorase-positive neurons in the striatum or cerebral cortex. Concentrations of neuropeptide Y-like and somatostatin-like immunoreactivity were unchanged despite a significant 25% depletion of substance P-like immunoreactivity and gamma-aminobutyric acid. Ischemic brain damage may be mediated by a neurotoxic effect of glutamate acting at the N-methyl-D-aspartate (NMDA) receptor. Previous studies of NMDA excitotoxin lesions in rat striatum have shown a sparing of neurons containing NADPH-diaphorase, somatostatin, and neuropeptide Y. The similar sparing of these neurons following ischemic lesions in gerbil striatum provides further evidence that NMDA receptor activation may play a role in ischemic injury.
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PMID:Selective sparing of NADPH-diaphorase-somatostatin-neuropeptide Y neurons in ischemic gerbil striatum. 197 76

Cellular protein synthesis was investigated in the rat hippocampus 2-100 h following 20 min of cerebral ischemia induced by four-vessel occlusion. [3H]-Phenylalanine was retrogradely infused through the external carotid artery for 30 min. This method limited the distribution of the tracer to one hemisphere and required 1/50th of the tracer amount used for intravenous tracer infusion. Cellular [3H]phenylalanine incorporation was examined in hematoxyline and eosin-stained sections coated with nuclear emulsion. A score for relative protein synthesis was estimated from counts of silver grains across neuron somata with undamaged morphology. Shortly after ischemia a generalized complete arrest of protein synthesis was observed. In CA1 pyramidal cells, this was followed by a transient incomplete regeneration (9-20 h) and later (46-100 h) persistent cessation of protein synthesis. By contrast protein synthesis in interneurons, CA3c pyramidal cells and granule cells recovered to preischemic levels 9-100 h after ischemia, as did the CA3ab pyramidal cells 46-100 h postischemia. Moreover, eosinophilic cell changes were seen in hilar and CA3c neurons at all postischemic stages and in CA1 pyramidal cells 46-72 h after ischemia. [3H]Phenylalanine incorporation was absent in neurons demonstrating eosinophilic cell changes. From the rapid recovery of protein synthesis in hippocampal interneurons, we conclude that changes in interneuronal protein synthesis per se are not involved in the pathophysiology of the delayed ischemic CA1 pyramidal cell death.
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PMID:Temporal profile of interneuron and pyramidal cell protein synthesis in rat hippocampus following cerebral ischemia. 208 91

The present study investigates the effects of the 5-hydroxytryptamine1A agonist ipsapirone on electroencephalography and somatosensory evoked potentials after middle cerebral artery occlusion in the rat. We implanted 17 silver ball electrodes symmetrically distributed over the skull in 14 rats and registered electroencephalography activity and somatosensory evoked potentials before, 1 hour, and 1 week after permanent occlusion of the left middle cerebral artery. Before vessel occlusion, a symmetric distribution of electroencephalography power was seen over both hemispheres. Middle cerebral artery occlusion caused a complete abolishment of electroencephalography power in the frontolateral aspects of the affected hemisphere. When electroencephalographic recordings 7 days after the insult were superimposed with three-dimensional-reconstructed pictures of the infarct, a close correspondence of the extention and spatial orientation was noted. Two negative and two positive peaks were consistently recorded before middle cerebral artery occlusion. In both control and ipsapirone-treated (30 mg/kg i.p. 30 minutes after induction of ischemia) animals, the vessel occlusion caused a severe reduction in amplitudes of somatosensory evoked potentials in all areas under record (p less than 0.05). One week after middle cerebral artery occlusion, amplitudes of somatosensory potentials over the lesioned hemisphere were still significantly (p less than 0.05) lower than preischemic values in the control group. When compared with the corresponding values 1 hour after middle cerebral artery occlusion, an albeit insignificant tendency toward increased amplitudes was observed in most areas under record. By contrast, in ipsapirone-treated animals, significant differences compared with preischemic values were no longer present 1 week after the vessel occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of ipsapirone on spatial and temporal changes in somatosensory evoked potentials after middle cerebral artery occlusion in the rat. 226 Jan 43

We studied eight anesthetized and physiologically monitored adult baboons (Papio cyanocephalus); four were subjected to hemorrhagic hypotension alone and four to hemorrhagic hypotension plus unilateral carotid artery occlusion. Cerebral blood flow was measured using xenon-133, the electroencephalogram was recorded using silver-silver chloride epidural electrodes, and histologic examination was carried out after perfusion-fixation. In the baboons subjected to hypotension alone (mean arterial blood pressure of 28 mm Hg) cerebral blood flow was 28.5 +/- 5.0 ml/100 g/min, whereas in the baboons subjected to hypotension plus unilateral carotid artery occlusion it was 21.8 +/- 1.8 ml/100 g/min at a mean arterial blood pressure of 27 mm Hg. There was no ischemic damage in the former group, but in the latter group there was necrosis in the arterial boundary zones of three baboons and in the distribution of the middle cerebral artery in one. We conclude that, when combined with hypotension, unilateral carotid artery occlusion may lead to hemodynamic ischemia accentuated in the arterial boundary zones of the ipsilateral cerebral hemisphere.
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PMID:Neuropathologic consequences of internal carotid artery occlusion and hemorrhagic hypotension in baboons. 230 67

