Ischaemic brain damage in the gerbil in the absence of 'no-reflow'1

Ames and his co-workers (Ames et al., 1968; Cantu et al., 1969) observed in rabbits that periods of cerebral ischaemia (circulatory arrest) of more than five minutes were followed by multifocal deficits in brain reperfusion as assessed by the post-ischaemic, intra-arterial injection of a suspension of carbon black. These zones of non-perfusion increased in number and size with increasing length of ischaemia, and it was concluded that 'no-reflow' resulting from ischaemic vascular damage was an important factor preventing the recovery of the brain parenchyma after ischaemia. This conclusion, that the vessels of the brain rather than its neurones are initially vulnerable to ischaemia, diverges sharply from long-held concepts about the effects of hypoxia on the brain. Furthermore, the zones of 'no-reflow' in their initial experiments did not conform with the distribution of neuropathological alterations in most studies of circulatory arrest and other types of ischaemia. In a rat preparation of cerebral hypoxiaischaemia (Levy et al., 1975a), impaired reperfusion or 'no-reflow' was rare and not important