抄録
Previously we showed the existence of tenderness (DOMS) after lengthening contraction (LC) by nocifensive behavioral tests and c-Fos protein expression in the spinal dorsal horn in rats. The mechanical withdrawal threshold of the EDL muscle underwent LC decreased 1 day after LC and remained decreased up to 3 days after LC. It returned to the pre-LC value 4 days after LC (Taguchi, 2005). To know if inflammatory mediators are involved in DOMS, we examined effects of NSAIDS and BK receptor antagonists. We used two selective COX2 inhibitors, Zaltoprofen (additionally having BK blocking effect) and Celecoxib, and BK receptor antagonists (des-Arg-HOE 140 : B1 receptor antagonist, HOE-140 : B2 receptor antagonist). We administered these drugs 1 hr (NSAIDS, p.o.) or 0.5 hr (BK antagonists, s.c.) before LC and 2 days after LC. Zaltoprofen and Celecoxib (10 mg/kg) administered before LC blocked the development of the mechanical hyperalgesia, but failed to reverse the developed mechanical hyperalgesia when administered 2 days after LC. Zaltoprofen was effective at a lower dosage (5 mg/kg) than Celecoxib (10 mg/kg). Administration of HOE-140 before LC inhibited the development of mechanical hyperalgesia but des-Arg-HOE 140 did not. Both drugs failed to reverse the mechanical hyperalgesia when administered 2 days after LC. These results suggest that prostaglandins and BK through B2 receptor are involved in the development of mechanical hyperalgesia but not in its maintenance. [J Physiol Sci. 2007;57 Suppl:S112]
