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1 Department of Materials Technology, Department of Biomedical Engineering, Eindhoven University of Technology, Eindhoven, NB, The Netherlands
2 Biomedical NMR, Department of Biomedical Engineering, Eindhoven University of Technology, Eindhoven, NB, The Netherlands
3 Department of Materials Technology, Department of Biomedical Engineering, Eindhoven University of Technology, Eindhoven, NB, The Netherlands; Department of Engineering and IRC in Biomedical Materials, Queen Mary, University of London, London, United Kingdom
* To whom correspondence should be addressed. E-mail: a.stekelenburg{at}tue.nl.
The underlying mechanisms leading to deep tissue injury after sustained compressive loading are not well understood. It is hypothesized that initial damage to muscle fibers is induced mechanically by local excessive deformation. Therefore, in this study an animal model was used to study early damage after compressive loading to elucidate on the damage mechanisms leading to deep pressure ulcers. The tibialis anterior of Brown Norway rats was loaded for 2 hours by means of an indenter. Experiments were performed in a magnetic resonance (MR) -compatible loading device. Muscle tissue was evaluated with T2-weighted MRI both during loading and up to 20 hours after load removal. In addition, a detailed examination of the histopathology was performed at several time points (1, 4 and 20 hours) after unloading. Results demonstrated that immediately after unloading T2-weighted MR images showed localized areas with increased signal intensity. Histological examination at 1 and 4 hours after unloading showed large necrotic regions with complete disorganization of the internal structure of the muscle fibers. Hypercontraction zones were found bilateral to the necrotic zone. Twenty hours after unloading an extensive inflammatory response was observed. The proposed relevance of large deformation was demonstrated by the location of damage indicated by T2-weighted MRI and the histological appearance of the compressed tissues. Differences in damage development distal and proximal to the indenter position suggested a contribution of perfusion status in the measured tissue changes that, however, appeared be to reversible.
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