RELATION BETWEEN CEREBRAL OXYGEN DELIVERY AND NEURONAL CELL-DAMAGE INFETAL SHEEP NEAR-TERM

Asphyxia is one of the major causes for fetal brain damage. Although t he quality of life of the so affected children is mostly very limited, the pathogenesis of hypoxic fetal brain damage is poorly understood. Particularly, there is a lack of studies, in which cerebral oxygen del ivery is directly correlated to the extent of neuronal cell damage in the same brain specimens. Therefore, we measured cerebral oxygen deliv ery before (-1 h), during (+3 min & +27 min) and after (+10 min, +4 h, +72 h) 30 min of ischaemia in 5 chronically catheterized normoxemic f etal sheep at 129+/-1 days gestation (term is at 147 days) using the m icrosphere method. In contrast to previous studies (Williams et al. 19 90), we arrested carotid arterial blood flow above the lingual artery for 30 min during surgery. Seventy-two hours later the fetal brains we re fixed in vivo under barbiturate anaesthesia of both the fetus and t he ewe. After cerebral blood flow analysis neuronal cell damage was as sessed with light microscopy in 43 specimens of the fetal brain after cresyl violet/fuchsin staining using a scoring system. After arrest of carotid arterial blood flow cerebral blood flow was reduced by 80%. N euronal cell damage was focussed on the cerebral cortex. Almost no dam age could be detected in deeper parts of the brain. In the cerebrum th ere was a threshold oxygen delivery of 3 mi O-2/100 g tissue/min, belo w which neuronal damage occurred. However, there was no correlation be tween cerebral oxygen delivery and neuronal cell damage in specimens o f the cerebrum, in which oxygen delivery was less than 3 mi O-2/100 g tissue/min, suggesting selective vulnerability. Therefore, in addition to the reduction in cerebral oxygen delivery, other variables, e.g. n eurotransmitter release, receptor pattern or oxygen radicals, may be i nvolved in the development of brain damage.