Affiliation:
1. College of Nursing, University of Arizona, Tucson, Arizona,
2. College of Nursing, University of Arizona, Tucson, Arizona
Abstract
Traumatic brain injury (TBI) is a leading cause of morbidity and mortality. A cascade of events is initiated with TBI that leads to degradation of the membrane lipid bilayer of neurons and neuroglia. The purpose of this study was to (a) describe changes in the cerebrospinal fluid (CSF) phospholipid concentration over time for those who survived and those who died following TBI; and (b) determine whether there were differences in the CSF phospholipid concentration between those who survived and those who died following TBI. Thirty-nine CSF samples were obtained from 10 participants who sustained a TBI. Following extraction, phospholipids were separated and quantified by normal-phase high performance liquid chromatography with ultraviolet detector. For those who died, the highest median concentration was on Day 1 after TBI for lysophosphatidylcholine and on Day 4 after TBI for phosphatidylethanolamine, phosphatidylserine, phosphatidylcholine, and sphingomyelin. For those who survived, the highest median concentration was on Day 1 after TBI for phosphatidylcholine, on Day 3 after TBI for phosphatidylethanolamine and phosphatidylserine, on Day 4 after TBI for sphingomyelin, and on Day 5 after TBI for lysophosphatidylcholine. There were significant differences in the concentrations of phosphatidylethanolamine and phosphatidylserine on Days 1—2 and of phosphatidylethanolamine, phosphatidylcholine, and sphingomyelin on Days 3—4 after TBI between those who survived and died, with the highest concentrations in those who died. These findings provide preliminary evidence of greater disruption of central nervous system membrane phospholipids in participants who died after TBI.
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39 articles.
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