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

Cerebral infarction was produced in rats by a combination of transient unilateral common carotid artery occlusion and systemic hypoxia. Horseradish peroxidase (HRP) and Evans blue were given 5 minutes prior to sacrifice to assess the integrity of the blood-brain barrier (BBB) at 1 minute, 30 minutes, and 2 hours following the ischemic insult. There was immediate permeability to HRP in the early (1 minute and 30 minutes) post-ischemic period, whereas, Evans blue was not seen until the late (1.5 to 2 hours) post-ischemic period. Ultrastructural examination showed two routes of barrier permeability to HRP. In the early post-ischemic period, HRP was transported by pinocytosis through endothelial cells in areas of brain containing ischemic neurons. In the late post-ischemic period, HRP diffusely leaked into the brain through the necrotic walls of vessels in areas of infarction. In contrast to previous reports, these results show that the BBB becomes permeable immediately following hypoxia-ischemia. In addition, this study shows that BBB permeability to HRP during cerebral ischemia occurs through two mechanisms: an active, energy-requiring permeability through enhanced pinocytosis within endothelial cells and a passive leakage of protein tracers through necrotic vessel walls.
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PMID:Early and late mechanisms of increased vascular permeability following experimental cerebral infarction. 43 63

The aim of this paper has been to review and discuss the past and the recent investigations concerned with the study of cerebral transport phenomena in pathological conditions which have been divided into two main parts: (1) the effects of experimentally induced blood brain barrier (BBB) injury by (a) HgCl2 or (b) hyper-osmolar intracarotic perfusate; and (2) the effects of ischemia or of an altered oxygen saturation and pCO2 tension on glucose and/or amino acids and/or protein transport across the BBB, in the syanptosomes and cerebral capillaries. The most important observations were as follows: (1) HgCl2 or hyperosmolar perfusates produced an increased BBB permeability to protein tracers but the brain uptake of glucose analogues was found decreased following the former, and increased (except for lactamide) after the latter treatment. (2) (a) In ischemia, the noted increased vesicular transport of peroxidase, as well as the increased saturable and non-saturable passage of glucose analogues across the BBB depended on the duration of cerebral deprivation of blood supply which never resulted in degeneration of endothelial cells of the brain vessels. (b) The progressively decreased specific 2-deoxy-D-glucose uptake in the synaptosomes seen during cerebral ischemia of 30-180 minutes returned to the level of controls 1 hour after reestablishment of cerebral circulation. (c) A decrease in brain uptake of glucose analogues and amino acids (with few exceptions) was observed in severe hypoxia and hypercapnia while an increase or no change in the brain uptakes was seen in hypocapnia. (d) Preliminary investigations of the 2-DG uptake by the cerebral capillaries obtained by fractionation of the brain from animals subjected to normal or altered oxygen saturation and pCO2 tension suggested that cerebral glucose uptake may be directly related to its capillary function.
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PMID:Pathological aspects of brain transport phenomena. 78 95

Cerebral ischemia was induced by occlusion of the left common carotic artery in adult Mongolian gerbils. The period of occlusion was 3, 6, or 18 h. Horseradish peroxidase (HRP) was intravenously injected in animals with clear neurological signs 1 h release of the clip. The HRP was allowed to circulate for 5 min. Fixation was carried out by perfusion with aldehydes. Tissue, incubated for peroxidatic activity, from the left side of the brain was treated for electron microscopy. During the postischemic period enhanced permeability was demonstrated in the brains of all animals. The amount of HRP transferred into the neuropil depended on the duration of ischemia. Thus the gerbils with 18 h occlusion showed the greatest content. The cells comprising the neuropil adjacent to vessels were studied and the degree of the pathological changes described below was increased proportionally to the time period of occlusion. The intercellular spaces, often filled with peroxidase, were expanded and the astrocytes swollen, especially the endfeet. Sometimes the astrocytes were pervious to HRP. The neurons were also swollen, but to a lesser degree than the astrocytes. No endothelial cell damage was observed. Even 18 h of occlusion did not change the plasma membranes. The intercellular spaces were free of HRP from the first luminal to the first abluminal tight junction. The cytoplasm exhibited HRP-containing vesicles of various types and shapes. Some were freely situated; others were connected to the plasma membrane and then open to the vessel lumen or to the basement membrane. Since no cell damage was demonstrated, and since no HRP was diffusely dispersed in the cytoplasm it is assumed that vesicles are responsible for the enhancement of the vesicular transport that normally occurs after intravenous injection of HRP.
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PMID:Increased permeability of cerebral vessels to horseradish peroxidase induced by ischemia in Mongolian Gerbils. 96 82

