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[Experimental study on pathogenesis of neonatal hypoxic-ischemic encephalopathy. II. Energy metabolism in the brain]
K Nishizawa1, K Tanaka, M Shimada
1Department of Pediatrics, Shiga University of Medical Science.
Insights
Hypoxia after carotid artery ligation in young rats caused brain damage. Energy metabolism changes, like decreased ATP and increased lactate, were specific to the cortex and hippocampus on the affected side.
Area of Science:
- Neuroscience
- Biochemistry
- Pathology
Context:
- Perinatal hypoxic-ischemic encephalopathy (HIE) in humans shares similarities with brain injury in young rats following hypoxia and unilateral carotid artery ligation.
- Understanding energy metabolism during such events is crucial for developing effective treatments.
Purpose:
- To evaluate regional brain energy metabolism during hypoxia after unilateral carotid artery ligation in developing rats.
- To investigate changes in tissue pH, lactate, pyruvate, ADP, and ATP levels in different brain areas.
Summary:
- Hypoxia following carotid artery ligation led to rapid declines in cortical tissue pH on the ligated side.
- ATP decreased and lactate increased significantly in the cortex and hippocampus of the ligated side.
- While lactate elevated in subcortical areas, overall energy metabolite levels showed no significant difference between ligated and non-ligated sides, despite observed neuropathology.
Impact:
- Findings suggest distinct pathogenetic mechanisms for cerebral damage in the cerebral cortex versus subcortical structures under hypoxic-ischemic conditions.
- This research provides insights into the regional differences in brain injury following perinatal hypoxia-ischemia.
Abstract:
In a preceding paper, we showed that the exposure to hypoxia after unilateral carotid artery ligation of sucking rat on 7 days of age caused various pathological changes in the ipsilateral forebrain, which had close similarity to human perinatal hypoxic-ischemic encephalopathy. To evaluate the energy metabolism in various regions of the brain during hypoxia after unilateral carotid artery ligation, tissue pH was monitored in the cortex by direct insertion of an electrode. The contents of the lactate, pyruvate, ADP and ATP were also measured during hypoxia. The tissue pH in the cortex of ligated side declined rapidly after initiation of hypoxia as compared to non-ligated side. The contents of pyruvate and ADP showed no particular changes through various regions. Only in the cortex and hippocampus of ligated side, ATP was decreased, and elevation of lactate was more salient than in non-ligated side. In the striatum and thalamus, only elevation of lactate was indicated. However, the levels of lactate, pyruvate, ADP and ATP disclosed no significant difference between the ligated side and non-ligated side, although neuropathological changes were observed only in their ligated side. These results suggest that pathogenesis of the cerebral damage caused by hypoxic-ischemic condition may be different between the cerebral cortex and subcortical structures.