Gelgor Linda, Phillips Sally, Mitchell Duncan
Department of Physiology, University of the Witwatersrand Medical School, Parktown, Johannesburg 2193 South Africa.
Pain. 1986 Feb;24(2):251-257. doi: 10.1016/0304-3959(86)90047-3.
We have investigated the effects of ischaemia on responses to a subsequent noxious stimulus in rats. Tail flick latencies to a noxious thermal stimulus were determined by immersing the tail in water at temperatures ranging from 39 to 49 degrees C. We then produced ischaemia by occluding the blood supply to the tail; ischaemia was terminated at the first signs of an escape response. Tail flick latencies were recorded immediately after termination of ischaemia and at 30 min intervals for another 2 h. Each rat acted as its own control. Tail flick latency decreased after ischaemia; we found a decrease of about 39% immediately after ischaemia, at immersion temperatures above 39 degrees C. The duration of the hyperalgesia increased with increasing water temperatures. Thus noxious ischaemia of the rat tail induced hyperalgesia to subsequent noxious thermal stimuli. The hyperalgesia could have arisen through either central or peripheral mechanisms.
我们研究了局部缺血对大鼠随后对伤害性刺激反应的影响。通过将大鼠尾巴浸入39至49摄氏度的水中，测定其对伤害性热刺激的甩尾潜伏期。然后通过阻断尾巴的血液供应制造局部缺血；在出现逃避反应的最初迹象时终止局部缺血。局部缺血终止后立即记录甩尾潜伏期，并在接下来的2小时内每隔30分钟记录一次。每只大鼠自身作为对照。局部缺血后甩尾潜伏期缩短；我们发现在高于39摄氏度的浸浴温度下，局部缺血后立即缩短约39%。痛觉过敏的持续时间随水温升高而增加。因此，大鼠尾巴的伤害性局部缺血会诱发对随后伤害性热刺激的痛觉过敏。痛觉过敏可能是通过中枢或外周机制产生的。
