Oxygen treatment restores energy status following experimental neonatal hypoxia-ischemia

The purpose of this study was to determine whether oxygen treatment could attenuate the alterations in cerebral energy metabolism found in the brain following hypoxia-ischemia.

Seven-day-old rat pups were subjected to unilateral carotid artery ligation followed by 2 hrs of hypoxia (8% oxygen at 37 degrees C). The concentrations of high-energy phosphate compounds and glycolytic intermediates and the activity of Na+/K+-adenosine triphosphatase were measured at 4-72 hrs of recovery. Brain weight was used to determine the severity of the brain injury at 2 wks after insult.

Experimental setting.

Rat pups.

Pups were treated with 100% oxygen 1 hr after the insult at 2.5 atmospheres absolute (hyperbaric oxygen) or at normobaric pressure for a duration of 2 hrs.

During the initial period of recovery from hypoxia-ischemia, values of adenosine triphosphate and phosphocreatine remained at levels below normal, whereas the levels of glucose and other glycolytic intermediates were elevated. Hyperbaric oxygen and normobaric oxygen both attenuated brain injury, restored the levels of adenosine triphosphate and phosphocreatine, decreased the levels of the glycolytic intermediates, and increased the utilization of energy.

These results suggest that oxygen treatment during the initial period of recovery from a hypoxia-ischemic insult is able to attenuate energy deficits in the brain, which ultimately leads to a reduction in brain injury.