Pressure-induced skin lesions in pigs: reperfusion injury and the effects of vitamin E

Abstract

The pathogenesis of the development of pressure ulcers is still unclear. The aim of this study was to investigate the role of ischaemia and reperfusion in pressure-induced tissue necrosis in the trochanteric region in pigs. Pressure application was achieved with a newly developed computer-controlled pressure device. Histological examination showed damage in the subcutis and muscle tissue comparable with inflammation, extending in a vascular pattern beyond the area of pressure application. Electron-microscopic studies revealed neutrophil adherence to the capillary endothelium, which showed signs of injury. These observations were manifest two hours after the cessation of pressure. Pre-treatment with 500 mg vitamin E per day resulted in significantly less tissue damage compared with untreated animals. Pressure alone caused a significant decrease in reduced glutathione and total glutathione, suggesting oxidative stress. After pressure release there was a significant increase in hydrogen peroxide concentration, suggesting a decreased antioxidant protection. After pre-treatment with vitamin E, however, there was no increase of hydrogen peroxide. It is concluded that the early signs of necrosis after pressure application are concordant with typical ischaemia-reperfusion damage and this can be prevented in part by treatment with vitamin E. Prophylactic administration of vitamin E may influence the occurrence of pressure ulcers in humans undergoing elective surgery.