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Elektronenmikroskopische Untersuchungen zur formalen Genese der Balkenläsionen nach experimenteller Cyanvergiftung

Electron microscopic findings concerning the pathogenesis of callosal lesions after experimental cyanide intoxication

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Summary

Subletal cyanide intoxication was produced in 17 rats by daily subcutaneous application of a solution of 0.2% KCN. The total daily dosis was divided in 3 injections. Duration of the intoxication period: up to 2 weeks (6 animals); up to 9 weeks (6 animals). Light- and electron-microscopic examination after surviving times up to 9 weeks. All animals were killed by perfusion with glutaraldehyde. Some animals received only a single injection and were examined within the following 3 days. In all cases appeared 1. necrotic lesions in the caudal part of the corpus callosum, accompanied by 2. spongy tissue alterations at the margin of these lesions. In the necrotic region disintegration of all tissue components appeared (histotoxic hypoxidosis). Phagocytotic activity could be observed only from 2 days after the last toxin application. Astrocytic fiber gliosis followed. After 10 weeks remyelinated axons could be seen. In the marginal region which had a spongy appearance the most important changes were swelling of the inner and outer oligodendrocytic covering of the myelin sheaths, supplemented by intramyelinic vacuolisation and mild astrocytic swelling. They are considered as a selective cyanide effect on these parts of oligodendrocytes (cytotoxic edema of the inner glial loop and the outer glial tongue). Disintegration of the myelin sheaths and degeneration of the axon were secondary phenomena. No criteria indicating a direct toxic myelin damage (primary myelinolysis) were found. The perikarya of oligodendrocytes were involved only by reversible swelling of endoplasmatic reticulum. A special vulnerability of the myelin covering oligodendrocytic processes in cyanide intoxication is suggested.

Zusammenfassung

Subletale Cyanidintoxikation wurde an 17 Ratten durch tägliche Applikation einer 0,2% igen Kaliumcyanidlösung (je drei subcutane Injektionen täglich) erzeugt. Dauer der Intoxikation: bis zu 2 Wochen (6 Tiere), länger als 2 Wochen (6 Tiere). Licht- und elektronenmikroskopische Untersuchung nach Überlebenszeiten bis zu 9 Wochen. Glutaraldehyd-Perfusionsfixierung. Einige Tiere erhielten eine einzige Injektion, Untersuchung innerhalb der folgenden 3 Tage. In allen Fällen traten 1. umschriebene Nekrosen im caudalen Abschnitt des Corpus callosum und 2. spongiöse Gewebsveränderungen in der Randzone dieser Läsionen auf. In der Nekrosezone Zerfall aller Gewebsbestandteile (Cytolyse) als Ausdruck einer histotoxischen Hypoxidose der Marksubstanz. Abräumung und Reparation waren während der Dauer der Intoxikation gehemmt, sie kamen erst 2 Tage nach der jeweils letzten Toxingabe in Gang. Nach 10 Wochen waren Remyelinsationsvorgänge nachweisbar. In der Randzone spongiöse Auflockerung der Marksubstanz infolge Schwellung des inneren und äußeren oligodendrocytären Hüllplasmas der Markmäntel, sowie intramyelinärer Vacuolenbildung und Astrocytenschwellung. Die Hüllplasmaschwellungen der Markmäntel werden als cytotoxisches Ödem der äußeren und inneren oligodendrocytären Gliascheiden (selektive Cyanidwirkung) angesehen. Sie führten sekundär zum Zerfall der Markscheiden, und zur Schädigung der Axone. Anzeichen für eine unmittelbare Toxinwirkung auf die Markscheiden-membranen (primäre Myelinolyse) fehlten. Die Perikarya der Oligodendrocyten zeigten lediglich reversible Schwellung des endoplasmatischen Reticulums. Es wird eine besondere Vulnerabilität der die Markscheiden einschließenden plasmatischen Ausläufer der Oligodendrocyten gegenüber der Cyanidvergiftung vermutet.

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  1. Institut für Hirnforschung-Korbinian-Brodmann-Haus-der Universität Tübingen, Calwer Str. 3, Tübingen

    Andreas Hirner

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Sonderdruckanforderungen an: Prof. Dr. J. Peiffer Direktor des Institutes für Hirnforschung der Universität Tübingen 74 Tübingen, Calwer Str. 3

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Hirner, A. Elektronenmikroskopische Untersuchungen zur formalen Genese der Balkenläsionen nach experimenteller Cyanvergiftung. Acta Neuropathol 13, 350–368 (1969). https://doi.org/10.1007/BF00686123

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