Faculty of Biomedical Engineering, Technion - Israel Institute of Technology, Haifa, Israel.
Bio-Analytical Microsystems Lab, Department of Chemical Engineering, Ariel University, Room 4.1.20, Building 4, P.O.B. 3, 40700, Ariel, Israel.
Biomech Model Mechanobiol. 2019 Dec;18(6):1847-1866. doi: 10.1007/s10237-019-01181-x. Epub 2019 Jun 27.
Ischemia reperfusion injury (IRI) involvement in pressure ulcers (PU) progression via a surge of oxidative stress and inflammatory responses is well documented. IRI strongly depends on the mechanical loading history. We present a generalized IRI model considering external loading, dynamic tissue healing capacity, accumulating mechanical and reperfusion-mediated damages and competing repair processes of saturating nature. Reperfusion depends on strain and strain rate to enhance loading history sensitivity. Tissue-specific ulceration susceptibility is assumed dependent on variable accumulated damage. We study damage evolution under cyclic loading having several strain expulsion profiles and demonstrate load relief history has critical impact on PU progression. Abrupt load removal generally follows existing models representing extreme repair/damage. We show (first time in silico) that under certain conditions (previously experimentally identified), IRI becomes repairing rather than damaging. In particular, we recapitulate the preconditioning and postconditioning IRI hallmarks. Finally, it is customary among physicians and nurses to promptly alleviate mechanical load applied to patients lying in bed for extended periods and in risk of developing PUs. We demonstrate this practice can be harmful. If load removal is performed early while reperfusion is still beneficial, then this conduct is suitable. However, if critical tissue damage has been crossed, then abrupt expulsion can constitute the worst-case scenario for patient outcome. If no preliminary patient documentation is available, we recommend gradual load removal since risks of accelerated damage eventually leading to ulceration supersede the improved repair potential benefit.
缺血再灌注损伤（IRI）通过氧化应激和炎症反应的激增参与压疮（PU）的进展已有充分记录。IRI 强烈依赖于机械加载历史。我们提出了一个考虑外部加载、动态组织愈合能力、累积机械和再灌注介导损伤以及饱和性质的竞争修复过程的广义 IRI 模型。再灌注取决于应变和应变速率，以增强加载历史的敏感性。组织特异性溃疡易感性被认为取决于可变的累积损伤。我们研究了具有几种应变排出曲线的循环加载下的损伤演化，并证明了负载缓解历史对 PU 进展具有关键影响。突然的负载移除通常遵循代表极端修复/损伤的现有模型。我们首次（在计算机模拟中）表明，在某些条件下（先前在实验中确定），IRI 会变成修复而不是损伤。特别是，我们再现了预处理和后处理 IRI 的特征。最后，医生和护士通常会及时减轻长时间卧床且有发展为 PU 风险的患者所承受的机械负荷。我们证明这种做法可能是有害的。如果在再灌注仍然有益时及早去除负载，则这种方法是合适的。然而，如果已经越过了临界组织损伤，那么突然的排出可能对患者的结果构成最坏情况。如果没有初步的患者记录，则建议逐渐减轻负载，因为加速损伤导致溃疡的风险最终超过了改善修复的潜在益处。
