Abebe Worku, Maddux William F, Schuster George S, Lewis Jill B
Department of Oral Biology and Maxillofacial Pathology, School of Dentistry, CB 3710, Medical College of Georgia, Augusta, Georgia 30912-1128, USA.
J Biomed Mater Res A. 2003 Jul 1;66(1):155-61. doi: 10.1002/jbm.a.10568.
The increasing use of acrylate-based resins in dentistry has raised questions about the biocompatibility of these substances with oral tissues. The focus of the present investigation was to assess the responsiveness of blood vessels to the resin polymerization accelerating agent dimethylaminoethyl methacrylate (DMAEMA) and its degradation products dimethylethanolamine (DME) and methacrylic acid (MAA), using the rat aortic ring preparation as a tissue model. DMAEMA induced concentration-dependent relaxation of norepinephrine (NE)-contracted aortic rings with and without endothelium. N-nitro-L-arginine methyl ester (L-NAME) selectively inhibited the endothelium-dependent relaxation induced by DMAEMA, suggesting the release of nitric oxide from the endothelium by DMAEMA. Both indomethacin and glybenclamide attenuated the vasorelaxation elicited by DMAEMA in the presence as well as in the absence of endothelium, providing evidence for the role of vasorelaxant prostanoid(s) and K(ATP) channel activation in the responses observed. On the other hand, while MAA was without any apparent effect on the rat aorta, DMAEMA at high and DME at relatively low concentrations caused contraction of the tissues with and without endothelium in the absence of NE. The DME-induced contraction was inhibited by indomethacin, suggesting the involvement of contractile arachidonic acid metabolite(s) in the action of DME. This observation was supported by the findings of increased thromboxane A(2) (TXA(2)) production in aortic rings incubated with DME. Taken together, the data suggest that both DMAEMA and its degradation product, DME, are vasoactive, inducing vasorelaxation and contraction by various mechanisms that may involve the release of nitric oxide from the endothelium, the activation of smooth muscle K(ATP) channels, and the generation of vasorelaxant prostanoid(s) and TXA(2). These effects may play a role in tissue homeostasis and certain adverse conditions associated with the use of dental resin materials containing DMAEMA and/or DME.
牙科领域中丙烯酸酯基树脂使用的日益增加引发了关于这些物质与口腔组织生物相容性的问题。本研究的重点是使用大鼠主动脉环制备作为组织模型，评估血管对树脂聚合促进剂甲基丙烯酸二甲氨基乙酯（DMAEMA）及其降解产物二甲基乙醇胺（DME）和甲基丙烯酸（MAA）的反应性。DMAEMA在有内皮和无内皮的情况下均能诱导去甲肾上腺素（NE）收缩的主动脉环出现浓度依赖性舒张。N-硝基-L-精氨酸甲酯（L-NAME）选择性抑制DMAEMA诱导的内皮依赖性舒张，表明DMAEMA可使内皮释放一氧化氮。吲哚美辛和格列本脲在有内皮和无内皮的情况下均能减弱DMAEMA引起的血管舒张，这为血管舒张性前列腺素和K（ATP）通道激活在观察到的反应中的作用提供了证据。另一方面，虽然MAA对大鼠主动脉没有明显影响，但在无NE的情况下，高浓度的DMAEMA和相对低浓度的DME会导致有内皮和无内皮的组织收缩。吲哚美辛可抑制DME诱导的收缩，提示收缩性花生四烯酸代谢产物参与了DME的作用。与DME孵育的主动脉环中血栓素A2（TXA2）生成增加的结果支持了这一观察。综上所述，数据表明DMAEMA及其降解产物DME均具有血管活性，通过多种机制诱导血管舒张和收缩，这些机制可能涉及内皮释放一氧化氮、平滑肌K（ATP）通道激活以及血管舒张性前列腺素和TXA2的生成。这些作用可能在组织稳态以及与使用含DMAEMA和/或DME的牙科树脂材料相关的某些不良状况中发挥作用。
