Background: Impaired energy metabolism during HI may induce apoptosis. This could have implications for neural rescue therapies.
Subjects and Interventions: Apoptotic and necrotic cells were counted in the cingulate gyrus in 8 newborn piglets subjected to transient HI while observed by magnetic resonance spectroscopy, and 5 controls.
Results: 48 hours after HI mean 11.9% (SD 6.7%) of cells were apoptotic and 11.4% (8.4%) necrotic, while in controls 4.1% (2.7%) were apoptotic and 0.7% (1.3%) necrotic. Apoptotic and necrotic cell counts were related to: (1) the decline in the ratio of nucleotide triphosphates to the exchangeable phosphate pool during HI; (2) the fall in the ratio of phosphocreatine to inorganic phosphate 8-48 hours after HI; and (3) an increased ratio of lactate to total creatine at both these times.(p<0.05).
Conclusion: Apoptosis is related to impairment of energy metabolism following transient HI.
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Mehmet, H., Yue, X., Penrice, J. et al. Relation of Energy Metabolism To Apoptosis Following Cerebral Hypoxia-Ischaemia (Hi). Pediatr Res 42, 386 (1997). https://doi.org/10.1203/00006450-199709000-00028
Issue Date:
DOI: https://doi.org/10.1203/00006450-199709000-00028