caa a22 4500 465767109 CHVBK 20180323111917.0 cr unu---uuuuu 170327e19900101xx s 000 0 eng 10.1007/BF00308722 doi (NATIONALLICENCE)springer-10.1007/BF00308722 Pattern of neuronal vulnerability in the cat hippocampus after one hour of global cerebral ischemia [Elektronische Daten] [R. Schmidt-Kastner, B. Grosse Ophoff, K. Hossmann] Summary: 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. Postischemic resuscitation was carried out using an intensive care regimen with continuous neurophysiological monitoring. Brains of controls (n=4) and postischemic 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. Springer-Verlag, 1990 Ischemia nationallicence Cat nationallicence Selective vulnerability nationallicence Immunohistochemistry nationallicence Glial fibrillary acidic protein (GFAP) nationallicence Schmidt-Kastner R. Abteilung für experimentelle Neurologie, Max-Planck-Institut für neurologische Forschung, Osthierheimer Straβe 200, D-5000, Koln 91, Federal Republic of Germany aut Grosse Ophoff B. Abteilung für experimentelle Neurologie, Max-Planck-Institut für neurologische Forschung, Osthierheimer Straβe 200, D-5000, Koln 91, Federal Republic of Germany aut Hossmann K. Abteilung für experimentelle Neurologie, Max-Planck-Institut für neurologische Forschung, Osthierheimer Straβe 200, D-5000, Koln 91, Federal Republic of Germany aut Acta Neuropathologica Springer-Verlag 79/4(1990-01-01), 444-455 0001-6322 79:4<444 1990 79 401 https://doi.org/10.1007/BF00308722 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF00308722 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Schmidt-Kastner R. Abteilung für experimentelle Neurologie, Max-Planck-Institut für neurologische Forschung, Osthierheimer Straβe 200, D-5000, Koln 91, Federal Republic of Germany aut NATIONALLICENCE 700 1- Grosse Ophoff B. Abteilung für experimentelle Neurologie, Max-Planck-Institut für neurologische Forschung, Osthierheimer Straβe 200, D-5000, Koln 91, Federal Republic of Germany aut NATIONALLICENCE 700 1- Hossmann K. Abteilung für experimentelle Neurologie, Max-Planck-Institut für neurologische Forschung, Osthierheimer Straβe 200, D-5000, Koln 91, Federal Republic of Germany aut NATIONALLICENCE 773 0- Acta Neuropathologica Springer-Verlag 79/4(1990-01-01), 444-455 0001-6322 79:4<444 1990 79 401 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer