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Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The dorsal hippocampus of cat was investigated by light microscopy and immunohistochemistry following 1 h global cerebral ischemia and various recirculation times from 1 day to 1 year. Complete ischemia was produced by combining hypotension with intrathoracic occlusion of major arteries. Post-ischemic resuscitation was carried out using an intensive care regimen with continuous neurophysiological monitoring. Brains of controls (n = 4) and post-ischemic animals (n = 12) were fixed in formaldehyde and prepared for histology and immunohistochemistry of glial fibrillary acidic protein (GFAP). In all post-ischemic animals the hilus and the regio superior of dorsal hippocampus which encompasses the CA1 subfield were severely damaged. Neurons in these regions exhibited the typical sequela of neuronal death. GFAP staining revealed vivid astroglial proliferation in stratum lacunosum-moleculare and stratum oriens. Changes in the regio inferior of dorsal hippocampus, i.e., CA3 subfield, and in dentate gyrus granular layer, were variable. Although most animals exhibited moderate to severe neuronal and glial alterations, groups of surviving cells were observed in the stratum oriens and in the granular layer of dentate gyrus. In one animal the majority of CA3 pyramidal cells and granule cells was preserved. These findings demonstrate that after 1 h of complete cerebral ischemia dorsal hippocampus exhibits two different types of injury: a consistent pattern of selective vulnerability in the hilus and the regio superior, and a variable pattern of non-selective injury in the regio inferior and dentate gyrus. The two patterns can be best explained by intrinsic (pathoclitic) and extrinsic (hemodynamic/edema) factors, respectively and are likely to represent basically different mechanisms of ischemic injury.
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PMID:Pattern of neuronal vulnerability in the cat hippocampus after one hour of global cerebral ischemia. 233 96

The data presented are indicative of the general stabilizing action of exogenous formaldehyde on membrane structures and specific retention of macromolecular structures in membrane complexes in the presence of exogenous formaldehyde in acute cerebral ischemia. It is assumed that stabilizing effect of exogenous formaldehyde might be accounted for by its influence on the activity of lipid peroxidation in the brain tissue. High lipid content in the brain tissue resulting from exogenous formaldehyde presence in cerebral ischemia is thought to influence the stabilizing effect on the membrane structures.
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PMID:[Action of exogenous formaldehyde in acute cerebral ischemia at the level of membrane structures]. 335 23

A model is described in which transient complete cerebral ischemia is induced in rats by intracardiac injection of potassium chloride. The animals were intubated and mechanically ventilated with a nitrous oxide/oxygen (70:30) mixture. Cardiac arrest was achieved following a brief period of ventricular fibrillation. After 5-6 min, the circulation was restored by cardiopulmonary resuscitation and partial exchange transfusion. Local CBF (LCBF) during ischemia and cardiac resuscitation was studied by injection of [14C]iodoantipyrine into the right auricle at various periods during cardiac arrest, and was subsequently analyzed by autoradiography. No radioactive tracer could be visualized in any brain structure, demonstrating the absence of CBF during the cardiac standstill. LCBF was also studied at 5 min and 6.5 h after cardiac resuscitation. Five minutes of recirculation showed an increase in blood flow in all brain structures studied, ranging between 130 and 400% of control values. After 6.5 h of recirculation, the CBF was decreased in 13 of 24 brain structures by 20-50%, concomitantly with the depressed rate of glucose utilization found in 15 brain structures. The neocortical, hippocampal, and striatal concentrations of labile phosphates, lactate, pyruvate, phosphocreatine, glucose, and glycogen were measured 5 min after cardiac arrest. Extensive energy failure and elevation of lactate levels were observed and were similar to earlier reported values. One week following recovery from the ischemic insult, the animals were perfusion-fixed with formaldehyde. The brains were embedded in paraffin, subserially sectioned, and stained with cresyl violet/acid fuchsin. Histopathological changes were assessed by light microscopy as the number of acidophilic or pyknotic neurons. Morphological changes were observed in the hilus of the dentate gyrus, the hippocampal CA1 and subicular regions, the dorsal and lateral septum, the olfactory tubercle, the primary olfactory cortex, the entorhinal cortex, the amygdaloid nuclei, and the reticular nucleus of the thalamus. The distribution of the morphological changes suggests a transsynaptic mechanism, causing neuronal necrosis primarily in the limbic brain areas.
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PMID:Ischemic brain damage in rats following cardiac arrest using a long-term recovery model. 403 Sep 19