Silver impregnation performed 1-2 days after transient forebrain ischemia in the Mongolian gerbil demonstrated terminal-like granular deposits in the outer two-thirds of the hippocampal dentate molecular layer (perforant path terminal zone), even though neither the cell bodies of origin of the perforant path nor the dentate granule cells were destroyed. Electron microscopic studies of the dentate gyrus were performed in an effort to discover the identity of these degenerating structures. Electron microscopy revealed that the granular silver deposits corresponded to electron-dense profiles. Many of these were degenerating boutons and some were degenerating postsynaptic dendritic fragments, but most of them could not be identified with certainty. Electron-dense profiles were less numerous than expected from the density of granular silver deposits. These structures were probably the degenerating axons, axon terminals and dendrites of CA4 neurons. The granular silver deposits and electron-dense boutons observed in the inner third of the dentate molecular layer 5 days after transient ischemia can probably be explained by the ischemia-induced degeneration of CA4 mossy cells, which give rise to the dentate associational-commissural projection. Finally, most mossy fiber boutons in area CA4 and some boutons in the molecular layer appeared watery and enlarged on postischemia days 1 and 2. Mossy fiber boutons with this ultrastructural appearance have previously been observed in seizure-prone animals and in animals undergoing convulsant-induced seizures. Although no postischemic seizures occur under the conditions of this study, these findings support the idea that excitatory pathways become hyperactive after transient ischemia.
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PMID:Electron microscopic study of the gerbil dentate gyrus after transient forebrain ischemia. 233 92

In animal models of transients ischemia, selective vulnerability and delayed neuronal death in the hippocampus have been extensively described. However, little is known about selective damage in the neocortex and the thalamus, even though deficits in sensorimotor function are common in humans surviving hypoxic/ischemic episodes. This study investigated the neurodegenerative effects of transient ischemia in the gerbil neocortex and thalamus with use of Cresyl Violet and silver impregnation staining methods. In addition, immunohistochemistry of an astrocyte-associated protein, glial fibrillary acidic protein, was used to assess the astrocytic response to ischemia. Pyramidal cells in layers 3 and 6 of somatosensory and auditory cortex were exceptionally sensitive to ischemia, whereas the neurons in layers 2, 4 and 5 were more resistant to ischemia. More pyramidal cells were killed in layer 3 than in layer 6. This bilaminar pattern of neuronal death developed after periods of ischemia ranging from 3 to 10 min and was identifiable at post-ischemic survival times of 6 h to one month. Somatodendritic argyrophilia in the neocortex was identified as early as 6-12 h after 5 min of ischemia. The greatest number of degenerating cortical neurons were stained two to four days after ischemia. With 10 min of ischemia, argyrophilic neurites and neurons were also found as early as 8 h after the occlusion. The most extensive damage was noted in the ventroposterior nucleus, the medial geniculate nucleus, and the intralaminar nuclei two to four days after ischemia. Thus, selective vulnerability and delayed neuronal death are evident in both the neocortex and the thalamus after transient ischemia. These regions need to be examined when considering the efficacy of potential neuroprotective drugs.
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PMID:Selective neocortical and thalamic cell death in the gerbil after transient ischemia. 238 10

Recent evidence indicates that different forms of stress, including hypoxia, can induce specific proteins called heat-shock or stress proteins in various types of mammalian cells. These studies examined whether myocardial ischemia can result in increased levels of proteins with molecular weight and isoelectric point characteristics similar to those described for heat-shock or stress proteins. The left anterior descending coronary artery of the dog heart was completely occluded; normal and ischemic myocardial samples were obtained 6 hours after occlusion; and total cardiac proteins and RNA were prepared. Ribonucleic acid was translated in vitro in a modified rabbit reticulocyte lysate system, and [35S]-methionine-labelled translational products as well as unlabelled cardiac proteins were separated by two-dimensional gel electrophoresis. Total proteins were visualized by silver staining and in vitro translation products quantified by fluorometry. A translatable mRNA coding for a 71,000 dalton peptide with an isoelectric point of 5.8 was markedly increased in the ischemic myocardium after 6 hours of ischemia. A protein with similar migration characteristics was detected in ischemic myocardium but not in normal myocardium. These results indicate that an mRNA coding for a translational product with similar migration characteristics of heat-shock protein 71 is induced by ischemia in the dog heart.
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PMID:Ischemia of the dog heart induces the appearance of a cardiac mRNA coding for a protein with migration characteristics similar to heat-shock/stress protein 71. 242 3

