Abelson Klas S P, Kommalage Mahinda, Höglund A Urban
Department of Neuroscience, Division of Comparative Medicine, Biomedical Center, Uppsala University, P.O. Box 572, S-751 23 Uppsala, Sweden.
Neurosci Lett. 2004 Sep 16;368(1):116-20. doi: 10.1016/j.neulet.2004.06.070.
Aspirin and paracetamol have been shown to suppress non-inflammatory pain conditions like thermal, visceral and mechanical pain in mice and rats. The non-inflammatory antinociception appears to be mediated by central receptor mechanisms, such as the cholinergic system. In this study, we tested the hypothesis that the non-inflammatory antinociception of aspirin and paracetamol could be mediated by an increase of intraspinal acetylcholine release. Microdialysis probes were placed intraspinally in anesthetized rats for acetylcholine sampling. Subcutaneously administered aspirin 100 and 300 mg/kg increased, while paracetamol 300 mg/kg decreased intraspinal acetylcholine release. Intraspinal drug administration did not affect acetylcholine release. Our results suggest that an increased intraspinal acetylcholine release could be involved in part of the non-inflammatory pain suppression by aspirin, but not by paracetamol.
阿司匹林和对乙酰氨基酚已被证明可抑制小鼠和大鼠的非炎性疼痛状况,如热痛、内脏痛和机械性疼痛。非炎性抗伤害感受似乎由中枢受体机制介导,如胆碱能系统。在本研究中,我们检验了以下假设:阿司匹林和对乙酰氨基酚的非炎性抗伤害感受可能通过脊髓内乙酰胆碱释放增加来介导。将微透析探针置于麻醉大鼠的脊髓内以采集乙酰胆碱。皮下注射100和300mg/kg的阿司匹林可增加脊髓内乙酰胆碱释放,而300mg/kg的对乙酰氨基酚则降低脊髓内乙酰胆碱释放。脊髓内给药不影响乙酰胆碱释放。我们的结果表明,脊髓内乙酰胆碱释放增加可能部分参与了阿司匹林对非炎性疼痛的抑制作用,但对乙酰氨基酚并非如此。