Linder-Ganz Eran, Engelberg Santiego, Scheinowitz Mickey, Gefen Amit
Department of Biomedical Engineering, Faculty of Engineering, Tel Aviv University, Tel Aviv 69978, Israel.
J Biomech. 2006;39(14):2725-32. doi: 10.1016/j.jbiomech.2005.08.010. Epub 2005 Sep 30.
Deep pressure sores (DPS) are associated with inadequate soft tissue perfusion and excessive tissue deformation over critical time durations, as well as with ischemia-reperfusion cycles and deficiency of the lymphatic system. Muscle tissue shows the lowest tolerance to pressure injuries, compared with more superficial tissues. In this communication, we present new histopathology data for muscle tissue of albino (Sprague-Dawley) rats exposed to pressures for 15 or 30 min. These data are superimposed with an extensive literature review of all previous histopathology reported for albino rat skeletal muscles subjected to pressure. The pooled data enabled a new mathematical characterization of the pressure-time threshold for cell death in striated muscle of rats, in the form of a sigmoid pressure-time relation, which extends the previous pressure-time relation to the shorter exposure periods. We found that for pressure exposures shorter than 1 h, the magnitude of pressure is the important factor for causing cell death and the exposure time has little or no effect: even relatively short exposures (15 min - 1 h) to pressures greater than 32 kPa (240 mmHg) cause cell death in rat muscle tissue. For exposures of 2 h or over, again the magnitude of pressure is the important factor for causing cell death: pressures greater than 9 kPa (67 mmHg) applied for over 2 h consistently cause muscle cell death. For the intermediate exposures (between 1 and 2 h), the magnitude of cell-death-causing pressure strongly depends on the time of exposure, i.e., critical pressure levels drop from 32 to 9 kPa. The present sigmoidal pressure-time cell death threshold is useful for design of studies in albino rat models of DPS, and may also be helpful in numerical simulations of DPS development, where there is often a need to extrapolate from tissue pressures to biological damage.
深部压疮（DPS）与关键时间段内软组织灌注不足、组织过度变形有关，还与缺血再灌注循环及淋巴系统功能缺陷有关。与更浅表的组织相比，肌肉组织对压力损伤的耐受性最低。在本报告中，我们展示了白化（斯普拉格-道利）大鼠肌肉组织在承受15或30分钟压力后的新组织病理学数据。这些数据与对之前所有关于白化大鼠骨骼肌受压的组织病理学报告的广泛文献综述相结合。汇总的数据使得能够以S形压力-时间关系的形式对大鼠横纹肌细胞死亡的压力-时间阈值进行新的数学表征，这将之前的压力-时间关系扩展到了更短的暴露时间段。我们发现，对于短于1小时的压力暴露，压力大小是导致细胞死亡的重要因素，而暴露时间影响很小或没有影响：即使相对较短时间（15分钟 - 1小时）暴露于大于32 kPa（240 mmHg）的压力下也会导致大鼠肌肉组织细胞死亡。对于2小时或更长时间的暴露，压力大小同样是导致细胞死亡的重要因素：施加超过2小时的大于9 kPa（67 mmHg）的压力会持续导致肌肉细胞死亡。对于中间暴露时间（1至2小时之间），导致细胞死亡的压力大小强烈依赖于暴露时间，即临界压力水平从32 kPa降至9 kPa。当前的S形压力-时间细胞死亡阈值对于设计DPS白化大鼠模型的研究很有用，也可能有助于DPS发展的数值模拟，在这种模拟中通常需要从组织压力推断生物损伤情况。
