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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 633 (1991), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 0891-5849
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 0014-5793
    Keywords: Atmospheric spectrum (a.t.B.) ; C6-glioma cell ; Correlation
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-0533
    Keywords: Brain ischemia ; Demyelination ; Hyperoxia ; Lipid peroxidation ; Myelin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Carotid arteries were occluded bilaterally for 15 min in two groups of Mongolian gerbils. The first group received 100% oxygen during the first 3 h of reperfusion. During that period, room air was given to the second group. After 3 h, both groups received room air. Brains of gerbils that died within 14 days after occlusion were removed, fixed in formalin and embedded in paraffin. Gerbils that survived 15–28 days were perfused with formalin before their brains were removed and embedded in paraffin. Adjacent, serially cut sections were stained with luxol fast blue (LFB)-H&E, cresyl violet, according to the Bodian method, or immunocytochemically with antisera raised against myelin basic protein (MBP) and glial fibrillary acidic protein (GFAP). In brain sections of gerbils receiving 3 h of 100% oxygen, there were circumscribed white matter lesions in the corpus striatum, lateral thalamus, mesencephalon and posterior limb of the internal capsule. Myelin sheaths were swollen, fragmented and were less intensely stained by MBP antiserum. MBP and LFB-stained myelin fragments were present extracellularly and in macrophages. Many axons in these areas appeared undamaged. Previously described ischemic changes were found in gray matter and some areas of white matter in both groups. However, neurons in the deeper laminae of the cerebral cortex appeared to be better preserved in gerbils given oxygen. The results suggest that hyperoxia, if present immediately after transient brain ischemia, may damage myelin more severely than other cellular elements.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Der Anaesthesist 46 (1997), S. S61 
    ISSN: 1432-055X
    Keywords: Schlüsselwörter Ketamin ; S-(+)-Ketamin ; NMDA- Antagonisten ; Glutamat ; Ischämie ; globale zerebrale ; Neuroprotektion ; Key words Ketamine ; S-(+)-Ketamine ; NMDA- antagonists ; Glutamate ; Ischaemia ; global cerebral ; Neuroprotection ; Review
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Abstract This review focuses on the significance of S-(+)-ketamine as a neuroprotective agent. Evidence in the literature supporting or contradicting a neuroprotective or even therapeutic role of ketamine in global cerebral ischaemia is critically reviewed, and data from an ongoing study in a rat global cerebral ischaemia model (15 min ischaemia with S(+)-ketamine administered 15 min after reperfusion) are reported. The number of experimental studies available so far limited, however, and therefore results cannot be considered conclusive at the present time. Only at higher ketamine dosages was protection found reliably, especially in models of complete forebrain ischaemia lasting over 10 min. In our own study, only after 90 mg/kg S(+)-ketamine was there significantly better preservation of cortical neurons than without treatment; 30 and 60 mg/kg did not produce this effect.
    Notes: Zusammenfassung Dieser Überblick konzentriert sich auf die Wirksamkeit von Ketamin und, spezieller, von S-(+)-Ketamin als Neuroprotektivum bei globaler zerebraler Ischämie. Indizien aus der Literatur, die für oder gegen einen neuroprotektiven oder gar therapeutischen Einsatz von Ketamin bei globaler zerebraler Ischämie sprechen, werden kritisch analysiert. Leider sind zitierbare Arbeiten zum Thema immer noch in zu geringer Zahl verfügbar, um ein ausgewogenes Urteil zu ermöglichen. Zusätzlich werden Ergebnisse einer eigenen Studie referiert, bei der S-(+)-Ketamin 15 min nach Einleitung der Reperfusion verabreicht wurde. Leider ist die Zahl relevanter Veröffentlichungen zum Thema immer noch begrenzt. Die Ergebnisse sind vor allem wegen der geringen Anzahl nicht eindeutig: Nur bei höherer Dosierung von Ketamin scheint es regelmäßig zu protektiven oder therapeutischen Effekten zu kommen, speziell bei zerebraler Ischämie von mehr als 10 min Dauer. In der eigenen Untersuchung fand sich nur bei 90 mg/kg S-(+)-Ketamin i.p. eine Protektion kortikaler Neurone 6 Tage nach einer 15minütigen Ischämie. Bei 30 oder 60 mg/kg blieb dieser Effekt aus.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 74 (1987), S. 329-334 
