摘要

Ischemic-reperfusion (I/R) is common in various pathological conditions like diabetic complication, complex regional pain syndrome type 11 (CRPS 11), necrotizing vascular occlusive disease and trauma. We have developed an animal model of ischemic-reperfusion injury induced nociceptive sensory neuropathy in rats. The model was validated after 2,4 and 6 h of ischemia followed by prolonged reperfusion. The sensory behavioral assessment revealed thermal and mechanical hyperalgesia in paw and in tail which expressed the peripheral and central neuropathic pain respectively. We observed a decrease in the serum IL-10 and nerve conduction velocity and increase in the serum nitrate, malondialdehyde (MDA) and TNF-alpha levels in the 4 and 6 h I/R groups in biochemical and electrophysiological evaluations. Histo pathological study had revealed the decrease in nerve fiber density in the moderate and severe I/R groups. We selected the moderate (4 h) ischemic-reperfusion injury as beneficial model because of the good correlation with clinical status for the development of neuropathy in human associated with severe pain disorders. This model can be used to explore pathophysiological mechanisms implied in the genesis of neuropathic pain and also to evaluate the new analgesic agents, peripheral neuro-vasoactive substances and neuroprotective drugs.

  • 出版日期2010-2-15