Superoxide production was measured as the superoxide dismutase (SOD)-inhibitable portion of nitro blue tetrazolium (NBT) reduction after cerebral ischemia-reperfusion in anesthetized cats equipped with cranial windows. Significant superoxide production was found in the early reperfusion period and continued for more than 1 h after ischemia. Superoxide was not detected in control animals not subjected to ischemia, during ischemia, and at 120 min of reperfusion. After ischemia, the vasoconstrictor response to arterial hypocapnia was reduced. This effect was prevented by pretreatment with SOD plus catalase or by deferoxamine. The response to topical acetylcholine was converted to vasoconstriction after ischemia. The normal vasodilator response reappeared spontaneously at 120 min of reperfusion. The vasodilator response to acetylcholine was preserved in animals pretreated with SOD plus catalase. Blood-brain barrier permeability to labeled albumin and horseradish peroxidase was increased after ischemia. These effects were minimized by pretreatment with SOD and catalase. We conclude that superoxide generation occurs during reperfusion after cerebral ischemia for a fairly long period and that superoxide and its derivatives are responsible at least in part for the vasodilation and the abnormal reactivity as well as for the increase in blood-brain barrier permeability to macromolecules seen after ischemia. Furthermore, the findings suggest that the agent responsible for the vascular abnormalities is hydroxyl radical generated via the iron-catalyzed Haber-Weiss reaction.
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PMID:Oxygen radicals in cerebral ischemia. 133 9

As brain capillaries do various works necessary for maintaining the homeostasis of neurons, their disruptions may play an important role in the establishment of ischemic brain damage. It is also said that brain capillaries response to ischemia more functionally than structurally and their microstructural features remain unchanged for a long time of ischemia. Therefore, a new method is expected to be introduced that can evaluate the ischemic changes of endothelial cells on a histological level more sensitively than conventional histological methods. In the present study we investigated immunohistochemical reactivity of factor VIII related antigen (F VIII RAg), a specific and representative marker of vascular endothelial cells, in normal and ischemic brains. In the experiment, cerebral ischemia was induced by occlusion of the unilateral common carotid artery in adult mongolian gerbils. The periods of occlusion were 1, 2, 3, 6, 12, and 24 hours, in five animals respectively. After occlusion each brain was obtained by decapitation and quickly frozen at -80 degrees C and 5-6 micron sections were cut in a cryostat at -20 degrees C and dried at 37 degrees C. The staining for F VIII RAg was done by the peroxidase-antiperoxidase method using specific antiserum to human F VIII RAg. In normal gerbil's brains, the positive staining for F VIII RAg was observed in endothelial cells of arteries, veins and capillaries. In major vessels the staining was intense, but neurons and glia were not stained.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Brain ischemia and endothelial cell damage--immunohistochemical study using factor VIII related antigen as a marker]. 245 25

Experimental cerebral ischaemia was produced by microembolization in rats. HRP (horseradish peroxidase) was then injected into the cerebral cortex and the extracellular fluid dynamics were observed. In the control group, there was a basic pattern in the migration of the tracer. In the ischaemic group, a 'dense tracer distribution around the focus' was found in addition to the basic pattern. This phenomenon could be observed from the second day after the ischaemic insults. The perivascular DAB reaction was marked, particularly around the focus. There was a vesicular uptake of the tracer in the vascular endothelium. This phenomenon appeared almost simultaneously with the active resolution of the oedema fluid. In addition, frequent mitotic figures were seen around the focus. It was thus possible to hypothesize that the 'dense tracer distribution around the focus' appeared at the site of active tissue reaction and had a close relationship with oedema resolution.
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PMID:Dynamics of ischaemic brain oedema fluid: 'dense tracer distribution around the focus', evaluated by peroxidase injection in the rat cortex. 256 82

Although cerebral infarction is a destructive process of nerve cells and brain tissue, the nature is not exclusively disintegrating but also includes active cellular reaction which may modify the progression of tissue damage. Most prominent cellular reaction in the area surrounding infarction can be recognized as a trophic or proliferative change of glial cells. In the present study we produced a focal cerebral ischemia in Mongolian gerbils and investigated the dynamic change of astrocytes in the brain adjacent to thalamic infarction. Using immunohistochemical methods, astrocytes were identified with the antibody to astroprotein (GFAP) and the DNA synthesizing (S phase) cells were detected with the antibody to bromodeoxyuridine (BrdU). The posterior communicating artery of a gerbil was occluded by coagulation through the trans-tympanic bulla approach under general anesthesia with ketamine hydrochloride (80 mg/kg, i.p.). Thirty min after intravenous administration of BrdU (200 mg/kg), animals were sacrificed by transcardiac perfusion with 75% ethanol on days 1, 2, 3, 5 and 7 post-infarction. Ethanol-fixed, paraffin-embedded blocks were cut coronally into 6 microns-thick sections at the level of dorsal hippocampus. Double-labeled immunohistochemical technique (avidin biotin peroxidase-complex method) was carried out with each antibody using 3,3'-diaminobenzidine tetrahydrochloride and 4-chloro-1-naphthol as chromogens. The population of GFAP-positive cells and their S-phase fraction (the number of BrdU-positive nuclei divided by the number of GFAP-positive cells expressed in per cent, %) were examined. The data demonstrated that the regional GFAP-positive cells increased continuously between days 1 to 5 (105.9 to 528.8 cells/mm2) postinfarction (44.6 cells/mm2 in normal brain).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Astrocytic proliferation in the brain adjacent to infarcted lesion: immunohistochemical study of astroprotein (GFAP) and bromodeoxyuridine (BrdU)]. 276