    ISSN: 1432-0533
    Keywords: Cerebromicrovascular endothelium ; Arachidonic acid ; Indomethacin ; Dexamethasone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Permeability of cerebromicrovascular endothelium has been investigated in a new model of cultured cells. The endothelial cells are grown on dextran microcarriers and constitute a barrier for trypan blue (TB) binding to the dextran beads. Changes in the permeability of microcarrier-cultured endothelium have been investigated during the exposure of cells to arachidonic acid or substances involved either in arachidonate metabolism or stimulation of cAMP. The results demonstrate enhanced TB passage through the endothelial barrier during exposure to high concentrations of arachidonic acid and indomethacin, but not to ibuprofen. The effect of indomethacin could be prevented by pretreatment with dexamethasone. Dexamethasone alone did not influence the barrier. Forskolin, a drug which stimulates the catalytic unit of adenylate cyclase, did not affect the endothelial permeability to TB. These findings support the contention that substances derived from a disturbed cellular membrane contribute to the altered blood-brain barrier function found under pathological conditions.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 0942-0940
    Keywords: Leucocytes ; ischaemia ; rat ; selective vulnerability ; quantitative histology
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Leucocytes play an important role in inflammation and immunologic responses. They might be of special significance under pathophysiological conditions of the brain i.e. ischaemia or stroke. It has been shown that neutropenic animals undergoing reversible ischaemia show higher post-ischaemic blood flow, suggesting improved post-ischaemic perfusion. In this study it was investigated therefore, whether polymorphonuclear leucocytes contribute to the nerve cell loss in the hippocampus after a reversible period of ischaemia. Rats were made neutropenic with a specific anti-serum against rat polymorphonuclear leucocytes yielding leucocyte counts less than 10% of normal. The animals were then subjected to 15 min reversible forebrain ischaemia. Quantitative histology was performed after a survival period of 7 days. Nerve cell counts in the frontal cortex and in the CA1 and CA3 sectors of the hippocampus did not reveal any differences between neutropenic rats and animals with normal leucocyte counts. From the results it might be concluded that neutrophils do not significantly contribute to the selective post-ischaemic nerve cell damage in the rat.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Metabolic brain disease 3 (1988), S. 247-255 
    ISSN: 1573-7365
    Keywords: forebrain ischemia ; hippocampus ; mortality ; gerbil ; hematocrit ; osmolarity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Mongolian gerbils were exposed to 15 min of cerebral ischemia. Quantitative histology was used to establish neuronal damage in the CA1, CA2/3, and CA3 sectors of the hippocampus 2 weeks after the insult. Seven moribund animals were sacrificed earlier to examine whether there is a correlation between hippocampal damage and mortality. Surviving animals had a 86.6% loss of CA1 neurons. In the CA2/3 and CA3 sectors 62.7 and 72.6% of the neurons were preserved. Moribund animals had a further dramatic loss of nerve cells in these sectors, to 14.8 and 20.3%, respectively. The reduction of CA2/3 neurons and survival time were correlated. In addition, gerbils which would later become moribund were found to have a significant increase in plasma osmolarity from 319 to 342 mosm/liter and of hematocrit from 47.4 to 53.9 at day 4 after ischemia.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1435-2451
    Keywords: Mesenteric vascular occlusion ; Leucocyte accumulation ; Tonometry ; Reperfusion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Der Epithelschaden und die Leukozytenakkumulation in der Wand des Ileums nach Ischämie und Reperfusion wurden experimentell am Schwein untersucht. Die A. mesenterica superior wurde für 1 h (Gruppe 2; n=9), 2 h (Gruppe 3; n=6) und 3 h (Gruppe 4; n=7) abgeklemmt und 2 h reperfundiert. Die histologische Beurteilung erfolgte an Hämatoxylin-Eosin- und NaphtolAS-D-Chlorazetatesterase-gefärbten Präparaten. Es entwickelte sich ein Reperfusionsschock in Abhängigkeit von der Ischämiedauer. Nach lstündiger Ischämie stabilisierte sich der Blutdruck mit erniedrigten Werten sowie einer Normalisierung des Serumlaktatspiegels und des intramuralen pHi des Dünndarms. Eine