AJP - Heart and Circulatory Physiology, Vol 262, Issue 3 672-H677, Copyright © 1992 by American Physiological Society

ARTICLES

Cerebral energy metabolism during hypoxia-ischemia and early recovery in immature rats

J. Y. Yager, R. M. Brucklacher and R. C. Vannucci
Department of Pediatrics (Pediatric Neurology), Milton S. Hershey Medical Center, Pennsylvania State University, Hershey 17033.

Persistent alterations in cellular energy homeostasis may contribute to the brain damage that evolves from perinatal cerebral hypoxia-ischemia. Accordingly, the presence and extent of perturbations in high-energy phosphate reserves were analyzed during hypoxia-ischemia and the early recovery period in the immature rat. Seven-day postnatal rats were subjected to unilateral common carotid artery ligation and hypoxia with 8% oxygen at 37 degrees C for 3 h, an insult that produces damage (selective neuronal necrosis or infarction) of the cerebral hemisphere ipsilateral to the common carotid artery ligation in 92% of animals. Rat pups were quick frozen in liquid nitrogen during hypoxia-ischemia and at 10, 30, and 60 min and 4 and 24 h of recovery for enzymatic, fluorometric analysis of phosphocreatine (PCr), creatine, ATP, ADP, and AMP. During hypoxia-ischemia, PCr, ATP, and total adenine nucleotides were decreased by 87, 72, and 50% of control, respectively. During recovery, PCr, ATP, and total adenine nucleotides exhibited a rapid (within 10 min) although incomplete and heterogeneous recovery that persisted for at least 24 h. Mean values for PCr remained between 55 and 85% of control, whereas ATP values remained between 57 and 67% of control. Individual ATP values were inversely related to tissue water content at 10 min of recovery, indicating a close correlation between failure of energy restoration and the extent of cerebral edema as a reflection of brain damage. Thus high-energy phosphate reserves display lingering alterations during recovery from hypoxia-ischemia. The interanimal variability in energy restoration presumably reflects the spectrum of brain damage seen in this model of perinatal cerebral hypoxia-ischemia.

This article has been cited by other articles:

				J. W. Calvert, J. Cahill, M. Yamaguchi-Okada, and J. H. Zhang Oxygen treatment after experimental hypoxia-ischemia in neonatal rats alters the expression of HIF-1{alpha} and its downstream target genes J Appl Physiol, September 1, 2006; 101(3): 853 - 865. [Abstract] [Full Text] [PDF]

				J. H Meek, C. E Elwell, D. C McCormick, A D. Edwards, J. P Townsend, A. L Stewart, and J. S Wyatt Abnormal cerebral haemodynamics in perinatally asphyxiated neonates related to outcome Arch. Dis. Child. Fetal Neonatal Ed., September 1, 1999; 81(2): 110F - 115. [Abstract] [Full Text]

				J. Y. Yager and J. Asselin Effect of Mild Hypothermia on Cerebral Energy Metabolism During the Evolution of Hypoxic-Ischemic Brain Damage in the Immature Rat Stroke, May 1, 1996; 27(5): 919 - 926. [Abstract] [Full Text]

				M. Qiao, K. L. Malisza, M. R. Del Bigio, and U. I. Tuor Transient Hypoxia-Ischemia in Rats: Changes in Diffusion-Sensitive MR Imaging Findings, Extracellular Space, and Na +-K+-Adenosine Triphosphatase and Cytochrome Oxidase Activity Radiology, April 1, 2002; 223(1): 65 - 75. [Abstract] [Full Text] [PDF]