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Background: Pressure ulcer (PU) is a significant and complicated health problem. Although ischemia–reperfusion (I/R) injury has been identified as the primary mechanism in the early stage of pressure ulceration, the cellular and molecular events contributing to I/R injury of PU development are unclear.
Objectives: The aim of this study was to characterize hypoxia-inducible factor-1α (HIF-1α) expression profile and elaborate the apoptotic pathways based on an I/R injury model of PU in rats.
Methods: Two related experiments were conducted. The purpose of Experiment 1 was to establish an animal model of early-stage PU (Stage I PU). Forty-eight rats were randomly divided into six groups of eight. Each group received three cycles of I/R, but with different magnitudes of pressure—which ranged from 100 to 270 mm Hg—except for Control Group A. On the basis of this established animal model, Experiment 2 focused on the I/R mechanism of early-stage PU. The 36 rats used in Experiment 2 were randomly divided into one control and two experimental groups; the experimental groups received the same magnitude of pressure (170 mm Hg), but either 3 or 5 I/R cycles. Tissue underneath the compressed region, including the skin and muscle tissue, was incised for immunohistochemistry, enzyme-linked immunosorbent assay, TdT-mediated dUTP nick-end labeling, and real-time polymerase chain reaction gene expression analysis.
Results: HIF-1α gene expression in the compressed muscle tissue was slightly reduced in the 3 I/R group, but significantly elevated in the 5 I/R group (p < .05). The compressed tissue showed inflammation and evidence of oxidative stress reaction. ATPase activity was lower when cycles of I/R were prolonged. TdT-mediated dUTP nick-end labeling analysis showed a significant increase in the compressed muscle tissue relative to the control. Bax and Bcl-2 proteins expressed reversely.
Discussion: These results suggest that mitochondria-mediated apoptotic pathways may be involved in the development of early-stage PU, and HIF-1α might play a potential role for promoting apoptosis. Inflammation, oxidative stress reaction, and energy depletion may cooperate in the process of I/R injury of early-stage PU.
