Ischemia-reperfusion injury has been hypothesized to play a major role in the physiopathology of acute stroke since it has been demonstrated that abrupt reperfusion induces secondary brain damages responsible for up to 70% of the final ischemic lesion size in rodents.
However, such a critical role for abrupt reperfusion on the ischemic injury has never been clearly demonstrated in human. Indeed, clinical data were still lacking up to recently. It is of importance considering that mechanical ischemia-reperfusion with a monofilament has been considered as a gold-standard model of stroke for decades. <\/p>\n\n\n\n