The density and distribution of brain damage after 2-10 min of cerebral ischemia was studied in the rat. Ischemia was produced by a combination of carotid clamping and hypotension, followed by 1 week recovery. The brains were perfusion-fixed with formaldehyde, embedded in paraffin, subserially sectioned, and stained with acid fuchsin/cresyl violet. The number of necrotic neurons in the cerebral cortex, hippocampus, and caudate nucleus was assessed by direct visual counting. Somewhat unexpectedly, mild brain damage was observed in some animals already after 2 min, and more consistently after 4 min of ischemia. This damage affected CA4 and CA1 pyramids in the hippocampus, and neurons in the subiculum. Necrosis of neocortical cells began to appear after 4 min and CA3 hippocampal damage after 6 min of ischemia, while neurons in the caudoputamen were affected first after 8-10 min. Selective neuronal necrosis of the cerebral cortex worsened into infarction after higher doses of insult. Damage was worst over the superolateral convexity of the hemisphere, in the middle laminae of the cerebral cortex. The caudate nucleus showed geographically demarcated zones of selective neuronal necrosis, damage to neurons in the dorsolateral portion showing an all-or-none pattern. Other structures involved included the amygdaloid, the thalamic reticular nucleus, the septal nuclei, the pars reticularis of the substantia nigra, and the cerebellar vermis.
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PMID:The density and distribution of ischemic brain injury in the rat following 2-10 min of forebrain ischemia. 650 48

The objectives were to study plasma and erythrocyte flow in an area of acute focal cerebral ischemia and define their relationship to developing microcirculatory obstruction as determined by morphological techniques. Eighteen adult cats, anesthetized with ketamine hydrochloride, had right middle cerebral artery (MCA) occlusion. Plasma flow was determined by measuring the transit of Iodine-131 (131I) albumin and erythrocyte flow was determined by measuring the transit of Technetium-99 (99Tc) labeled erythrocytes in the right Sylvian region. Transit studies were performed before and immediately after right MCA occlusion and at the end of the ischemic period, 1 hour, 3 hours, or 6 hours after occlusion. Intra-arterial perfusion with a buffered formaldehyde - colloidal carbon solution was carried out after completion of the isotope studies. Swelling of cerebral tissue and impaired carbon filling in the right MCA territory were seen initially after 3 hours occlusion and were more severe after 6 hours occlusion. Ischemic neuronal alterations, edema formation, and capillary luminal narrowing increased with longer periods of occlusion. 131I albumin transit time in the right Sylvian region was 8 +/- 2 seconds before occlusion and 10 +/- 2 seconds immediately after occlusion. 99Tc erythrocyte transit time was 10 +/- 2 seconds before occlusion and 12 +/- 3 seconds immediately after occlusion. 99Tc erythrocyte transit time was 10 +/- 2 seconds before occlusion and 12 +/- 3 seconds immediately after occlusion. Transit times increased progressively with longer periods of occlusion in cats developing cortical ischemic changes. No evidence of complete microcirculatory obstruction to albumin and erythrocyte transit was seen in cats with 6 hours of occlusion despite the impaired filling of the cortical microcirculation with carbon. There were no findings to substantiate the hypothesis that plasmapheresis develops during the early phases of cerebral infarction.
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PMID:Microcirculatory obstruction in focal cerebral ischemia: albumin and erythrocyte transit. 723 67

A chemical worker working with urea-formaldehyde resin hazard for 20 years suffered cerebral ischemia in association with an increase of blood beta2-glycoprotein I-dependent anticardiolipin antibody (aCL)-IgG and IgM isotype, and a prolongation of activated partial thromboplastin time (aPTT). Major histocompatibility complex antigen showed DR4 positivity. On follow-up for over 6 years, aCL-IgG and aPTT decreased to reference range but aCL-IgM was still abnormally high despite a cessation of exposure. This patient highlights the induction of antibody-mediated thrombosis in chronic chemical exposure, especially in an individual with subclinical autoimmune disorder. The role of environment for coagulopathic vascular thrombosis is warranted for investigation.
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PMID:An increase of anticardiolipin antibody in association with stroke and chronic chemical exposure. 1670 28