Free fatty acids and energy metabolites in ischemic cerebral cortex with noradrenaline depletion
Abstract
We tested whether cerebral noradrenaline (NA) may play a central role in mediating the increased production of free fatty acids (FFAs) during cerebral ischemia. Levels of FFAs, cyclic AMP, and NA, as well as ATP, ADP, and AMP, were measured in cerebral cortex during decapitation ischemia in rats 2 weeks after unilateral locus ceruleus lesion. Comparisons were made between the results obtained from the contralateral cortex with normal NA content and the NA-depleted ipsilateral cortex. Although NA depletion was associated with a diminished transient rise of cyclic AMP in response to ischemia, it failed to influence the magnitude of FFA increase or the decline of energy state within the 15-min period of ischemia. A more than twofold increase of total FFAs (sum of palmitic, stearic, oleic, arachidonic, and docosahexaenoic acids) was observed in both hemispheres at 1 min after decapitation, when energy failure became manifest. The increased production of FFAs continued throughout the 15 min of ischemia, with a preferential rise in the levels of stearic and arachidonic acids. There was an inverse correlation between FFA levels and total adenylate pool. The results do not support a major role for NA and cyclic AMP in increasing cortical FFAs during complete ischemia. Instead, they are consistent with the view that impaired oxidative phosphorylation activates deacylating enzymes. Disturbance of reacylation due to energy depletion is probably another factor contributing to the continuous increase of FFAs during prolonged ischemia.
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The synthesis of 10,17S-docosatriene after 1 h of MCAo coincides with free DHA availability that results from phospholipase A2 activation as well as with reperfusion reoxygenation.
“The synthesis of 10,17S-docosatriene after 1 h of MCAo coincides with free DHA availability that results from phospholipase A2 activation (Bazán, 1970; Bazan and Allan, 1998; Yoshida et al., 1984) as well as with reperfusion reoxygenation.”
From Docosanoids and elovanoids from omega-3 fatty acids are pro-homeostatic modulators of inflammatory responses, cell damage and neuroprotection (2018) · cites this paper as Yoshida et al., 1984
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- Authors
- Yoshida, S., Harik, S. I., Busto, R., Santiso, M., Martinez, E., & Ginsberg, M. D.
- Affiliations
- Case Western Reserve University (US)
- University of Miami (US)
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 1984-03
- Volume
- 42
- Issue
- 3
- Pages
- 711-717
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- OpenAlex
- W1968028706
- Cited by
- 46
- References
- 39
- Citations by year
- 2025: 1 · 2020: 1 · 2018: 1 · 2017: 2 · 2016: 1 · 2015: 1
- FWCI
- 4.88
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neurochemistry (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Neurology › Neurological Disorders and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Keywords
- free fatty acids, cerebral ischemia, norepinephrine depletion, cyclic AMP, energy metabolism, adenylate pool, ATP, arachidonic acid, stearic acid, docosahexaenoic acid, oxidative phosphorylation, reacylation, cerebral cortex
- MeSH terms
- Adenine Nucleotides, Cyclic AMP, Animals, Cerebral Cortex, Brain Ischemia, Energy Metabolism, Fatty Acids, Nonesterified, Kinetics, Functional Laterality, Locus Coeruleus, Male, Norepinephrine, Rats, Inbred Strains, Rats
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