An important feature of ischemic brain damage is the exceptional vulnerability of specific neuronal populations and the relative resistance of others. Silver impregnation was used to delineate the extent and time-course of neuronal degeneration produced by 5 min of complete forebrain ischemia in the Mongolian gerbil. Lesions were confined to four brain regions: (1) hippocampal areas CA1, CA2-CA3a and CA4; (2) the dorsomedial portion of the lateral septal nucleus; (3) the dorsolateral portion of the striatum; and (4) the somatosensory neocortex. The ischemic lesion evolved with time in all four regions, but at different rates. Somatic argyrophilia developed rapidly in the striatum and hippocampal area CA4 (maximal in 24 h or less), at intermediate rates in the somatosensory neocortex, hippocampal areas CA1a and CA2-CA3a and the lateral septal nucleus (maximal in 2 days), and slowly in hippocampal area CA1b (maximal in 3 days). These results emphasize that the extent and rate of neuronal degeneration can vary even within a presumably homogeneous neuronal population, as evidenced by the different results in areas CA1a and CA1b. Similar results were obtained from analysis of brain sections stained with Cresyl Violet, hematoxylin-eosin or hematoxylin-eosin/Luxol Fast Blue. Terminal-like silver granules were observed in the projection fields of degenerated neurons. They also appeared, however, in the perforant path terminal zone of the hippocampal dentate molecular layer 1-2 days after transient ischemia and in stratum oriens and stratum radiatum of area CA1b prior to somatic degeneration. These granular deposits could not be clearly related to the degeneration of neuronal somata. Novel findings of this study include the degeneration of some dentate basket cells and lateral septal neurons and the appearance of terminal-like argyrophilia in the hippocampal formation without any obvious relation to somatic degeneration. Some of our results lend support to the hypothesis that ischemic neuronal cell death constitutes an excitotoxic process. Other results, however, suggest that the selective vulnerability of neurons to transient ischemia must involve factors beyond excitotoxicity.
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PMID:Selective neuronal death after transient forebrain ischemia in the Mongolian gerbil: a silver impregnation study. 246 45

To clarify a possible cause of delayed neuronal death, synthesis of protein and ribonucleic acid (RNA) following transient forebrain ischemia was evaluated autoradiographically. Mongolian gerbils were subjected to transient forebrain ischemia for 5 minutes by occluding bilateral common carotid arteries. They were used for autoradiographic study at 1, 2, and 5 days after ischemia. Tracer dose of 14C-valine or 14C-uridine was injected intravenously, and animals were sacrificed 45 minutes thereafter. Brains were frozen and thin sliced for macroautoradiography. After the first autoradiogram was obtained, tissue sections were incubated in cold 5% trichloroacetic acid for 1 hour, dried and again used for autoradiogram. With this preparation we could differentiate the tracer incorporated into protein or RNA fraction from the total tissue radioactivity. In the different set of animals, microautoradiograms of 3H-valine and 3H-uridine was obtained to detect subcellular distribution of synthesized protein or RNA. At 1 day after ischemia, protein synthesis in the CA 1 region of the hippocampus was reduced by 57% of the sham control, but RNA synthesis was not reduced quantitatively. Microautoradiogram of 3H-uridine however, indicated that silver grains in the cytoplasms of the CA 1 pyramidal cells were much reduced as compared to sham controls, though the amount of silver grains in the nucleus was the same as sham controls. Therefore, synthesized RNA in the nucleus was not transported to the cytoplasm. At 2 days after ischemia, protein and RNA synthesis was preserved to the same level as sham controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Malfunction of gene expression as a possible cause of delayed neuronal death]. 246 13

We studied functional disturbances following left middle cerebral artery occlusion in rats. Neuronal function was evaluated by [14C]2-deoxyglucose autoradiography 1 day after occlusion. We analyzed the mechanisms of change in glucose utilization outside the infarct using Fink-Heimer silver impregnation, axonal transport of wheat germ agglutinin-conjugated-horseradish peroxidase, and succinate dehydrogenase histochemistry. One day after occlusion, glucose utilization was remarkably reduced in the areas surrounding the infarct. There were many silver grains indicating degeneration of the synaptic terminals in the cortical areas surrounding the infarct and the ipsilateral cingulate cortex. Moreover, in the left thalamus where the left middle cerebral artery supplied no blood, glucose utilization significantly decreased compared with sham-operated rats. In the left thalamus, massive silver staining of degenerated synaptic terminals and decreases in succinate dehydrogenase activity were observed 4 and 5 days after occlusion. The absence of succinate dehydrogenase staining may reflect early changes in retrograde degeneration of thalamic neurons after ischemic injury of the thalamocortical pathway. Terminal degeneration even affected areas remote from the infarct: there were silver grains in the contralateral hemisphere transcallosally connected to the infarct and in the ipsilateral substantia nigra. Axonal transport study showed disruption of the corticospinal tract by subcortical ischemia; the transcallosal pathways in the cortex surrounding the infarct were preserved. The relation between neural function and the neuronal network in the area surrounding the focal cerebral infarct is discussed with regard to ischemic penumbra and diaschisis.
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PMID:Neuronal network disturbance after focal ischemia in rats. 247 23


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