Characterization of tissue morphology, angiogenesis, and temperature in the adaptive response of muscle tissue to chronic heating.
Characterization of tissue morphology, angiogenesis, and temperature in the adaptive response of muscle tissue to chronic heating.
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发表时间：
1998-12
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通讯作者：
T. Seese;H. Harasaki;G. Saidel;C. Davies
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作者：
T. Seese;H. Harasaki;G. Saidel;C. Davies
先前关于慢性热对组织的体内影响的研究表明，加热的组织温度随着时间的推移而降低。这种反应与局部血管生成一起发生，这可能通过增加局部灌注和增强组织传热而导致温度降低。我们自己的研究是第一个使用慢性热源在40摄氏度和46摄氏度之间的初始界面温度下加热组织。初始温度高于45.3+/-2.2 ℃导致邻近组织坏死。通过适应性反应，坏死在7周内被去除，并在41.8+/-0.5 ℃下被高度血管化的组织囊所取代。本研究试图描述与这种适应性反应相关的空间分布，毛细血管数量和温度。在以0.08 W/cm 2加热2、4和7周后，取出加热和对照肌肉组织切片。组织层厚度和毛细血管密度进行了测量，并与相应的组织温度。在第2周和第4周，热源附近出现坏死;然而，到第7周，高度血管化的纤维组织囊几乎取代了所有坏死。毛细血管密度，特别是靠近热源，显着大于在7周比在2或4周。加热组织毛细血管前沿中的毛细血管密度从2周到7周增加了两倍（106.4+/-14.3帽/mm 2 vs 39.1+/-18.5帽/mm 2）。此外，在所有持续时间内，在加热的组织毛细血管前沿测量到41.7+/-0.9 ℃的平均温度，表明这可能是热诱导血管生成或内皮细胞存活的阈值温度。这些发现更完整地表征了当前组织传热数学模型的灌注组件，并将有助于建立可植入产热器械可能允许的功能性热损失指南。
Previous investigations on the in vivo effects of chronic heat on tissue suggest a response whereby heated tissue temperatures decrease over time. This response occurred in conjunction with localized angiogenesis, which possibly contributed to the temperature decreases by increasing local perfusion and enhancing tissue heat transfer. Our own studies were the first to use a chronic heat source to heat tissue at initial interfacial temperatures between 40 degrees C and 46 degrees C. Initial temperatures above 45.3+/-2.2 degrees C caused necrosis of adjacent tissue. Through an adaptive response, the necrosis was removed by 7 weeks and replaced by a highly vascularized tissue capsule at 41.8+/-0.5 degrees C. The present study sought to characterize the spatial distribution, number of capillaries, and temperatures associated with this adaptive response. Heated and control muscle tissue sections were removed after 2, 4, and 7 weeks of heating at 0.08 W/cm2. Tissue layer thicknesses and capillary densities were measured and correlated with corresponding tissue temperatures. Necrosis was present adjacent to the heat source at 2 and 4 weeks; however by 7 weeks, a highly vascularized fibrous tissue capsule had replaced nearly all necrosis. Capillary densities, particularly near the heat source, were significantly greater at 7 weeks than at either 2 or 4 weeks. Capillary densities in heated tissue capillary fronts tripled from 2 to 7 weeks (106.4+/-14.3 caps/mm2 versus 39.1+/-18.5 caps/mm2). Furthermore, a mean temperature of 41.7+/-0.9 degrees C was measured in heated tissue capillary fronts at all durations, suggesting that this may be a threshold temperature for heat-induced angiogenesis or endothelial cell survival. These findings more completely characterize the perfusion component of the current mathematical model for heat transfer in tissue and will help to establish guidelines for the functional heat loss that an implantable, heat-producing device may allow.