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Titolo:
Effects of atropine sulphate on seizure activity and brain damage producedby soman in guinea-pigs: ECoG correlates of neuropathology
Autore:
Carpentier, P; Foquin, A; Rondouin, G; Lerner-Natoli, M; de Groot, DMG; Lallement, G;
Indirizzi:
Ctr Rech, Serv Sante Armees, Unite Neuropharmacol, F-38702 La Tronche, France Ctr Rech La Tronche France F-38702 pharmacol, F-38702 La Tronche, France Ecole Natl Super Chim Montpellier, CNRS UPR 8402, INSERM U249, F-34053 Montpellier 1, France Ecole Natl Super Chim Montpellier Montpellier France 1pellier 1, France TNO, Nutr & Food Res Inst, NL-3700 AJ Zeist, Netherlands TNO Zeist Netherlands NL-3700 AJ Res Inst, NL-3700 AJ Zeist, Netherlands
Titolo Testata:
NEUROTOXICOLOGY
fascicolo: 4, volume: 21, anno: 2000,
pagine: 521 - 540
SICI:
0161-813X(200008)21:4<521:EOASOS>2.0.ZU;2-J
Fonte:
ISI
Lingua:
ENG
Soggetto:
CHOLINESTERASE INHIBITOR SOMAN; CONVULSIVE STATUS EPILEPTICUS; RAT HIPPOCAMPUS; LONG-TERM; INTOXICATED RATS; POISONED RATS; PYRIDOSTIGMINE; ELECTROENCEPHALOGRAM; ACETYLCHOLINE; STRESS;
Keywords:
soman; atropine sulphate; pyridostigmine; analogue ECoG; ECoG power spectrum analysis; neuropathology; guinea-pig;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
73
Recensione:
Indirizzi per estratti:
Indirizzo: Carpentier, P Ctr Rech, Serv Sante Armees, Unite Neuropharmacol, BP 87, F-38702 La Tronche, France Ctr Rech BP 87 La Tronche France F-38702 La Tronche, France
Citazione:
P. Carpentier et al., "Effects of atropine sulphate on seizure activity and brain damage producedby soman in guinea-pigs: ECoG correlates of neuropathology", NEUROTOXICO, 21(4), 2000, pp. 521-540

Abstract

The present study describes the effects of pyridostigmine (PYR; 0.2 mg/kg)and atropine sulphate (AS; 5 mg/kg) on guinea-pigs intoxicated by a high dose (2xLD50) of the organophosphate compound, oman, an irreversible inhibitor of acetylcholinesterase. The medication was shown to counteract the acute respiratory distress and lethality normally produced by the intoxication. Moreover, due to the central activity of AS, soman-induced electrocorticographic (ECoG) seizure activity was either totally prevented, or reduced in duration and overall intensity. In addition, as established in the 24-hr survivors, seizure-related neuropathology was either prevented, or reduced intopographical extent and severity. An attempt to correlate our electrographic and morphological findings gives evidence that (a), the occurrence of seizure activity is the primary factor necessary for the development of acute neuropathology; (b) the duration of ECoG seizures is a secondary factor, on which the topographical distribution of brain damage finally depends; (c), the minimal duration of seizures necessary to produce 24 hr-damage in the most sensitive areas (e.g. the amygdala) is less than 70 min; (d), the overall intensity/power of epileptifbrm discharges is a tertiary factor whichinfluences the severity of damage; (e), in addition, ECoG power spectral analysis suggested that an acute increase of relative power in the lower (delta) frequency band might be a real-time external marker of the starting cerebral lesions and is thus predictive for their future installation. All these data confirm the tight relationships which exist between seizure activity and neuropathology in soman poisoning, and suggest that refined, standardized analysis of electrographic parameters drawn from ECoG tracings and power spectrum might serve as a useful tool to predict the presence, localization, and severity of soman-induced brain damage. (C) 2000 Intox Press, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/11/20 alle ore 15:35:21