Vascular responsiveness to dimethylaminoethyl methacrylate and its degradation products

Worku Abebe, William F. Maddux, George S. Schuster, Jill B. Lewis

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

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 KATP 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 A2 (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 KATP channels, and the generation of vasorelaxant prostanoid(s) and TXA2. 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.

Original languageEnglish (US)
Pages (from-to)155-161
Number of pages7
JournalJournal of Biomedical Materials Research - Part A
Volume66
Issue number1
DOIs
StatePublished - Jul 1 2003

Fingerprint

Deanol
Methacrylates
Norepinephrine
Blood Vessels
Resins
Nitric oxide
Tissue
Endothelium
Degradation
Acids
Rats
Tissue homeostasis
Chemical activation
Dentistry
Arginine
Blood vessels
Metabolites
Biocompatibility
KATP Channels
Muscle

Keywords

  • DMAEMA
  • DME
  • Rat aorta
  • TXA
  • Vascular responsiveness

ASJC Scopus subject areas

  • Ceramics and Composites
  • Biomaterials
  • Biomedical Engineering
  • Metals and Alloys

Cite this

Vascular responsiveness to dimethylaminoethyl methacrylate and its degradation products. / Abebe, Worku; Maddux, William F.; Schuster, George S.; Lewis, Jill B.

In: Journal of Biomedical Materials Research - Part A, Vol. 66, No. 1, 01.07.2003, p. 155-161.

Research output: Contribution to journalArticle

Abebe, Worku ; Maddux, William F. ; Schuster, George S. ; Lewis, Jill B. / Vascular responsiveness to dimethylaminoethyl methacrylate and its degradation products. In: Journal of Biomedical Materials Research - Part A. 2003 ; Vol. 66, No. 1. pp. 155-161.
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