1998
DOI: 10.1046/j.1471-4159.1998.70010325.x
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Selective Acceleration of Arachidonic Acid Reincorporation into Brain Membrane Phospholipid Following Transient Ischemia in Awake Gerbil

Abstract: Awake gerbils were subjected to 5 mm of forebrain ischemia by clamping the carotid arteries for 5 mm and then allowing recirculation. Radiolabeled arachidonic or palmitic acid was infused intravenously for 5 mm at the start of recirculation, after which the brains were prepared for quantitative autoradiography or chemical analysis. Dilution of specific activity of the acyl-C0A pool was independently determined for these fatty acids in control gerbils and following 5 mm of ischemia and 5 mm of reperfusion. Usin… Show more

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Cited by 28 publications
(18 citation statements)
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“…The apparent increase in the rate of incorporation and turnover of AA in PtdIns and increased turnover of ChoGpl, suggest that there are compensatory changes in other phospholipid-metabolizing enzymes. However, the reported resistance of the knockout mouse to middle cerebral artery occlusion (17,18) may arise from reduced availability and release of esterified AA during insult as a result of the absence of cPLA 2 activity (61)(62)(63). This interpretation is consistent with evidence that chronically administered LiCl in rats increases their resistance to cerebral ischemia (64), while decreasing brain cPLA 2 expression and AA turnover (21,54).…”
Section: Discussionmentioning
confidence: 54%
“…The apparent increase in the rate of incorporation and turnover of AA in PtdIns and increased turnover of ChoGpl, suggest that there are compensatory changes in other phospholipid-metabolizing enzymes. However, the reported resistance of the knockout mouse to middle cerebral artery occlusion (17,18) may arise from reduced availability and release of esterified AA during insult as a result of the absence of cPLA 2 activity (61)(62)(63). This interpretation is consistent with evidence that chronically administered LiCl in rats increases their resistance to cerebral ischemia (64), while decreasing brain cPLA 2 expression and AA turnover (21,54).…”
Section: Discussionmentioning
confidence: 54%
“…Excess AA metabolism can contribute to neuronal damage in experimental ischemia, glutamate excitotoxicity, neuroinflammation, and cerebral trauma 45,[60][61][62][63][64] . This, among other factors, may explain why an n-3 PUFA dietary deficiency might increase brain vulnerability to these insults.…”
Section: Enzymes Of the Brain Aa And Dha Cascades In Relation To Dietmentioning
confidence: 99%
“…The majority of unesterified AA and DHA are re-esterified into the phospholipid membrane 44 , whereas a small portion (~3%) is converted via non-enzymatic or enzymatic pathways into oxylipins 41, 4547 that regulate the brain’s response to injury 24 . This response involves oxylipins that acutely down-regulate neuronal hyperexcitability 48 and enhance vasodilation 49 as a protective mechanism.…”
Section: Introductionmentioning
confidence: 99%