Abstract
Although ischemia has been considered the main factor of pressure ulcers, increasing evidence demonstrates a principal role of ischemia-reperfusion (IR). This study assessed the mechanism of pressure ulcer formation using a cutaneous IR injury model by external application of two magnetic plates. In this model, monocyte chemoattractant protein-1 (MCP-1) was remarkably increased, and following infiltration of macrophages and augmented expression of proinflammatory cytokines and inducible nitric oxide synthase (iNOS) were observed. Therefore, IR cycles were performed in MCP-1 deficient (MCP-1-/-) mice to evaluate the role of this chemokine in pressure ulcer development. MCP-1-/- mice showed reduced macrophage infiltration and expression of tumor necrosis factor-α and iNOS during IR cycles leading to attenuated skin injury. MCP-1 played a role in injury during the reperfusion rather than the ischemic period. These findings suggest that recruitment of macrophages from increasing MCP-1 and subsequent release of proinflammatory cytokines and toxic oxygen-derived free radicals induce the development of pressure ulcers during IR cycles.
