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首页> 外文期刊>Journal of biomedical materials research. Part B, Applied biomaterials. >Vascular responsiveness to dimethylaminoethyl methacrylate and its degradation products.
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Vascular responsiveness to dimethylaminoethyl methacrylate and its degradation products.

机译：对甲基丙烯酸二甲氨基乙酯及其降解产物的血管反应性。

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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.
机译：丙烯酸酯类树脂在牙科中的使用越来越多，引起了人们对这些物质与口腔组织的生物相容性的疑问。本研究的重点是使用大鼠主动脉环制剂作为组织模型，评估血管对树脂聚合促进剂甲基丙烯酸二甲基氨基乙酯（DMAEMA）及其降解产物二甲基乙醇胺（DME）和甲基丙烯酸（MAA）的响应能力。 。 DMAEMA诱导有或没有内皮的去甲肾上腺素（NE）收缩的主动脉环的浓度依赖性松弛。 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，提示DMAEMA从内皮释放一氧化氮。吲哚美辛和格列本脲在存在和不存在内皮的情况下均减弱了DMAEMA引起的血管舒张作用，为血管舒张性前列腺素和K（ATP）通道活化在观察到的反应中的作用提供了证据。另一方面，虽然MAA对大鼠主动脉没有任何明显影响，但高浓度的DMAEMA和相对低浓度的DME会导致在缺乏NE的情况下有或无内皮的组织收缩。吲哚美辛抑制了DME诱导的收缩，表明收缩型花生四烯酸代谢物参与了DME的作用。这一发现得到了血栓烷A（2）（TXA（2））生产在与DME孵育的主动脉环中增加的发现的支持。两者合计，数据表明DMAEMA及其降解产物DME均具有血管活性，并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中一氧化氮的释放，平滑肌K（ATP）通道的激活以及血管松弛素类前列腺素和TXA（2）的产生。这些作用可能在组织稳态和与使用含有DMAEMA和/或DME的牙科树脂材料相关的某些不利条件中起作用。

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