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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 30 (1978), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 26 (1976), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: -Eight metabolites were measured in the post-ischemic period following either 1 or 3 h of unilateral ischemia in the gerbil cerebral cortex. The levels of ATP, P-creatine, glucose, glycogen and GABA were essentially restored by 1 h after ischemia. In the 3 h ischemic animals. glycogen continued to increase to greater than control values aftcr 5 and 20 h of recirculation. The Icvels of glutamate were unchanged during the ischemic episode, but decreased to 60% of control at Smin and 1 h after either period of ischemia. The concentrations of cyclic AMP, which were 4-to 5-fold elevated during ischemia. increased an additional 6-fold 5 min after recirculation in both groups. Arter 1 h of recovery. the levels were not different from control values. After the 1 h ischemic period, lactate levels recovered between 5 and 20 h of recirculation. In the 3 h ischemic animals. lactate concentrations were still elevated even after 20 h of recirculation. These data suggest that with the exception of lactate. recovery of metabolites is not sevcrely compromiscd by either 1 or 3 h of ischemia. Furthermore, the changes in glycogen. glutamate and cyclic AMP after recirculation suggest that the recovery process is not just a rcversal of the changes observed during ischemia.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract— Several enzyme activities were determined in gerbil cerebral cortex during unilateral ischemia or in the post-ischemic period following 1 h of ischemia. Adenylate cyclase and Na + -K + -activated ATPase showed essentially the same pattern. Neither enzyme changed during ischemia but the activities decreased on recirculation to 40–60% of right side control by 5 h. The ATPase had returned to control level by 20h; the adenylate cyclase by 7 days of recirculation. Particulate cyclic AMP-dependent protein kinase in the ischemic left hemisphere decreased throughout the 6h of ischemia. It remained depressed in the first 5 h of the post-ischemic period but returned to control by 20 h. The soluble protein kinase activity, the soluble cyclic AMP and cyclic GMP phosphodiesterase and the Mg2+ dependent ATPase did not change significantly during the ischemic or post-ischemic periods. The results suggest that ischemia and/or recirculation may affect cellular membranes and membrane-bound enzymes, in particular. Furthermore, the results imply that despite apparent metabolite recovery during the post-ischemic period, enzymatic changes are occurring that may be important for both the quality of recovery and the response to further ischemic insult.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    BBA - Biochimica et Biophysica Acta 28 (1958), S. 656-657 
    ISSN: 0006-3002
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Medicine , Physics
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Cellular and molecular life sciences 32 (1976), S. 732-734 
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Cortical glycogen levels decreased after both 1 and 3 h of unilateral ischemia. After 1 h of recirculation, the levels of glycogen were restored to control values in both groups. Subsequently, glycogen increased above normal levels after 1 week of recirculation in the 1 h ischemic groups, and after 5 h in the 3 h ischemic group. Thus, the onset of the excess glycogen accumulation appears to be dependent on the intensity of the ischemic insult.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Cellular and molecular life sciences 34 (1978), S. 169-170 
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary The influence of Na pentobarbital anesthesia on the activity of specific and nonspecific cholinesterase was studied in the synaptosomal fraction of Mongolian gerbils' brains. These studies have shown that this barbiturate inhibits the specific activity of acetylcholinesterase only.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 46 (1979), S. 123-131 
    ISSN: 1432-0533
    Keywords: Cerebral ischemia ; Mitochondria ; Lysosomes ; Golgi apparatus ; Histochemistry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The ischemic effect on cerebral enzymes and glycogen content was histochemically evaluated in mongolian, gerbils subjected to unilateral common carotid artery occlusion for various periods of time from 1/2 to 9h. In early stages (up to 2h), the only enzyme affected was the phosphorylase which revealed a decreased activity. Thereafter, the observed changes inclusive of glycogen and other enzymes such as the dehydrogenase, nonspecific acid and alkaline phosphatases, leucine aminopeptidase and thiamine pyrophosphatase progressed proportionally to the duration of ischemia. There was an overall inverse appearance of histochemically demonstrated enzymatic disturbances between the severely damaged ischemic regions and its marginal zones; the former revealing a conspicuous decrease and/or loss of enzymatic activities while the latter showing an increase of the same enzymes. Correlating the various ischemic responses of the intracellular organelles it appears that the changes in the lysosomes and Golgi apparatus occurred slower than those of mitochondria.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-0533
