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ToxSci Advance Access published online on October 20, 2004
Toxicological Sciences, doi:10.1093/toxsci/kfi010
Toxicological Sciences © Society of Toxicology 2004; all rights reserved
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Received May 20, 2004
Accepted September 6, 2004

Respiratory Toxicology

Effects of Trichloroethylene and Perchloroethylene on Muscle Contractile Responses and Epithelial Prostaglandin Release and Acetylcholinesterase Activity in Swine Trachea

Hwei-Hsien Chen 1, Yi-Ruu Lin 2, Quan-Guo Peng 1, and Ming-Huan Chan 3*

1 Institute of Pharmacology and Toxicology, Tzu Chi University, No 701, Section 3, Chung Yang Road, Hualien 970, Taiwan
2 Institute of Medical Sciences, Tzu Chi University, No 701, Section 3, Chung Yang Road, Hualien 970, Taiwan
3 Institute of Pharmacology and Toxicology, Tzu Chi University, No 701, Section 3, Chung Yang Road, Hualien 970, Taiwan; Department of Pharmacology, Tzu Chi University, No 701, Section 3, Chung Yang Road, Hualien 970, Taiwan

* To whom correspondence should be addressed.
Ming-Huan Chan, E-mail: ming{at}mail.tcu.edu.tw


  Abstract

Trichloroethylene (TCE) and perchloroethylene (PERC) have been reported to induce respiratory complications such as airway hyperactivity and asthma. The present study was to investigate their influence on smooth muscle contraction and epithelial release of prostanoids in swine trachea. Results showed that TCE and PERC exposure did not alter the basal tone of tracheal smooth muscle. However, TCE and PERC concentration-dependently increased the ACh- and high K+-induced muscle contraction. In addition to potentiation of muscle contractile responses evoked by ACh or histamine, pretreatment of smooth muscle with PERC at higher concentration significantly suppressed the relaxant ability of beta-adrenergic agonist. The epithelial PGE2, but not PGD2, release from tracheal epithelium was significantly increased by TCE and PERC. The AChE activity of tracheal epithelia was reduced by TCE and PERC. In conclusion, our results suggest that the enhancement of spasmogen-evoked muscle contractile responses and epithelial PGE2 secretion as well as reduction of epithelial AChE activity may participate in airway impairment and hyperresponsiveness after TCE and PERC exposure.

Keywords: Tricholoroetylene; Perchloroethylene; Trachea; Swine; Prostaglandin; Acetylcholinesterase.
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