PSJ Web Site
J-STAGE
  Software Requirements
Microsoft Internet Explorer 5.01 or higher and Netscape Navigator 4.75 or higher are recommended.


J.Health Sci., 55(4), 525-531, 2009

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

Yng-Tay Chen,a Dong-Zong Hung,b Chi-Chung Chou,a Jaw-Jou Kang,c Yu-Wen Cheng,d Chien-Ming Hu,e and Jiunn-Wang Liao*, f

aDepartment of Veterinary Medicine, National Chung-Hsing University, 250, Kuo-Kuang Road, Taichung 40227, Taiwan, Republic of China, bToxicology Center, China Medical University Hospital, and Graduate Institute of Drug Safety, China Medical University, 2, Yuh-Der Rd., Taichung 40402, Taiwan, Republic of China cInstitute of Toxicology, College of Medicine, National Taiwan University, 1, Jen-Ai Road, Section 1, Taipei 10051, Taiwan, Republic of China, dSchool of Pharmacy, Taipei Medical University, 250, Wu-Shing Street, Taipei 11031, Taiwan, Republic of China, eEmergency Department, Taipei Medical University Hospital, 252, Wu-Shing Street, Taipei 11031, Taiwan, Republic of China and fGraduate Institute of Veterinary Pathobiology, National Chung-Hsing University, 250, Kuo-Kuang Road, Taichung 40227, Taiwan, Republic of China

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 vasorelaxation. 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 vasorelaxation and showed dose dependency in endothelium-intact and -denuded aortic rings. The half inhibitory concentration (IC50) of 2-CE exceeded 50 mM; meanwhile, the IC50 values of CAA in the endothelium-intact and -denuded aortic rings were 3.3 and 2.7 mM, respectively. The CAA-induced relaxation could be significantly attenuated by adding calcium (CaCl2) and various Ca2+ channel blockers, dantrolene, nifedipine, and NiCl2. Nifedipine presents the most strong inhibition effect among the calcium blockers. In conclusion, it is suggested that the hypotension effect of 2-CE intoxicated cases may be mainly mediated by its metabolite CAA, and calcium channels are partially involved inducing the vasorelaxation.