    Keywords: Neuronal activity ; Ischemia ; Hippocampus ; Gerbil
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Spontaneous neuronal activity was recorded in the cerebral cortex and the CA1 sector of the hippocampus in gerbils during and after 5-min ischemia, produced by bilateral clamping of the common carotid arteries. It was found that spontaneous activity in both cortical and CA1 neurons ceased within 60 s after the onset of ischemia and that it began to reappear 10–20 min after the recirculation. During the next 24 h most CA1 neurons which were recorded showed hyperactivity. This was evident primarily by an increase in spike discharges, whereas recordings from the cerebral cortex were within the preocclusion ranges. On the 2nd day after ischemia, functioning CA1 neurons could not be found, as if they were in a state of functional death, although histological sections showed a general preservation of their cellular structure at that time.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-0533
    Keywords: Cerebral ischemia ; Blood-brain barrier ; Cerebral blood flow ; Glucose utilization
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Changes in morphology, behavior of the blood-brain barrier (BBB), regional cerebral blood flow (rCBF), and local cerebral glucose utilization (LCGU) were assessed and correlated in Mongolian gerbils following 5 min cerebral ischemia, produced by bilateral clamping of the common carotid arteries. The morphological changes were confined to the hippocampus and revealed a conspicuously delayed destruction of the CA1 neurons, occurring after 3 days. Following release of carotid occlusions, there were two separate openings of the BBB. One, occurring shortly after recirculation, was associated with focal hyperemia in the cerebral cortex, hippocampus and basal ganglia; the second opening was observed after several days and was associated with severe neuronal destruction in the CA1 sector. Correlation of quantitative and qualitative rCBF assays with14C-deoxyglucose autoradiographic observations indicated an uncoupling between blood flow and glucose metabolism, observed in the hippocampus at 10 min after recirculation. The described changes provide a further insight into the post-ischemic events which determine the outcome of ischemic injury.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1432-0533
    Keywords: Cold-lesion injury ; Brain edema ; Blood-brain barrier ; Alkaline phosphatase ; Anionic sites
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Micro-blood vessels (MBVs), located in the area of edema, were studied in cat brain at various time intervals (1 h, 24 h, 7 days) after cold-lesion injury. Both cold-injured and adjacent gyri were examined for blood-brain barrier (BBB) permeability to i. v. injected horseradish peroxidase (HRP) with circulation times of 40 min and 24 h. Evans blue (EB) was used as a tracer for gross evaluation of the extension of brain edema. Localization of alkaline phosphatase (AP) and binding of cationized ferritin (CF), considered as a marker of anionic sites, were also studied ultrastructurally. Twenty-four hours after cold injury, the extravasated edema fluid, outlined by EB tracer, was observed to be spreading through the white matter (WM) into the adjacent gyrus. At this time, numerous, larger than capillary MBVs, presumably arterioles and venules located in the edematous WM, showed accumulations of HRP injected at the time of the operation, in the basement membrane, in abluminal pits, and in numerous pinocytotic vesicles and vacuoles of endothelial cells (ECs). The animals killed after 24 h with 40 min HRP circulation showed extravasation of HRP tracer in a zone underlying the necrotic cold injury lesion. On the other hand, there was no evidence of an abnormal HRP leakage in the further removed areas of edema in the WM, particularly in the adjacent gyrus. These observations suggest that a reverse, vesicular transport of HRP across the ECs of some MBVs represents one of several possible mechanisms responsible for the removal of extravasated proteins and of edematous fluid from brain extracellular space. This reverse transport is accompanied by a disruption of the surface anionic layer and changed polarity of ECs manifested by the relocation of AP activity from luminal to abluminal plasmalemma.
    Type of Medium: Electronic Resource
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