NADH Fluorescence and Regional Energy Metabolites During Focal Ischemia and Reperfusion of Rat Brain

Transient focal ischemia was produced in rat brain using simultaneous, reversible occlusion of the middle cerebral artery (MCA) and both carotid arteries. NADH tissue fluorescence and regional levels of ATP and lactate were measured after occlusion for 1 or 2.5 h and after reperfusion for 1 or 24 h...

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Bibliographic Details
Published in:Journal of cerebral blood flow and metabolism 1991-05, Vol.11 (3), p.459-465
Main Authors: Welsh, Frank A., Marcy, Val Robert, Sims, Reneé E.
Format: Article
Language:English
Subjects:
Adenosine Triphosphate - metabolism
Animals
Biological and medical sciences
Brain - metabolism
Cerebral Arteries
Cerebral Cortex - metabolism
Energy Metabolism
Fluorescence
Ischemic Attack, Transient - metabolism
Lactates - metabolism
Lactic Acid
Male
Medical sciences
NAD - metabolism
Nervous system involvement in other diseases. Miscellaneous
Neurology
Rats
Rats, Inbred Strains
Reperfusion
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Summary:Transient focal ischemia was produced in rat brain using simultaneous, reversible occlusion of the middle cerebral artery (MCA) and both carotid arteries. NADH tissue fluorescence and regional levels of ATP and lactate were measured after occlusion for 1 or 2.5 h and after reperfusion for 1 or 24 h following a 2.5-h insult. Occlusion for 1 or 2.5 h caused a marked but microheterogenous increase in NADH fluorescence, which was restricted to the MCA territory of the ipsilateral cortex. In this ischemic core, tissue levels of ATP were nearly depleted, while lactate accumulated to 10–13 mmol/kg. Metabolic alterations were less pronounced in regions adjacent to the ischemic core; however, one border region experienced a progressive increase in lactate between 1 and 2.5 h. NADH fluorescence and metabolite levels were not significantly altered in subcortical structures. In animals reperfused after a 2.5-h insult, NADH fluorescence diminished in the ischemic core to abnormally low levels, ATP was restored only to 37–50% of control, and lactate remained elevated. By 24 h, histologic infarction was evident in the regions with metabolic impairment. These results indicate that focal depletion of energy metabolites for 2.5 h caused irreversible impairment of energy metabolism and focal infarction even though lactate accumulation was moderate.
ISSN:0271-678X
1559-7016
DOI:10.1038/jcbfm.1991.88