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2-Chloroethanol (2-CE) is a commonly used solvent in industry; unfortunately, severe hypotension is one of main toxic signs during intoxication. Calcium ion modulation is considered to be an important role of vasorelax- ation. The aim of this study is to evaluate either 2-CE or its main metabolite, chloroacetaldehyde (CAA), possible cause of hypotension, by using isolated rat aortic rings. Results revealed that 2-CE caused a weakly relaxation in the phenylephrine (PE) pre-induced endothelium-intact aortic rings. However, its metabolite, CAA induced vasore- laxation and showed dose dependency in endothelium-intact and -denuded aortic rings. The half inhibitory con- centration (IC50 )o f2 -CE exceeded 50 mM; meanwhile, the IC50 values of CAA in the endothelium-intact and -de- nuded aortic rings were 3.3 and 2.7 mM, respectively. The CAA-induced relaxation could be significantly attenu- ated by adding calcium (CaCl2 )a nd various Ca2+ channel blockers, dantrolene, nifedipine, and NiCl2 .N ifedipine presents the most strong inhibition effect among the calcium blockers. In conclusion, it is suggested that the hy- potension effect of 2-CE intoxicated cases may be mainly mediated by its metabolite CAA, and calcium channels are partially involved inducing the vasorelaxation.

Vasorelaxation Effects of 2-Chloroethanol and Chloroacetaldehyde in the Isolated Rat Aortic Rings