A model for compression trauma: pressure-induced injury in cell cultures.
An increase in pressure up to 15 atm was used to condense the cellular membrane of cells in culture thereby eliciting a mechanical-like trauma. This trauma is similar to a compression-like spinal cord injury or brain injury. The cells used in this study were ROC-1 oligodendroglia, N1E-115 neuroblastoma, and human umbilical vein endothelial (HUVE) cells. Total fatty acid (FA) release and release of lactate dehydrogenase (LDH) into the extracellular medium were used as indices of cellular trauma. Pressure-induced FA release, dependent on pressure and pressure duration, occurred with all cell types. The level of pressure needed to cause the greatest increase in FA levels was 10 atm for ROC-1 cells (3 min duration), 15 atm for N1E-115 cells (3 min duration), and 15 atm for HUVE cells (10 min duration). With each cell type, the released FA were reacylated or metabolized between 10 and 30 min of recovery. Following a 12- to 24-h recovery period, N1E-115 and HUVE cells release more FA, indicating that the initial perturbation of the membrane was not fully reversible. LDH levels were significantly increased in both the N1E-115 and HUVE cultures following 24 h of recovery. This efflux of LDH indicates irreversible membrane damage, suggesting that the trauma may be irreversible at longer recovery times.[1]References
- A model for compression trauma: pressure-induced injury in cell cultures. Murphy, E.J., Horrocks, L.A. J. Neurotrauma (1993) [Pubmed]
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