The aim is the study of basic processes or potential therapeutic interventions in this disease, and the extension of the pathophysiological knowledge on and/or the improvement of medical treatment of human ischemic stroke.
Ischemic stroke has a complex pathophysiology involving the interplay of many different cells and tissues such as neurons, glia, endothelium, and the immune system.
This approach is useful to study hypoxic ischemia in the developing brain, since newborn rat pups are utilized in this model.
Briefly, 7 day old rat pups undergo a permanent unilateral carotid artery ligation with a subsequent 3 hour exposure to a hypoxic environment (8% oxygen).
This model creates a unilateral infarct in the hemisphere ipsilateral to the ligation, since the hypoxia alone is subthreshold for injury at this age.
The following models are established [2]: Endothelin-1 is a potent vasoconstrictor which is produced endogenously during ischemic stroke and which contributes to overall loss of cells and disability.
However, the quality of MCAO – and thus the volume of brain infarcts – is very variable, a fact which is further aggravated by a certain rate of spontaneous lysis of injected blood clots.
The technique of endovascular filament (intraluminal suture) MCAO as an animal model of ischemic stroke was described first by Koizumi [7].
In this animal model of ischemic stroke the middle cerebral artery (MCA) is surgically dissected and subsequently permanently occluded, e.g. by electrocautery or ligation.