Linder-Ganz Eran, Gefen Amit
Department of Biomedical Engineering, Faculty of Engineering, Tel Aviv University, Tel Aviv, 69978, Israel.
Ann Biomed Eng. 2007 Dec;35(12):2095-107. doi: 10.1007/s10439-007-9384-9. Epub 2007 Sep 27.
Deep tissue injury (DTI) is a severe pressure ulcer, which initiates in muscle tissue under a bony prominence, and progresses outwards. It is associated with mechanical pressure and shear that may cause capillaries to collapse and thus, induce ischemic conditions. Recently, some investigators stipulated that ischemia alone cannot explain the etiology of DTI, and other mechanisms, particularly excessive cellular deformations may be involved. The goal of this study was to evaluate the functioning of capillaries in loaded muscle tissue, using animal and finite element (FE) models. Pressures of 12, 37, and 78 kPa were applied directly to one gracilis muscle of 11 rats for 2 h. Temperatures of the loaded and contralateral muscles were recorded with time using infrared thermography (IRT) as a measure of the ischemic level. In addition, a non-linear large deformation muscle-fascicle-level FE model was developed and subjected to pressures of 12-120 kPa without and with simultaneous shear strain of up to 8%. For each simulation case, the accumulative percentage of open capillary cross-sectional area and the number of completely closed capillaries were determined. After 2 h, temperature of the loaded muscles was 2.4 +/- 0.3 degrees C (mean +/- standard deviation) lower than that of the unloaded contralateral limbs (mean of plateau temperature values across all pressure groups). Temperature of the loaded muscles dropped within 10 min but then remained stable and significantly higher than room temperature for at least 30 additional minutes in all pressure groups, indicating that limbs were not completely ischemic within the first 40 min of the trials. Our FE model showed that in response to pressures of 12-120 kPa and no shear, the accumulative percentage of open capillary cross-sectional area decreased by up to 71%. When shear strains were added, the open capillary cross-sectional area decreased more rapidly, but even for maximal loading, only 46% of the capillaries were completely closed. Taken together, the animal and FE model results suggest that acute ischemia does not develop in skeletal muscles under physiological load levels within a timeframe of 40 min. Since there is evidence that DTI develops within a shorter time, ischemia is unlikely to be the only factor causing DTI.
深部组织损伤（DTI）是一种严重的压疮，起始于骨隆突下的肌肉组织，并向外发展。它与机械压力和剪切力有关，这些力可能导致毛细血管塌陷，从而引发缺血状况。最近，一些研究人员规定，仅缺血不能解释DTI的病因，可能还涉及其他机制，特别是过度的细胞变形。本研究的目的是使用动物模型和有限元（FE）模型评估加载肌肉组织中毛细血管的功能。将12、37和78 kPa的压力直接施加于11只大鼠的一条股薄肌上，持续2小时。使用红外热成像（IRT）随时间记录加载肌肉和对侧肌肉的温度，作为缺血水平的一种度量。此外，开发了一个非线性大变形肌肉-肌束水平的有限元模型，并在无剪切应变和有高达8%的同时剪切应变的情况下，对其施加12 - 120 kPa的压力。对于每个模拟案例，确定开放毛细血管横截面积的累积百分比和完全闭合毛细血管的数量。2小时后，加载肌肉的温度比未加载的对侧肢体低2.4 +/- 0.3摄氏度（平均值 +/- 标准差）（所有压力组的平台温度值的平均值）。加载肌肉的温度在10分钟内下降，但随后保持稳定，并且在所有压力组中至少在接下来的30分钟内显著高于室温，这表明在试验的前40分钟内肢体并未完全缺血。我们的有限元模型表明，在12 - 120 kPa的压力且无剪切的情况下，开放毛细血管横截面积的累积百分比最多可降低71%。当添加剪切应变时，开放毛细血管横截面积下降得更快，但即使在最大加载情况下，也只有46%的毛细血管完全闭合。综合来看，动物模型和有限元模型的结果表明，在40分钟的时间范围内，生理负荷水平下的骨骼肌不会发生急性缺血。由于有证据表明DTI在更短的时间内发展，缺血不太可能是导致DTI的唯一因素。
