Yes and no. Most hypoxic brain damage occurs in the form of re-perfusion injuries. If that cascade could somehow be halted, prolonged anoxic episodes would not necessarily lead to the cell death landslides we see today after strokes and cardiac arrests. While anoxia most certainly depolarizes the whole structure, leading to the loss of whatever is currently in short term memory, the more permanent structures of the brain should survive episodes of maybe an hour or more, if we could only stop the apoptosis triggers from happening as soon as blood flow is restored.
The status quo of efforts basically discards the totally anoxic tissue after a stroke, focussing on protecting the (often large) partially perfused border region. This is what's practical now, but the fight about the totally ischemic core regions is far from over.
It's a race between anoxic necrosis (which is the point of no return, where passive cell dissolution happens) and active cell death cascades that are triggered in the fully or partially reperfused cell. The latter one can potentially be halted, the first one leads to irreversible information loss. What the actual timing windows are on both of these in the human brain is subject to active research and the view on them is likely to change over the coming years.
I posted links mainly to stroke and TBI-relevant articles, because that's where the research happens. However it's important to keep in mind that the fully dead brain is relatively static, whereas damaged areas in the living brain are subject to internal "cleanup" mechanisms pretty much right away. In this context, prolonged cardiac arrest might turn out to be preferrable to a stroke.
