L A Horrocks, P Demediuk, R D Saunders, L Dugan, N R Clendenon, E D Means, D K Anderson
{"title":"The degradation of phospholipids, formation of metabolites of arachidonic acid, and demyelination following experimental spinal cord injury.","authors":"L A Horrocks, P Demediuk, R D Saunders, L Dugan, N R Clendenon, E D Means, D K Anderson","doi":"10.1089/cns.1985.2.115","DOIUrl":null,"url":null,"abstract":"<p><p>Spinal cord injury has been studied using a cat compression model. Very early changes in lipid metabolism were found that compromise the integrity of the plasma membrane and decrease the activities of ATPases. Up to 18% of the ethanolamine plasmalogens are lost, with very marked elevations of the free fatty acids, arachidonic acid, diacylglycerols, prostaglandins, thromboxanes, and leukotrienes. These changes result in edema, inflammation, necrosis of oligodendroglia, demyelination, and paralysis.</p>","PeriodicalId":77690,"journal":{"name":"Central nervous system trauma : journal of the American Paralysis Association","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"1985-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1089/cns.1985.2.115","citationCount":"31","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Central nervous system trauma : journal of the American Paralysis Association","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1089/cns.1985.2.115","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 31
Abstract
Spinal cord injury has been studied using a cat compression model. Very early changes in lipid metabolism were found that compromise the integrity of the plasma membrane and decrease the activities of ATPases. Up to 18% of the ethanolamine plasmalogens are lost, with very marked elevations of the free fatty acids, arachidonic acid, diacylglycerols, prostaglandins, thromboxanes, and leukotrienes. These changes result in edema, inflammation, necrosis of oligodendroglia, demyelination, and paralysis.
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