Abstract
Objective: Lactic acid accumulation or glucose depletion may contribute to the development of cortical infarction after cerebral ischaemia. The aim of this study was to determine the changes of extracellular glucose and lactate levels within the parasagittal cortex following 30-minute of cerebral ischaemia.
Study Design: Eight chronically instrumented near-term fetal sheep (119-133 days) were studied. Microdialysis probes were implanted in the parasagittal cortex. The relative recoveries for lactate and glucose were 25 ±6% and 22±3% respectively. Electrocorticographic (ECoG) activity and cytotoxic oedema were measured by continuous spectral analysis and impedance techniques respectively.
Results: Brain lactate levels increased 3-fold (0.36±0.07 to 1.08±0.19mM, p < 0.05) from 1-4h preceding the onset of ECoG epileptiform activity and secondary cytotoxic oedema (8-36h). The maximum lactate concentration was 5.8 mM during 8-16h. Glucose levels rose 2-fold (0.10±0.02 to 0.22±0.03 mM, p<0.05) from 8-64h.
Conclusion: These results suggest a metabolic disturbance during the postisehaemie phase. However, the maximum lactate concentration was less than the threshold thought to cause infarction (20 mM). Glucose depletion does not occur during die onset of epileptiform activity and secondary cytotoxic oedema. Thus, tissue availability of glucose and accumulation of lactate are probably not major pathogenetic factors during the development of parasagittal cortical infarction alter hypoxic-isehaemic injury in fetal sheep.
Article PDF
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Tan, W., Williams, C., Bossano, D. et al. Changes In extracellular lactate and glucose during the development of parasagittal cortical infarction after hyposic-ischaemic injury in fetal sheep. Pediatr Res 35, 262 (1994). https://doi.org/10.1203/00006450-199402000-00046
Issue Date:
DOI: https://doi.org/10.1203/00006450-199402000-00046