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Cell-level temperature distributions in skeletal muscle post spinal cord injury as related to deep tissue injury

机译：脊髓损伤后骨骼肌中细胞水平温度分布与深层组织损伤有关

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Deep tissue injury (DTI) is a severe pressure ulcer, which initiates in skeletal muscle tissue under intact skin. Patients with spinal cord injury (SCI) are especially vulnerable to DTI, due to their impaired motosensory capacities. The underlying mechanisms that lead to DTI are, however, still poorly understood. This study focuses on cell-level temperature distributions in muscles of patients with SCI, which typically contain thinner muscle fibers and fewer capillaries. It has been shown previously by our group that ischemic muscles of rat models of DTI cool down mildly and locally, which is very likely to slow the diffusivity of metabolites in the ischemic regions. However, it is unclear how these temperature decreases affect diffusivity at the scale of individual muscle cells in the microanatomy of SCI patients. We hypothesize that a 2°C drop in the temperature of inflowing capillary blood, as shown in our animal studies, has a substantial effect on lowering the diffusivity of metabolites in skeletal muscle, but the pathological microanatomy in the chronic phase of SCI is less dominant in affecting the local temperatures in and around muscle cells. In order to test this hypothesis, two-dimensional finite element (FE) models of cross sections through the microanatomy of muscle tissue were developed using COMSOL Multiphysics software for normal and SCI muscles. The models included muscle cells, extracellular matrix (ECM), and capillaries, each with its own geometrical, thermal, and heat production properties. The SCI model configuration specifically included reduced cross section of myofibrils in favor of more ECM, less capillaries, and decreased blood inflow rate. After a 20-s heat transfer simulation, it was found that temperatures around the cells of the SCI muscle were approximately 2°C lower than that in the normal muscle, that is, heat production from the muscle cell metabolism did not compensate for the lower inflowing blood temperature in the SCI model. We conclude that the temperature and rate of inflowing capillary blood are the dominant factors determining the localized temperatures in the microarchitecture of an ischemic SCI muscle tissue. The altered SCI microanatomy was shown to be less influential. Taken together with the Stokes–Einstein theory, our results indicate that diffusivity of metabolites would be approximately 50% less around the cells of SCI muscle due to local cooling, which is yet another factor compromising tissue viability in the patients with SCI. Keywords Pressure ulcer - Deep tissue injury - Striated muscle - Heat transfer - Rehabilitation
机译：深层组织损伤（DTI）是一种严重的压疮，其始于完整皮肤下的骨骼肌组织。脊髓损伤（SCI）患者的运动感觉能力受损，因此特别容易受到DTI的伤害。但是，导致DTI的基本机制仍然知之甚少。这项研究的重点是SCI患者肌肉中细胞水平的温度分布，这些温度通常包含较细的肌肉纤维和较少的毛细血管。我们的研究小组先前已经证明，DTI大鼠模型的缺血性肌肉会轻度和局部冷却，这很可能会减慢代谢产物在缺血区域的扩散。但是，尚不清楚这些温度降低如何影响SCI患者微观解剖结构中单个肌肉细胞的扩散性。我们假设，如我们的动物研究所示，流入的毛细血管温度下降2°C会对降低骨骼肌代谢产物的扩散性具有实质性影响，但SCI慢性期的病理微观解剖学作用并不明显影响肌肉细胞内和周围的局部温度。为了检验该假设，使用COMSOL Multiphysics软件针对正常和SCI肌肉开发了通过肌肉组织的微观解剖结构的横截面的二维有限元（FE）模型。这些模型包括肌肉细胞，细胞外基质（ECM）和毛细血管，每个模型都有自己的几何，热和热产生特性。 SCI模型配置特别包括减少了肌原纤维的横截面，有利于增加ECM，减少毛细血管和降低血液流入速度。经过20 s的传热模拟，发现SCI肌肉细胞周围的温度比正常肌肉的温度低大约2°C，也就是说，肌肉细胞代谢产生的热量无法弥补温度的降低。 SCI模型中的流入血液温度。我们得出结论，毛细血管血液的流入温度和速率是决定局部缺血性SCI肌肉组织微结构中局部温度的主要因素。改变的SCI显微解剖显示出影响较小。结合斯托克斯-爱因斯坦理论，我们的结果表明，由于局部冷却，代谢产物在SCI肌肉细胞周围的扩散将减少约50％，这也是损害SCI患者组织生存能力的另一个因素。关键词压疮-深层组织损伤-横纹肌-传热-康复

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