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.

Biomechanics of Pressure Ulcer in Body Tissues Interacting with External Forces during Locomotion

“…However, at higher pressures (35kPa and 70kPa), extensive damage was reported immediately after the first day of loading. On the other hand, 50kPa pressure on pig trochanter for 2 hrs did not result in noticeable histopathological signs immediately upon cessation of loading (134). Histological signs of damage in subcutaneous tissues and muscles started to appear 1 hr after pressure cessation.…”

“…In animal studies, ischemia reperfusion injury has been demonstrated in the context of pressure ulcers (92,(134)(135)(136)). An adaptive effect of skin perfusion was reported in healthy subjects, where tissue oxygenation remained unaffected after a number of loading cycles.…”

Oxidative Stress Mediates Chemical Hypoxia-Induced Injury and Inflammation by Activating NF-κb-COX-2 Pathway in HaCaT Cells

“…Previous studies showed that hypoxic injury of skin was intimately associated with oxidative stress and inflammatory responses (Houwing et al, 2000;Peirce et al, 2001). Mounting evidence suggested that cyclooxygenase-2 (COX-2) and its product prostaglandin E 2 (PGE 2 ) played a pivotal role in inflammatory response (Birnbaum et al, 2005;Chi and Kim, 2005).…”

Toward real-time detection of deep tissue injury risk in wheelchair users using Hertz contact theory

“…Other theories for the onset of tissue damage include collapse of capillaries and lymph nodes [29][30][31], reperfusion injury [32][33][34], and cell deformation under pressure [5,33,35]. The last has been studied using finite element (FE) models with a damage threshold law derived from previous experiments [4,36].…”