The relative contributions of compression and hypoxia to development of muscle tissue damage: an in vitro study.
Deep pressure ulcers develop in tissues subjected to sustained mechanical loading. Though it has been hypothesized that this damage mechanism results from local tissue ischemia, it has recently been shown with a cell model that sustained compression can cause cell deformation, leading to tissue breakdown. The present study focuses on the assessment of cell viability during compression and ischemia in an in vitro muscle model to determine their relative contributions to damage development. A model system was developed consisting of engineered skeletal muscle produced from the culture of murine muscle cells in a collagen gel. The tissue was subjected to 0, 20, or 40% compression under hypoxic or normoxic conditions. Experiments were performed on the stage of a microscope and cell viability was monitored using fluorescent markers for apoptotic and necrotic 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 with time. No additional effect of hypoxia on cell death was observed. These data show that contrary to existing theories, compression can cause development of muscle damage and that hypoxia does not contribute to cell death development within 22 h in engineered muscle.
Gawlitta
Debby
D
Department of Biomedical Engineering, Eindhoven University of Technology, WH 4.105, PO Box 513, 5600 MB, Eindhoven, The Netherlands. d.gawlitta@tue.nl
Li
Wei
W
Oomens
Cees W J
CW
Baaijens
Frank P T
FP
Bader
Dan L
DL
Bouten
Carlijn V C
CV
D000818:Animals; D015687:Cell Hypoxia; D002460:Cell Line; D002470:Cell Survival; D007511:Ischemia / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D051379:Mice; D018482:Muscle, Skeletal / Q000098:blood supply* / Q000473:pathology / Q000503:physiopathology*; D032446:Myoblasts; D010100:Oxygen / Q000378:metabolism*; D011312:Pressure / Q000009:adverse effects; D003668:Pressure Ulcer / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*
D010100:Oxygen