Data_Sheet_1_Heat Emitting Damage in Skin: A Thermal Pathway for Mechanical Algesia.ZIP

Mechanical pain (or mechanical algesia) can both be a vital mechanism warning us for dangers or an undesired medical symptom important to mitigate. Thus, a comprehensive understanding of the different mechanisms responsible for this type of pain is paramount. In this work, we study the tearing of porcine skin in front of an infrared camera, and show that mechanical injuries in biological tissues can generate enough heat to stimulate the neural network. In particular, we report local temperature elevations of up to 24°C around fast cutaneous ruptures, which shall exceed the threshold of the neural nociceptors usually involved in thermal pain. Slower fractures exhibit lower temperature elevations, and we characterise such dependency to the damaging rate. Overall, we bring experimental evidence of a novel—thermal—pathway for direct mechanical algesia. In addition, the implications of this pathway are discussed for mechanical hyperalgesia, in which a role of the cutaneous thermal sensors has priorly been suspected. We also show that thermal dissipation shall actually account for a significant portion of the total skin's fracture energy, making temperature monitoring an efficient way to detect biological damages.

机械性疼痛（Mechanical pain，或称机械性痛觉（mechanical algesia））既是预警危险的关键生理机制，也是亟需加以缓解的不良医学症状。因此，全面解析这类疼痛的不同致病机制至关重要。本研究针对红外摄像机拍摄下的猪皮肤撕裂过程展开实验分析，证实生物组织的机械损伤可产生足以激活神经网络的热量。具体而言，我们观测到快速皮肤破裂部位周围的局部温度可升高至多24°C，该温度超出了通常参与热痛感知的神经伤害性感受器（neural nociceptors）阈值。较慢的组织断裂则伴随更低的温度升高，我们还对这一随损伤速率变化的特性进行了系统表征。总体而言，本研究通过实验证实了一条全新的热传导直接机械性痛觉通路。此外，我们还讨论了该通路在机械性痛觉超敏（mechanical hyperalgesia）中的潜在意义——此前学界曾推测皮肤热传感器在该病理过程中发挥作用。我们同时证实，热耗散实际上可占皮肤断裂总能量的相当一部分，这使得温度监测成为检测生物组织损伤的高效手段。