CHRONIC EFFECTS OF HEATING ON TISSUE AND PERFUSION

完全植入式循环支持的可行性， 更换系统取决于身体消散的能力， 从驱动血泵的电源排出热量。 的 41 ℃至45 ℃的界面温度的影响 C对参与宿主防御、组织愈合和外来 然而，身体反应在很大程度上是未知。我们初步的体外试验 实验表明，温度依赖性抑制免疫活性 细胞和组织修复细胞 慢性持续散热 会产生新的生物学和医学问题 最近 在小牛中植入加热装置的慢性体内实验， 恒定的热通量显示持续的炎症反应，厚 组织囊形成和组织囊本身的坏死， 邻近器官的热通量远低于先前认为的 是可以接受的。 还发现， 界面温度存在于肌肉和肺组织之间， 散发同样的热量。 此外，吞噬细胞， 循环白细胞的趋化和随机迁移功能 在接受超过0.08W/cm 2热量的动物中受到抑制 通量 当功率输入被控制以产生恒定的加热器时， 表面温度，维持表面温度所需的热通量， 对于高于42摄氏度的温度，温度随时间增加。 这表明存在某种热适应机制。 不过， 有必要进行进一步的研究， 并且灌注可以在体内测量。 同时，热效应对 必须确定关键的细胞和免疫成分。 在这 这样，组织对热的响应的分析模型可以是 制定了 该方案的具体目标是：（1） 研究长期加热对生物成分的影响 对全身和局部热防御、伤口愈合和表面 （2）确定体内温度分布 对植入器械产生的慢性发热的反应，以识别 高温的安全范围，以及相应的组织 反应，以及（3）开发组织的数学模型 结合长期和短期的温度分布 通过血管生成和增加的适应机制来加热 灌注。 在拟议的 研究将是非常宝贵的，不仅对目前正在进行的人工 心脏计划，但也为慢性高热的未来应用 for cancer癌症patients病人.

The feasibility of totally implantable circulatory support and replacement systems depends on the ability of the body to dissipate the rejected heat from the power source driving the blood pump. The effects of the interfacial temperature of 41 degrees C to 45 degrees C on components involved in host defense, tissue healing and foreign body reaction are, however, largely unknown. Our preliminary in vitro experiments showed temperature dependent suppression of immunocompetent cells and tissue repair cells. Chronic and continuous heat dissipation into the body creates a new biological and medical problem. Recent chronic in vivo experiments in calves implanting heating devices with constant heat fluxes showed persistent inflammatory reaction, thick tissue capsule formation, and necrosis in the tissue capsule itself and adjacent organs at far lower heat fluxes than those previously thought to be acceptable. It was also found that a considerable difference in interface temperature exists between the muscle and lung tissues in dissipating the same amount of heat. In addition, phagocytic, chemotactic, and random migration functions of circulating leukocytes were suppressed in animals which received more than a 0.08W/cm2 heat flux. When the power input was controlled to yield constant heater surface temperature, the heat flux necessary to maintain that temperature increased with time for temperatures above 42 degrees C. This suggested the presence of some heat adaptation mechanism. Still, it is necessary to perform further studies in which tissue temperature and perfusion can be measured in vivo. Concurrently, heat effects on crucial cellular and immune components must be determined. In this way, an analytical model of the tissues' response to heat may be formulated. The specific aims of this proposed program are: (1) to investigate the effects of chronic heating on biological components crucial to systemic and local heat defense, wound healing, and surface interactions; (2) to determine the in vivo temperature distribution response to chronic heat generated by an implanted device, to identify the safe range of high temperature, and the corresponding tissue reactions, and (3) to develop a mathematical model of the tissue temperature distribution which incorporates both long- and short-term adaptation mechanisms to heat through angiogenesis and increased perfusion, respectively. The information obtained in the proposed studies will be invaluable not only for currently ongoing artificial heart programs, but also for future application of chronic hyperthermia for cancer patients.