The effects of pressure and shear on capillary closure in the microstructure of skeletal muscles
The effects of pressure and shear on capillary closure in the microstructure of skeletal muscles
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DOI：
10.1007/s10439-007-9384-9
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发表时间：
2007-12-01
影响因子：
3.8
通讯作者：
Gefen, Amit
中科院分区：
文献类型：
--
作者：
Linder-Ganz, Eran;Gefen, Amit
深部组织损伤（DTI）是一种严重的压力性溃疡，它始于骨突起下的肌肉组织，并向外发展。它与机械压力和剪切力有关，可能导致毛细血管塌陷，从而诱发缺血性疾病。近年来，一些研究者认为，单纯缺血不能解释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）模型评估毛细血管在负荷肌肉组织中的功能。直接对11只大鼠的一侧股薄肌施加12、37和78 kPa的压力2 h。使用红外热成像法（IRT）记录负荷和对侧肌肉的温度随时间的变化，作为缺血水平的测量。此外，一个非线性大变形肌肉束水平的有限元模型，并进行压力为12-120千帕没有和同时剪切应变高达8%。对于每个模拟情况，开放的毛细管横截面积的累积百分比和完全封闭的毛细管的数量被确定。2小时后，负荷肌肉的温度比未负荷对侧肢体的温度（所有压力组的平台温度值的平均值）低2.4 +/- 0.3 ℃（平均值+/-标准差）。在所有压力组中，负荷肌肉的温度在10分钟内下降，但随后保持稳定并显著高于室温至少30分钟，表明肢体在试验的前40分钟内没有完全缺血。我们的有限元模型表明，在12-120千帕的压力和无剪切，开放的毛细管横截面积的累积百分比减少了高达71%。当加入剪切应变时，开放的毛细管横截面积下降得更快，但即使在最大载荷下，也只有46%的毛细管完全关闭。两者合计，动物和FE模型的结果表明，急性缺血不会在40分钟的时间范围内的生理负荷水平下的骨骼肌发展。由于有证据表明，DTI发展在较短的时间内，缺血是不太可能是唯一的因素导致DTI。
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.