Nozaki-Taguchi N, Yaksh T L
Department of Anesthesiology, University of California, San Diego, La Jolla 92093-0818, USA.
Neurosci Lett. 1998 Sep 18;254(1):25-8. doi: 10.1016/s0304-3940(98)00648-x.
Secondary hyperesthesia was investigated in a rat thermal injury model. After a mild focal thermal injury (52 degrees C/45 s) to the rat heel, the response latency for a thermal stimulus directed at the injured site was reduced (10 --> 6 s; e.g. primary thermal hyperalgesia) but no change was seen at the distal site. Conversely, tactile threshold at the distal site was significantly reduced (15 --> 5 g; e.g. secondary tactile allodynia) but much less so at the injured site. Magnitude of the secondary tactile allodynia paralleled the severity of the primary injury. Accordingly, this model has the same characteristics seen in human post-tissue-injury hyperesthetic states and provides a tool for the study of mechanisms underlying primary and secondary hyperesthesia.
在大鼠热损伤模型中研究了继发性感觉过敏。对大鼠足跟进行轻度局灶性热损伤(52摄氏度/45秒)后,针对受伤部位的热刺激反应潜伏期缩短(10 --> 6秒;例如原发性热痛觉过敏),但在远端部位未见变化。相反,远端部位的触觉阈值显著降低(15 --> 5克;例如继发性触觉异常性疼痛),但在受伤部位降低程度较小。继发性触觉异常性疼痛的程度与原发性损伤的严重程度平行。因此,该模型具有人类组织损伤后感觉过敏状态中所见的相同特征,并为研究原发性和继发性感觉过敏的潜在机制提供了一种工具。