Verlängerung der Ischämie auf 2 h (Gruppe 3) führte zu einem Blutdruckabfall (54–69 mmHg), einem bleibend erhöhten Serumlaktatspiegel (5,2–6,0 mmol/1) und einem verzögerten Anstieg des pHi. Die Reperfusion nach 3stündiger Ischämie verursachte einen irreversiblen Schock. Der Epithelschaden des Dünndarms war abhängig von der Ischämiedauer. Es fand sich, kein Unterschied der Leukozytenakkumulation innerhalb der Submukosa im Vergleich zur Kontrollgruppe. Ein signifikanter Anstieg der Leukozytenzahl war jedoch in der Lamina interna und externa der Muskularis nach lstündiger Ischämie zu verzeichnen (106±5/mm2 bzw. 280/mm2; p〈0,05), der nach 2stündiger [92±5/mm2 (p〈0,05) bzw. 189±4/mm2 und 3stündiger Ischämiedauer (84±5/mm2 bzw. 185±23/mm2) nur geringgradig erhöht war. Während die intestinale Ischämie und der anschließende reperfusionsbedingte Schock nicht zu einer Beeinflussung der Leukozytenakkumulation innerhalb der Submukosa, aber zu einer signifikanten Akkumulation innerhalb der Muskularis nach einer lstündigen Ischämie führten, scheint bei ausbleibender Normalisierung des Serumlaktatspiegels und einem verzögerten oder fehlenden Anstieg der ischämischen intramuralen pHi-Werte als Hinweis auf eine intestinale Perfusionsstörung als Folge einer längeren Ischeämiedauer die Akkumulation der Leukozyten innerhalb der Muscularis mucosae abgescwächt zu sein.
    Notes: Abstract The epithelial damage and the accumulation of the leucocytes within intestinal wall layers after ischemia and reperfusion was investigated in a pig model. Superior mesenteric artery (SMA) was occluded for 1 h (group 2, n = 9), 2 h (group 3, n = 6) and 3 h (group 4, n = 7) with a consecutive 2 h reperfusion period. The histological evaluation was performed on hematoxylin-eosine and Naphtol AS-D chloracetate stained preparations. The intensity of reperfusion shock depended on the duration of the intestinal ischemia. After 1 h SMA occlusion systolic blood pressure stabilized at a lower level with a normalization of the serum lactate level and the intestinal intramural pHi within the reperfusion period. After 2 h SMA occlusion the decrease of the systolic blood pressure was intensified (54–69 mm Hg) with a persistent elevated serum lactate concentration and a delayed increase of the ischemic pHi values. Reperfusion after 3 h SMA occlusion caused an irreversible shock. The epithelial damage also depended on the duration of the SMA occlusion. There were no significant changes of the leucocytic accumulation within the submucosa. But a significant increase of the number of the leucocytes was seen within the inner and the outer layer of the muscularis after 1 h SMA occlusion (106±5/mm2 resp. 280/mm2; p〈0.05). This increase was less pronounced after 2 h (92±5/mm2 *resp. 189±4/mm2; *p〈0.05) and 3 h of SMA occlusion (84±5/mm2 resp. 185±23/mm2). Intestinal ischemia and reperfusion caused no changes of the leucocytic accumulation within the submucosa but a significantly increased accumulation within the muscularis after 1 h SMA occlusion, which was not seen after a more elongated occlusion period. A reperfusion shock without normalization of the serum lactate level and the intramural pHi suggesting intestinal perfusion disturbances may also lead to a depression of the leucocytic accumulation within the muscularis.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    New York, NY [u.a.] : Wiley-Blackwell
    Journal of Cellular Physiology 123 (1985), S. 51-54 
    ISSN: 0021-9541
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Regulation of cell volume as a fundamental cellular function of high biological priority was studied in cultured cerebrovascular endothelium. The use of a multiparameter flow cytometric system allowed simultaneous measurements of cell volume, viability, and membrane potential or intracellular pH. Endothelium, the cellular constituent of the blood-brain barrier (BBB), swells immediately on exposure to low osmolality. This is associated with membrane depolarization and a fall of intracellular pH. Within 30-60 min, cell volume and membrane potential recover completely, although the extracellular osmolality is kept low. Intracellular pH does not normalize fully. Measurements of intracellular K+ and Na+ concentrations reveal their involvement in the regulatory process. The findings strongly suggest that the cerebrovascular endothelium has a highly effective built-in capacity for homeostatic control essential for normal BBB function.
    Additional Material: 1 Ill.
    Type of Medium: Electronic Resource
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