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  • 1
    Electronic Resource
    Electronic Resource
    Changes in the bioenergetic state of rat hippocampus during 2.5 min of ischemia, and prevention of cell damage by cyclosporin A in hyperglycemic subjects (1997)
    Springer
    Experimental brain research 114 (1997), S. 44-50 
    Details
    ISSN: 1432-1106
    Keywords: Key words Forebrain ischemia ; Hyperglycemia ; Hippocampus ; Bioenergetic state ; Cyclosporin A ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  A recent study from this laboratory has shown that brief transient ischemia (2 min 30 s) in normo- and hyperglycemic rats leads to moderate neuronal necrosis in CA1 cells of the hippocampus, of equal density in the two groups. However, hyperglycemic animals failed to depolarize during the ischemia, nor did they show a decrease in extracellular calcium concentration. The present study was undertaken to study the metabolic correlates to these unexpected findings. Normoglycemic (plasma glucose ∼6 mM) and hyperglycemic (∼20 mM) rats were subjected to ischemic periods of 1 min and 2 min 15 s (2 min 30 s with freezing delay considered), and their brains were frozen in situ. Samples of dorsal hippocampus were dissected at –22°C and extracted for the measurement of phosphocreatine (PCr), creatine, ATP, ADP, AMP, glucose, glycogen, and lactate. Normoglycemic animals showed rapid depletion of PCr, ATP, glucose, and glycogen, and a rise in lactate content to 10–12 mM·kg–1 during the ischemia. Hyperglycemic animals displayed a more moderate rate of fall of PCr and ATP, with ATP values exceeding 50% of control after 2 min 30 s. Glycogen stores were largely maintained, but degradation of glucose somewhat enhanced the lactic acidosis. The results demonstrate that hyperglycemic rats maintained ATP at levels sufficient to prevent cell depolarization and calcium influx during the ischemic period. However, the metabolic perturbation observed must have been responsible for the delayed neuronal damage. We speculate that lowered ATP, increased inorganic P, and oxidative stress triggered a delayed mitochondrial permeability transition (MPT), which led to delayed neuronal necrosis. This assumption was supported by a second series of experiments in which CA1 damage in hyperglycemic rats was prevented by cyclosporin A, a virtually specific inhibitor of the MPT.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00005622
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  • 2
    Electronic Resource
    Electronic Resource
    Calcium metabolism of focal and penumbral tissues in rats subjected to transient middle cerebral artery occlusion (1998)
    Springer
    Experimental brain research 120 (1998), S. 503-509 
    Details
    ISSN: 1432-1106
    Keywords: Key words Extracellular calcium concentration ; Total tissue calcium content ; Middle cerebral artery occlusion ; Reperfusion ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The present experiments were undertaken to define changes in tissue calcium metabolism in focal and perifocal (“penumbral”) tissues following 2 h of transient middle cerebral artery occlusion (MCAO) in rats, induced with an intraluminal filament occlusion technique. The extracellular calcium concentration ([Ca2+]e) was measured with ion-selective microelectrodes in neocortical focus and penumbra. For measurement of total tissue calcium content, tissue samples from these areas were collected and analyzed with atomic absorption spectrometry. During MCAO, [Ca2+]e in a neocortical focal area fell from a normal value of about 1.2 mM to values around 0.1 mM, suggesting translocation of virtually all extracellular calcium to intracellular fluids. Recirculation was accompanied by re-extrusion of calcium within 5–7 min; however, [Ca2+]e never returned to normal but stabilized at about 50% of the control value for the first 6 h, and decreased further after 24 h. In penumbral areas, [Ca2+]e showed the expected transient decreases associated with spreading depression-like (or ischemic) depolarization waves. Recirculation was followed by return of [Ca2+]e towards normal values. In the focus, water content increased from about 79% to about 80.4% at the end of the 2-h period of ischemia. After 2 h and 4 h of recirculation, the edema was aggravated (mean values 81.9% and 81.2%, respectively). After 6 h and 24 h, the edema was more pronounced (83.6% and 83.8%, respectively). In the penumbra, no significant edema was observed until 6 h and 24 h of recirculation. The total tissue calcium content in the focus (expressed by unit dry weight) increased at the end of the ischemia period demonstrating calcium translocation from blood to tissue. After 6 h and 24 h, the content increased two- to threefold, compared with control. Changes in the penumbra were qualitatively similar but less pronounced, and a significant increase was not observed until after 6 h of recirculation. The results suggest that 2 h of MCAO leads to a profound perturbation of cell calcium metabolism. In focal areas, cells fail to extrude the calcium that is gradually accumulated during reperfusion and show massive calcium overload after the first 4–6 h of recirculation. Penumbral tissues show a similar increase in calcium concentration after 6 h of recirculation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002210050424
