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LEADER 03577nam 2200721Ia 4500

001 ocn227996336;

003 OCoLC;

005 20141212063332.0;

006 m d f ;

007 cr bn|||||||||;

008 080513s2002 mdua ob f000 0 eng d;

029 0 a| DTICEb| ADA402693;

035 a| (Sirsi) o227996336;

035 a| (OCoLC)227996336;

049 a| ERE#;

074 a| 0324-A-01 (online);

086 0 a| D 101.133:2738;

100 1 a| Zoltani, Csaba K.=| ^A1123599;

245 10 a| Organophosphonate caused cardiac toxicity :b| action potential dynamics in atrial tissue.;

260 a| Aberdeen Proving Ground, MD :b| U.S. Army Research Laboratory,c| [2002];

300 a| 1 online resource (viii, 15 pages) :b| illustrations.;

336 a| text2| rdacontent;

337 a| computer2| rdamedia;

338 a| online resource2| rdacarrier;

490 1 a| ARL-TR ;v| 2738;

500 a| Title from title screen (viewed on Feb. 24, 2011).;

500 a| "May 2002.";

500 a| DTIC reproduction in black and white.;

504 a| Includes bibliographical references (p. 11-12).;

506 a| Approved for public release.;

513 a| Final report;b| November 2000--August 2001.;

520 a| Highly effective treatments for the effect of organophosphonate and organophosphate (OP) nerve agents have eluded the medical community. It is known that acetylcholine overload is one of the effects of OP toxicity, but the cellular processes leading to cardiac toxicity are still incompletely understood. This study details high performance computer simulations of the electrophysiology in atrial toxicity. It shows that hyperkalemia of the tissue, one of the manifestations of OP intoxication, promotes the processes leading to reentry, a recursor of atrial fibrillation. Then, we demonstrate that changes in two of the potassium membrane currents, i(sub Kr) and i(sub Ks), can modulate the reentry process. This suggests that Class III anti-arrhythmic agents that primarily block these currents in the cardiac cells are important candidates for therapeutics of OP poisoning.;

536 a| U.S. Army Medical Research Institute of Chemical Defenseb| 1U590C 665803.731;

650 0 a| Cardiovascular toxicology.=| ^A1036883;

650 0 a| Phosphatesx| Physiological effect.=| ^A76078;

650 0 a| Acetylcholinex| Physiological effect.=| ^A800999;

650 17 a| Medicine and Medical Research.2| scgdst;

650 27 a| Chemical, Biological and Radiological Warfare.2| scgdst;

650 17 a| Toxicity.2| dtict;

650 17 a| Phosphonates.2| dtict;

650 17 a| Cardiovascular system.2| dtict;

650 17 a| Organic phosphorus compounds.2| dtict;

650 27 a| Computerized simulation.2| dtict;

650 27 a| Tissues(biology)2| dtict;

650 27 a| Poisoning.2| dtict;

650 27 a| Medical research.2| dtict;

650 27 a| Cells(biology)2| dtict;

650 27 a| Nerve agents.2| dtict;

650 27 a| Organophosphates.2| dtict;

650 27 a| Electrophysiology.2| dtict;

650 27 a| Acetylcholine.2| dtict;

650 27 a| Intoxication.2| dtict;

653 2 a| OP(ORGANOPHOSPHATES);

653 2 a| ATRIAL TISSUE;

700 1 a| Baskin, Steven I.=| ^A1024451;

710 2 a| U.S. Army Research Laboratory.=| ^A367731;

830 0 a| ARL-TR (Aberdeen Proving Ground, Md.) ;v| 2738.=| ^A566074;

856 40 u| http://purl.fdlp.gov/GPO/gpo4329;

949 a| Click on web addressw| ASISh| JOYNER94;

596 a| 1;

998 a| 2450325;

999 a| CLICK ON WEB ADDRESSw| ASISc| 1i| 2450325-1001l| JNETm| JOYNERr| Ys| Yt| JNE1DOu| 3/17/2011x| EDOCUMENTz| JERESOURCE;

Organophosphonate caused cardiac toxicity : action potential dynamics in atrial tissue.

Author/creator	Zoltani, Csaba K.
Other author	Baskin, Steven I.
Other author	U.S. Army Research Laboratory.
Format	Electronic
Publication Info	Aberdeen Proving Ground, MD : U.S. Army Research Laboratory, [2002]
Description	1 online resource (viii, 15 pages) : illustrations.
Supplemental Content	http://purl.fdlp.gov/GPO/gpo4329
Subjects	Cardiovascular toxicology. Phosphates--Physiological effect. Acetylcholine--Physiological effect.

Series	ARL-TR ; 2738 ARL-TR (Aberdeen Proving Ground, Md.) ; 2738. ^A566074
Abstract	Highly effective treatments for the effect of organophosphonate and organophosphate (OP) nerve agents have eluded the medical community. It is known that acetylcholine overload is one of the effects of OP toxicity, but the cellular processes leading to cardiac toxicity are still incompletely understood. This study details high performance computer simulations of the electrophysiology in atrial toxicity. It shows that hyperkalemia of the tissue, one of the manifestations of OP intoxication, promotes the processes leading to reentry, a recursor of atrial fibrillation. Then, we demonstrate that changes in two of the potassium membrane currents, i(sub Kr) and i(sub Ks), can modulate the reentry process. This suggests that Class III anti-arrhythmic agents that primarily block these currents in the cardiac cells are important candidates for therapeutics of OP poisoning.
General note	Title from title screen (viewed on Feb. 24, 2011).
General note	"May 2002."
General note	DTIC reproduction in black and white.
Bibliography note	Includes bibliographical references (p. 11-12).
Access restriction	Approved for public release.
Report note	Final report; November 2000--August 2001.
Funding information	U.S. Army Medical Research Institute of Chemical Defense 1U590C 665803.731
GPO item number	0324-A-01 (online)
Govt. docs number	D 101.133:2738

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Organophosphonate caused cardiac toxicity : action potential dynamics in atrial tissue.

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