Enhanced inflammatory hyperalgesia after recovery from burn injury

Severe burn induces severe pain. While chronic as well as acute pain syndromes are reported, the peripheral mechanisms of burn-induced chronic pain syndromes have not been studied. We tested the hypothesis that burn induces plastic changes in primary afferent nociceptors that predispose to chronic pain states. Mechanical nociceptive thresholds were measured using the Randall–Selitto paw-withdrawal test in male Sprague-Dawley rats, before and following a small (<1% total body surface area) partial-thickness thermal injury to the dorsal surface of one hind paw. This burn induced mechanical hyperalgesia, which lasted over 2 weeks. After recovery, local injection of prostaglandin E2 (PGE2), to mimic re-injury, induced an enhanced and markedly prolonged mechanical hyperalgesia compared to the hyperalgesic effect of PGE2 in the control contralateral paw. This prolonged PGE2-induced hyperalgesia was reversed by a selective inhibitor of protein kinase C-epsilon (PKC ). Our findings suggest PKC as a peripheral mechanism for burn-induced chronic pain syndromes.