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  • 3
    Electronic Resource
    Electronic Resource
    Current concepts on reperfusion injury following focal cerebral ischemia (1999)
    Springer
    Intensivmedizin und Notfallmedizin 36 (1999), S. 260-269 
    Details
    ISSN: 1435-1420
    Keywords: Schlüsselwörter Zerebralischämie ; Reperfusionsschädigung ; Mitochondria ; Key words Cerebral ischemia ; Reperfusion injury ; Mitochondria
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Reperfusion injury has become a scientific problem of increasing importance, in part because of recent developments of thrombolytic therapy. The mechanisms of reperfusion injury following focal cerebral ischemia, however, are not known in detail. Recent studies strongly suggest that reactive oxygen species (ROS) and calcium overload play an important role in reperfusion injury and that pharmacological interventions against calcium- or free radical-mediated damage could extend the therapeutic window in cerebral ischemia/reperfusion. The mediators involved are known to induce a mitochondrial permeability transition (PT) during the reperfusion period, which is associated with uncoupling of mitochondrial respiration, loss of mitochondrial membrane potential, and a burst production of ROS, leading to cellular death. The mitochondrial PT is considered to be a key process in reperfusion injury following cerebral ischemia, as also observed in other organs such as heart and liver. Pharmacological modulation of mitochondrial permeability changes have the potential to reduce tissue damage due to reperfusion.
    Notes: Zusammenfassung Die Reperfusionsschädigung ist ein an Wichtigkeit zunehmendes wissenschaftliches Problem, z. T. wegen der neueren Entwicklungen in der thrombolytischen Therapie. Die Mechanismen der Reperfusionsschädigung nach fokaler Zerebralischämie sind jedoch in Detail unbekannt. Neuere Studien deuten stark darauf hin, daß reaktive Sauerstoffspezien (ROS) und Kalziumüberladung eine wichtige Rolle bei der Reperfusionsschädigung spielen, und daß pharmakologische Interventionen gegen eine von Kalzium- oder freien Radikalen vermittelte Schädigung die therapeutische Breite bei der Zerebralischämie/ Reperfusion erweitern könnte. Es ist von den entsprechenden Vermittlern bekannt, daß sie eine mitochondriale Permeabilitätstransition (PT) während der Reperfusionszeit induzieren, und eine explosionsartige Produktion von ROS, welche zum Zelltod führt. Der mitochondrialen PT wird eine Schlüsselrolle bei der Reperfusionsschädigung nach Zerebralischämie zugeschrieben, wie auch in anderen Organen z. B. Herz und Leber beobachtet. Eine pharmakologische Modulation der Veränderung der mitochondrialen Permeabilität hat das Potential, reperfusionsbedingte Gewebeschädigung zu reduzieren.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s003900050237
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  • 4
    Electronic Resource
    Electronic Resource
    Effect of transient focal ischemia on blood-brain barrier permeability in the rat: correlation to cell injury (1997)
    Springer
    Acta neuropathologica 94 (1997), S. 158-163 
    Details
    ISSN: 1432-0533
    Keywords: Key words Brain ; Focal ischemia ; Reperfusion ; Albumin extravasation ; Blood-brain barrier
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Prolonged ischemia is known to damage the blood-brain barrier, causing an increase in vascular permeability to proteins. We studied the time course of extravasation of endogenous albumin in rats after 1 and 2 h of middle cerebral artery (MCA) occlusion followed by 6, 12, and 24 h of recirculation. In a separate group of rats that had undergone 1 h of MCA occlusion and 6 h of recirculation, influx of [14C]aminoisobutyric acid (AIB) from blood to brain was also measured. After 1 h of occlusion followed by 6 h of recirculation, neuronal damage was evident in caudoputamen, but there were no signs of blood-brain barrier leakage to either AIB or albumin. At 12 h, the caudoputamen contained extravasated albumin, and at 24 h extravasation was extended to the somatosensory cortex. Animals subjected to 2 h of MCA occlusion showed albumin extravasation in caudoputamen already at 6 h of recirculation, and at 12 and 24 h albumin was abundant in the major part of the right hemisphere. This study suggests that damage to neurons precedes leakage of the blood-brain barrier. Even a relatively short period of ischemia such as 1 h will result in markedly increased vascular permeability. However, a longer transient ischemic insult disrupts the blood-brain barrier earlier than a shorter one.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010050688
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