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ToxSci Advance Access originally published online on June 19, 2007
Toxicological Sciences 2007 99(1):354-361; doi:10.1093/toxsci/kfm167
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Published by Oxford University Press 2007.

Multiple Exposures to Sarin Vapor Result in Parasympathetic Dysfunction in the Eye but not the Heart

Paul A. Dabisch*,1, Filip To{dagger}, Edmund K. Kerut{ddagger}, Michael S. Horsmon* and Robert J. Mioduszewski*

* Operational Toxicology Team, U.S. Army Edgewood Chemical Biological Center, Aberdeen Proving Ground, Maryland 21010 {dagger} Department of Agricultural and Biological Engineering, Mississippi State University, Mississippi 39762 {ddagger} Louisiana State University School of Medicine, New Orleans, Louisiana 70112

1 To whom correspondence should be addressed at Operational Toxicology Team, US Army Edgewood Chemical Biological Center, ATTN: AMSRD-ECB-RT-TT, 5183 Blackhawk Road, Aberdeen Proving Ground, MD 21010-5424. Fax: (410) 436-7129. E-mail: paul.a.dabisch{at}us.army.mil.

Received April 19, 2007; accepted June 13, 2007


  Abstract

Several studies in conscious animals have reported parasympathetic dysfunction in the eyes following exposure to cholinesterase inhibitors. Given the similarities between the autonomic innervation in the eye and the heart, it is possible that parasympathetic dysfunction could also occur in the heart. Therefore, the present study assessed time domain indices of heart rate variability in conscious rats surgically implanted with telemetric transmitters to investigate the hypothesis that multiple exposures to the nerve agent sarin would result in muscarinic receptor desensitization and parasympathetic dysfunction in the heart. Animals exposed to sarin vapor on multiple occasions developed parasympathetic dysfunction in the eye characterized by an attenuated response to light and a diminished miotic response to sarin vapor exposure. However, the same dose of sarin vapor failed to produce any effects on either time domain indices of HRV or the magnitude of the tachycardia induced by atropine, suggesting that autonomic control in the heart was not affected. It is possible that the dose of sarin used in the present study was insufficient to inhibit cardiac acetylcholinesterase (AChE). Additional studies utilizing higher doses of sarin may be able to inhibit cardiac AChE, producing overstimulation of cardiac muscarinic receptors, ultimately resulting in desensitization and parasympathetic dysfunction.

Key Words: Sarin; organophosphate; heart rate variability; miosis; parasympathetic dysfunction.


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