Science Publications

Gawlitta,D; Li,W; Oomens,CW; Baaijens,FP; Bader,DL; Bouten,CV

Abstract Deep pressure ulcers develop in tissues subjected to sustained mechanicalloading. Though it has been hypothesized that this damage mechanism results from local tissueischemia, it has recently been shown with a cell model that sustained compression can cause celldeformation, leading to tissue breakdown. The present study focuses on the assessment of cellviability during compression and ischemia in an in vitro muscle model to determine their relativecontributions to damage development. A model system was developed consisting of engineered skeletalmuscle produced from the culture of murine muscle cells in a collagen gel. The tissue was subjectedto 0, 20, or 40% compression under hypoxic or normoxic conditions. Experiments were performed on thestage of a microscope and cell viability was monitored using fluorescent markers for apoptotic andnecrotic cell death. Hypoxia did not lead to significant cell death over a 22 h period. By contrast,compression led to immediate cell death that increased withtime. No additional effect of hypoxia oncell death was observed. These data show that contrary to existing theories, compression can causedevelopment of muscle damage and that hypoxia does not contribute to cell death development within22 h in engineered muscle.

Keywords Ischemia; Muscle, Skeletal; Myoblasts; Oxygen; Pressure Ulcer

Annals of Biomedical Engineering
0090-6964, Volume 35, Issue 2, 2007, Pages 3-284