Light and electron microscopy and quantitative estimates of pinocytotic activity in cerebral arterioles and capillaries were performed in two different rat models of altered blood-brain barrier permeability in order to determine the side of initially increased vesicular transport. Seizures were produced by 20 consecutive electroshocks, and ischemic neuronal damage was produced by a 30-minute period of combined right common carotid artery occlusion and systemic hypoxia. Horseradish peroxidase was used to evaluate blood-brain barrier permeability. Serial 1micronm.sections showed an ateriole within most foci of horseradish peroxidase extravasation. There were areas of brain in both experimental groups in which the only permeable vessels were arterioles, and in one ischemic animal, the only permeable vessels were arterioles. Pinocytotic activity was determined in capillaries and arterioles and expressed as the number of horseradish peroxidase-containing pinocytotic vesicles per square millimeter of endothelial cytoplasmic area +/- standard error. The pinocytotic activity in capillaries and arterioles, respectively, was 12.2 +/- 5.4 and 6.7 +/- 3.0 in normal rats, 86.7 +/- 22.1 and 267 +/- 46.1 after seizures, and 52.7 +/- 10.6 and 91.2 +/- 33.2 following cerebral ischemia. These results indicate the importance of the arterioles in maintaining and altering the blood-brain barrier and suggest that abnormal blood-brain barrier permeability occurs first within the arteriole.
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PMID:The importance of cerebral arterioles in alterations of the blood-brain barrier. 740 36

We report on a 3 year old girl with acute promyelocytic leukemia (APL) with cerebral infarction due to disseminated intravascular coagulation (DIC) at initial presentation. She was hospitalized because of unconsciousness and petechiae on the chest wall and extremities. Cerebral ischemia and infarction were found on computed tomography scan and magnetic resonance imaging. Peripheral blood content was hemoglobin 7.3 g/dL, white blood cells 1.0 x 10(3) cells/microL (31% blasts) and platelet count was 12 x 10(3) cells/microL. Fragmented erythrocytes were frequently observed on May-Giemsa stained blood smears. Bone marrow aspirates showed normal cellularity, with 60.4% blasts, containing faggot cells. The blasts were positive for peroxidase. Therapy was begun; however, the patient died 1 week after admission.
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PMID:Cerebral infarction in acute promyelocytic leukemia at initial presentation. 877 58

Hypothermia protects the brain and other vital organs during periods of ischaemia. We differentiate between mild (36-34 degrees C), moderate (33-29 degrees C), deep (28-17 degrees C) and profund (16-4 degrees C) hypothermia. During hypothermia, cerebral metabolic rate and cerebral blood flow decrease dependent on temperature. The relation between temperature and cerebral metabolism is expressed by the temperature coeffizient Q10, which is the ratio between two metabolic rates separated by 10 degrees C. The following factors contribute to decreases in cerebral blood flow seen during hypothermia: cerebral metabolic depression, decreases in cardiac output, and decreases in arterial blood pressure with pH-stat management, increases in hematocrit and in blood viscosity. Mild or moderate hypothermia reduces histopathological damage and neurological deficits if started before and during cerebral ischaemia. Hypothermia may also improve neurologic outcome if initiated following focal cerebral ischaemia, but is less effective after global ischaemic insults. Mild hypothermia appears to be safer and more effective compared to moderate hypothermia. In most instances, deep hypothermia renders neurologic outcome worse, which is most likely related to the generation of toxic metabolites and inadequate myocardial function during rewarming. The neuroprotective effects of hypothermia are related to several mechanisms along the ischaemic cascade: prevention of postischaemic hypoperfusion, reduction of functional and basal metabolism, decreased accumulation of lactic acid and oedema formation, inhibition of excitatory neurotransmitter release, prevention of Ca(++)- and Na(+)-influx, inhibition of lipid peroxidase activity, and free radical formation, stimulation of regenerative immediate early genes. The side effects of hypothermia include myocardial ischaemia, cardiac arrhythmias, decreased left ventricular contractility, coagulation abnormalities, and suppression of metabolic and immunological processes.
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PMID:[Mild and moderate hypothermia as a new therapy concept in treatment of cerebral ischemia and craniocerebral trauma. Pathophysiologic principles]. 928 20


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