Summary
A study was made on the blood-brain barrier (BBB) to protein tracers in focal cerebral ischemia and infarction caused by permanent or temporary occlusion of the middle cerebral artery (MCA) in the rhesus monkey.
Permanent occlusion of the MCA for 1–48 hrs only exceptionally caused extravasation of intravenously injected Evans blue, but temporary occlusion for 4 hrs followed by recirculation for 2 hrs frequently caused exudation of the tracer, particularly in the grey matter of the MCA territory. Reduction of the collateral supply during MCA occlusion of less than 4 hrs did not cause extravasation of the tracer.
If the temporary MCA occlusion caused no or only microscopical brain necrosis, no extravasation of the dye could be detected, irrespective of the survival time of the animal. Monkeys with medium-sized subcortical infarcts and survival times between 3 days and 3 weeks showed exudation of evans blue in 50% of the cases, whereas almost all animals with large cortical and subcortical infarcts showed abnormal blue staining in parts of the lesions. All animals examined 23 days or later after the MCA occlusion did not show any changes of the BBB. Extravasation of the tracer during the first 3 weeks after MCA occlusion is therefore related to thesize of the resulting brain necrosis, but restitution of the BBB occurs thereafter irrespective of infarct size.
Zusammenfassung
Die Bluthirnschranke (BHS) für Proteintracer bei focaler cerebraler Ischämie und bei Hirninfarkten infolge dauerndem oder passagem Verschluß der A. cerebri media (ACM) wurde beim Rhesusaffen untersucht.
Dauernder Verschluß der ACM für 1–48 Std verursachte nur ausnahmsweise einen Austritt von i.v. injiziertem Evansblau, während vorübergehende Klemmung von 4 Std Dauer gefolgt von Wiederdurchblutung durch 2 Std häufig einen Austritt der Markierungssubstanz, vor allem in den grauen Anteilen des Versorgungsgebietes der ACM bewirkte. Drosselung der Kollateralversorgung während Verschlusses der ACM für weniger als 4 Std verursachte keinen Austritt des Tracers.
Wenn der passagere Verschluß der ACM keine oder nur eine histologisch faßbare Hirngewebsnekrose verursachte, so war unabhängig von der Überlebenszeit des Tieres kein Farbstoffaustritt nachweisbar. Affen mit mittelgroßen subcorticalen Infarkten und Überlebenszeiten zwischen 3 Tagen und 3 Wochen zeigten Evansblauaustritte in 50% der Fälle, während fast alle Tiere mit großen corticalen und subcorticalen Infarkten eine abnorme Blaufärbung von Teilen der Läsionen aufwiesen. Keines der Tiere, die 23 Tage oder länger nach Verschluß der ACM untersucht wurden, zeigte Störungen der BHS. Der Austritt des Tracers während der ersultierenden Hirngewebsnekrose, doch ist die darauffolgende Restitution der BHS-Funktion unabhängig von der Größe des Infarkts.
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Olsson, Y., Crowell, R.M. & Klatzo, I. The blood-brain barrier to protein tracers in focal cerebral ischemia and infarction caused by occlusion of the middle cerebral artery. Acta Neuropathol 18, 89–102 (1971). https://doi.org/10.1007/BF00687597
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DOI: https://doi.org/10.1007/BF00687597