Animal models of stroke: Compromise between consistency and clinical relevance?

Abstract

Listen

Translate article

Experimental stroke can be induced by permanent or temporal reduction of oxygen supply in focal brain regions of a variety of animal species in order to produce a reliable functional deficit with or without the formation of reproducible infarcts. The resulting lesion depends on the size of the occluded vessels and the territory that they supply. This can include a complete hemisphere, a major perfusion territory, specific functional regions or unpredictable lacunar fields. The outcome depends on the residual flow to the affected area and the timely restoration of blood supply. Areas of low flow, either in the occluded region or in the apposing penumbra, deserve attention for therapeutic rescue. This is also true for areas remote from the compromised structure. Since the progression of injury and the response of the different brain constituents are multifactorial and behave in a rather unpredictable and variable way, treatment is a complex matter. The evolution of acute or delayed neuronal injury and secondary phenomena such as edema formation, inflammatory reaction and retrograde degeneration may require well-timed approaches based on various mechanisms of action. In this paper current experimental models are reviewed and pharmacotherapeutic measures will be discussed in relation to the pathogenesis of stroke.