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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.
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Gelgor et al. (1986) studied this question.
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