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An enzyme histochemical study of cerebral arteriosclerosis

dc.contributor.authorFriede, Reinhard L.en_US
dc.date.accessioned2006-09-11T18:43:42Z
dc.date.available2006-09-11T18:43:42Z
dc.date.issued1962-01en_US
dc.identifier.citationFriede, Reinhard L.; (1962). "An enzyme histochemical study of cerebral arteriosclerosis." Acta Neuropathologica 2(1): 58-72. <http://hdl.handle.net/2027.42/47221>en_US
dc.identifier.issn0001-6322en_US
dc.identifier.issn1432-0533en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/47221
dc.description.abstractThe distribution of two oxidative enzymes (DPN-diaphorase and succinic dehydrogenase), two hydrolytic enzymes (acid and alkaline phosphatase) and data on mitochondria were described as to their relationship to the histopathology of cerebral arteriosclerosis. Incomplete necrosis of gray matter was characterized by a patchy, irregular decrease of oxidative enzyme activity in the neuropil. Complete necrosis (infarcts) showed a loss of enzyme activity in the tissue except the walls of capillaries which still showed activity of oxidative enzymes and also alkaline phosphatase. Hypertrophic astrocytes in the adjacent tissue were characterized by excessive increase of oxidative enzyme activity. Microglia showed little oxidative enzyme activity but strong activity of acid phosphatase. Fatty degeneration of cells was consistently accompanied by decreased oxidative enzyme activity; there was no such inverse relationship for acid phosphatase. Study of capillarization, normal histochemistry, and of pathological changes of the periarterial tissue suggested that the wall of thick arteries normally provided sufficient nutrition of the periarterial tissue. Impairment of this function in arteriosclerosis was considered responsible for the formation of periarterial scars in arteriosclerosis. Die Verteilung zweier oxydativer Enzyme (DPN-Diaphorase und Succino-Dehydrogenase), zweier hydrolytischer Enzyme (saure und alkalische Phosphatase) und Befunde über Mitochondrien werden in ihrem Verhältnis zur Histopathologie der cerebralen Arteriosklerose beschrieben. Unvollständige Nekrosen der grauen Substanz waren gekennzeichnet durch stellenweise auftretende, unregelmäßige Verminderung der Aktivität oxydativer Enzyme im Neuropil. Vollständige Nekrosen (Infarkte) wiesen einen Verlust der Enzymaktivität im Gewebe auf, mit Ausnahme der Capillarwände, in denen noch Aktivität der oxydativen Enzyme und auch der alkalischen Phosphatase vorhanden war. Hypertrophische Astrocyten im angrenzenden Gewebe waren charakterisiert durch übermäßige Erhöhung der Aktivität der oxydativen Enzyme. Die Mikroglia zeigte nur geringe Aktivität der oxydativen Enzyme, jedoch starke Aktivität der sauern Phosphatase. Gleichzeitig mit der Zellverfettung kam es immer zu einer Aktivitätsverminderung der oxydativen Enzyme; für die saure Phosphatase konnte kein derartiges reziprokes Verhältnis nachgewiesen werden.en_US
dc.format.extent3532832 bytes
dc.format.extent3115 bytes
dc.format.mimetypeapplication/pdf
dc.format.mimetypetext/plain
dc.language.isoen_US
dc.publisherSpringer-Verlagen_US
dc.subject.otherPathologyen_US
dc.subject.otherMedicine & Public Healthen_US
dc.titleAn enzyme histochemical study of cerebral arteriosclerosisen_US
dc.typeArticleen_US
dc.subject.hlbsecondlevelPathologyen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumMental Health Research Institute, University of Michigan, Ann Arbor, Michiganen_US
dc.contributor.affiliationumcampusAnn Arboren_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/47221/1/401_2004_Article_BF00685744.pdfen_US
dc.identifier.doihttp://dx.doi.org/10.1007/BF00685744en_US
dc.identifier.sourceActa Neuropathologicaen_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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