Marsala M, Vanicky I, Yaksh T L
Department of Anesthesiology, University of California, San Diego, La Jolla 92093.
Stroke. 1994 Oct;25(10):2038-46. doi: 10.1161/01.str.25.10.2038.
We used a rat model of reversible spinal ischemia to assess the effect of spinal cord temperature on the development of neurological and histopathologic changes after 20 minutes of reversible aortic occlusion. Spinal cord blood flow and CO2 reactivity was tested by using laser Doppler before and 60 minutes after ischemia.
In halothane (1%)-anesthetized rats, the spinal cord temperature as assessed by using thermocouple in the paraspinal muscles was lowered to 34 degrees, 31 degrees, or 27 degrees C. After ischemia, spinal cord temperature was raised to 37 degrees C for the next 30 minutes. Animals were maintained in this normothermic condition for 8 hours, after which motor and sensory function were assessed. All animals were then anesthetized and perfused with 10% formalin for light microscopic analysis of spinal cords.
In normothermic animals, 20 minutes of ischemia resulted in a loss of CO2 reactivity and hind limb paraplegia with an attendant allodynia that persisted for the 8 hours of reperfusion. Even mild (34 degrees C) hypothermia resulted in significant improvement of neurological function compared with the normothermic group. In paraplegic animals, lumbosacral interneuronal pools localized primarily in laminae III through VII displayed heavy argyrophilic neurons and areas of localized necrosis. In moderate and deep hypothermic animals preservation of CO2 responsivity and complete recovery of neurological function were seen with no detectable histopathologic changes.
These results show that a slight decrease in spinal cord temperature in the peri-ischemic period provides significant protection as measured by histopathology and neurological function.
我们使用可逆性脊髓缺血大鼠模型，以评估脊髓温度对可逆性主动脉阻断20分钟后神经和组织病理学变化发展的影响。在缺血前及缺血60分钟后，使用激光多普勒检测脊髓血流和二氧化碳反应性。
在氟烷（1%）麻醉的大鼠中，通过椎旁肌中的热电偶评估，将脊髓温度降至34℃、31℃或27℃。缺血后，接下来30分钟将脊髓温度升至37℃。动物在这种正常体温条件下维持8小时，之后评估运动和感觉功能。然后将所有动物麻醉并用10%福尔马林灌注，以对脊髓进行光镜分析。
在正常体温的动物中，20分钟的缺血导致二氧化碳反应性丧失和后肢截瘫，并伴有持续8小时再灌注的伴随性痛觉过敏。与正常体温组相比，即使是轻度（34℃）低温也导致神经功能显著改善。在截瘫动物中，主要位于Ⅲ至Ⅶ层的腰骶中间神经元池显示嗜银神经元大量增加和局部坏死区域。在中度和深度低温的动物中，观察到二氧化碳反应性得以保留且神经功能完全恢复，未检测到组织病理学变化。
这些结果表明，在缺血周围期脊髓温度轻微降低，从组织病理学和神经功能方面衡量可提供显著保护。
