The CA1 and hilar fields of the hippocampus are highly vulnerable to lack of oxygen after interruption of blood flow to the brain. Severe anterograde memory loss, seen in a significant proportion of heart attack survivors, has been attributed to selective bilateral ischaemic damage to the hippocampus. Animal models of global ischaemia, induced by extracranial occlusion of the major ascending arteries, enable assessment of the neuropathological and functional consequences of transient interruption of cerebral blood flow, and can inform strategies to reduce or alleviate ischaemic brain damage. This review focuses firstly on the nature of cognitive deficits induced by global ischaemia, how far they are consistent with lesion-based accounts of hippocampal function, and the extent to which these deficits can be correlated with CA1 cell loss. The second focus of the review is to examine the limited evidence for graft-induced recovery of cognitive function in animals subjected to global ischaemia. Recent findings that grafted foetal cells from discrete hippocampal fields follow appropriate laminar routes to form functional connections with host neurons, and that growth factors protect cells from ischaemic damage, have suggested that CA1 or trophic grafts placed in the region of ischaemic CA1 cell loss might restore or protect this vulnerable sector, and reduce cognitive deficits.