of the skin proceeded to full-thickness necrosis and/or discoloration throughout or in part of the compressed area. Necrotic skin was replaced by black/brown eschar, accompanying exudation, and significant tissue hardening. The injuries considerably contracted a few days after completing the series of compressions. The eschar further decreased gradually in size and usually became detached with time, after which a skin ulcer formed. A small number of rats showed only erosion and/or severe redness of the skin, damage which was reversible to heal without eschar formation. Generally, skin injuries seemed most severe a few days after 5 compressions and essentially healed over the subsequent 20 days. This model should prove useful for developing preventive measures and treating pressure ulcers.
IntroductionP r e s s u r e u l c e r s c o n s t i t u t e a m a j o r p r o b l e m f o r persons who are unable or find it difficult to change the position of their bodies. Studying the pathogenesis and repair process of pressure ulcers is of great clinical importance to prevent and treat pressure ulcers. However, the mechanisms of development a n d p r o g r e s s i o n o f p r e s s u r e u l c e r s a r e n o t f u l l y understood because numerous factors are involved in their production (Stekelenburg et al., 2005), including the magnitude of pressure, exposure time, friction, shear forces Gefen, 2004, 2007), and temperature (Kokate et al., 1995 Summary. A better understanding of pressure ulcers requires animal models under precise experimental conditions. We here report on an improved and clinically more relevant model of pressure ulcers. Rats underwent implantation of a gold-plated magnet (25 20 2 mm) into their peritoneal cavities under anesthesia. At either 3 or 4 days postoperatively, the rat abdominal wall was repeatedly compressed at 100 mmHg (13.3 kPa) for 4 h daily for 5 consecutive days by applying another magnet to the skin while animals were conscious. The rats were reared without further treatment and the abdominal skin was photographed daily. Specimens were removed at appropriate intervals for histological examination. Edema and mild redness of the skin appeared at 1 day after the first compression. After a few repetitions of compression, edema and redness of the skin were enhanced. Subsequently, in the majority of rats, redness