Pressure-induced Tissue Injury Research Articles

Protective Effect of Unacylated Ghrelin on Compression-Induced Skeletal Muscle Injury Mediated by SIRT1-Signaling.

Unacylated ghrelin, the predominant form of circulating ghrelin, protects myotubes from cell death, which is a known attribute of pressure ulcers. In this study, we investigated whether unacylated ghrelin protects skeletal muscle from pressure-induced deep tissue injury by abolishing necroptosis and apoptosis signaling and whether these effects were mediated by SIRT1 pathway. Fifteen adult Sprague Dawley rats were assigned to receive saline or unacylated ghrelin with or without EX527 (a SIRT1 inhibitor). Animals underwent two 6-h compression cycles with 100 mmHg static pressure applied over the mid-tibialis region of the right limb whereas the left uncompressed limb served as the intra-animal control. Muscle tissues underneath the compression region, and at the similar region of the opposite uncompressed limb, were collected for analysis. Unacylated ghrelin attenuated the compression-induced muscle pathohistological alterations including rounding contour of myofibers, extensive nucleus accumulation in the interstitial space, and increased interstitial space. Unacylated ghrelin abolished the increase in necroptosis proteins including RIP1 and RIP3 and attenuated the elevation of apoptotic proteins including p53, Bax, and AIF in the compressed muscle. Furthermore, unacylated ghrelin opposed the compression-induced phosphorylation and acetylation of p65 subunit of NF-kB. The anti-apoptotic effect of unacylated ghrelin was shown by a decrease in apoptotic DNA fragmentation and terminal dUTP nick-end labeling index in the compressed muscle. The protective effects of unacylated ghrelin vanished when co-treated with EX527. Our findings demonstrated that unacylated ghrelin protected skeletal muscle from compression-induced injury. The myoprotective effects of unacylated ghrelin on pressure-induced tissue injury were associated with SIRT1 signaling.

Postoperative gluteal skin damage associated with latent development of gluteal muscle damage.

Preceding this study, we observed two cases of concurrent postoperative gluteal skin and muscle damage with extremely high serum creatine kinase (CK) levels, both of which were unrelated to pressure-induced tissue injury. However, postoperative gluteal skin damage accompanied by gluteal muscle damage has not been previously reported and the association between gluteal skin damage, gluteal muscle damage and pressure-induced tissue injury has not previously been investigated. Therefore, we conducted this study to determine the postoperative incidence of gluteal skin damage associated with gluteal muscle damage and assess associations with postoperative serum CK levels and pressure-induced tissue injury. We prospectively evaluated postoperative incidence of gluteal skin damage and measured serum CK levels in 929 consecutive patients who underwent abdominal, urological or gynecological surgery at our hospital. Magnetic resonance imaging (MRI) of the pelvis was performed in 67 patients who consented. As a result, two of 929 patients developed postoperative gluteal skin damage accompanied by gluteal muscle damage. Gluteal muscle damage without gluteal skin damage was observed in 23 of the 67 patients who underwent MRI, and volumes of damaged gluteal muscle and postoperative serum CK levels were positively correlated. Both gluteal skin and muscle damage were distinguishable from pressure-induced tissue injury. Based on the results of this study, we could confirm the occurrence of postoperative gluteal skin damage, distinct from pressure sores, accompanied by gluteal muscle damage. We also revealed latent development of postoperative gluteal muscle damage, distinguishable from compression-induced tissue injury, without accompanying gluteal skin damage.

Deep tissue injury rat model for pressure ulcer research on spinal cord injury

Many rat/mouse pressure ulcer (PU) models have been developed to test different hypotheses to gain deeper understanding of various causative risk factors, the progress of PUs, and assessing effectiveness of potential treatment modalities. The recently emphasized deep tissue injury (DTI) mechanism for PU formation has received increased attention and several studies reported findings on newly developed DTI animal models. However, concerns exist for the clinical relevance and validity of these models, especially when the majority of the reported rat PU/DTI models were not built upon SCI animals and many of the DTI research did not simulate well the clinical observation. In this study, we propose a rat PU and DTI model which is more clinically relevant by including chronic SCI condition into the rat PU model and to simulate the role of bony prominence in DTI formation by using an implant on the bone-tissue interface. Histological data and imaging findings confirmed that the condition of chronic SCI had significant effect on pressure induced tissue injury in a rat PU model and the including a simulated bony prominence in rat DTI model resulted in significantly greater injury in deep muscle tissue. Further integration of the SCI condition and the simulated bony prominence would result a rat PU/DTI model which can simulate even more accurately the clinical phenomenon and yield more clinically relevant findings.