Summary
Fourteen sheep were subjected to periods of cerebral ischaemia varying from 4–30 min. After prior bilateral ligation of the occipito-vertebral anastomoses linking the common carotid and vetebral arteries, ischaemia was induced by simultaneous clamping of both common carotic arteries resected into cutaneous loops.
The clinical signs following collapse were: defaecation, abnormal breathing, in some cases interrupted by repeated periods of apnoea, and loss of ocular reflexes. In all a state resembling decerebrate rigidity developed. One animal died after 17 min of cerebral ischaemia.
The rapidity and degree of recovery of the sheep following restoration of the cephalic circulation was inversely proportional to the duration of cerebral ischaemia. Twenty four hours after the ischaemic episode six sheep appeared to have fully recovered, five still showed signs of blindness and ataxia, and one was recumbent and comatose.
No lesions were found in brains of sheep subjected to the method for up to 10 min. Longer cerebral ischaemia produced neuronal changes which were first apparent in the striatum and/or cerebral cortex, later also in the hippocampus, thalamus and cerebellum. The nature and the distribution of the brain lesions were similar to those observed by other workers in other species.
The efficacy of the method for producing complete cerebral ischaemia and various aspects of ischaemic lesions found in the brain of sheep are discussed.
Zusammenfassung
14 Schafe wurden einer 4–30 min dauernden cerebralen Ischämie ausgesetzt. Nach vorheriger beidseitiger Ligatur der occipito-vertebralen Anastomosen zwischen Carotis communis und den Vertebralarterien wurde durch gleichzeitige Klipsung beider Carotiden die Ischämie herbeigeführt. Die klinischen Erscheinungen, die dem Kollaps folgten, bestanden in: Defäkation, abnormer Atmung, die in einigen Fällen von wiederholten Apnoeanfällen unterbrochen wurde, sowie Verlust der Augenreflexe. Bei allen Tieren entwickelte sich ein Zustand ähnlich der Enthirnungsstarre. 1 Tier starb nach 17 min dauernder cerebraler Ischämie. Die Schnelligkeit und der Grad der Erholung der Schafe nach erfolgter Wiederherstellung der Schädelzirkulation war umgekehrt proportional zur Dauer der cerebralen Ischämie. 24 Std nach der ischämischen Episode erschienen 6 Schafe voll wiederhergestellt, 5 boten noch Blindheit und Ataxie, 1 blieb liegen und war comatös. Inden Gehirnen von Schafen, die kürzer als 10 min der Behandlung unterworfen waren, fanden sich keine Veränderungen. Länger dauernde cerebrale Ischämie bewirkte Nervenzellveränderungen, die zuerst im Striatum und/oder in der Hirnrinde, später auch in Hippocampus, Thalamus und Kleinhirn erschienen. Die Art und Verteilung der Hirnläsionen war ähnlich den bei anderen Tierarten beschriebenen. Die Wirksamkeit der Methode zur Erzeugung kompletter cerebraler Ischämie und verschiedener Aspekte der im Schafhirn gefundenen ischämischen Läsionen werden erörtert.
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Terlecki, S., Baldwin, B.A. & Bell, F.R. Experimental cerebral ischaemia in sheep. Acta Neuropathol 7, 185–200 (1967). https://doi.org/10.1007/BF00686371
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DOI: https://doi.org/10.1007/BF00686371