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Titolo:
Cerebroprotective drugs shorten the hypoxia-induced onset of electrical silence in unanesthetized rats
Autore:
Zagvazdin, Y; Bodo, M; Sarkadi, A; Szporny, L;
Indirizzi:
Nova SE Univ, Coll Med Sci, Ft Lauderdale, FL 33328 USA Nova SE Univ Ft Lauderdale FL USA 33328 Sci, Ft Lauderdale, FL 33328 USA Natl Stroke Prevent Fdn, Silver Spring, MD 20904 USA Natl Stroke Prevent Fdn Silver Spring MD USA 20904 r Spring, MD 20904 USA Gedeon Richter Ltd, Chem Works, Budapest, Hungary Gedeon Richter Ltd Budapest Hungary Ltd, Chem Works, Budapest, Hungary
Titolo Testata:
PHARMACOLOGICAL RESEARCH
fascicolo: 3, volume: 42, anno: 2000,
pagine: 261 - 268
SICI:
1043-6618(200009)42:3<261:CDSTHO>2.0.ZU;2-R
Fonte:
ISI
Lingua:
ENG
Soggetto:
BLOOD-FLOW; BRAIN; PROTECTION; MICE; ISCHEMIA; HYPOTHERMIA; VINPOCETINE; SUPPRESSION; IDEBENONE; NEURONS;
Keywords:
hypoxia; isoelectric EEC; cerebroprotective drugs; cerebral blood flow; rat;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
50
Recensione:
Indirizzi per estratti:
Indirizzo: Bodo, M 212 Eldrid Dr, Silver Spring, MD 20904 USA 212 Eldrid Dr Silver Spring MD USA 20904 ver Spring, MD 20904 USA
Citazione:
Y. Zagvazdin et al., "Cerebroprotective drugs shorten the hypoxia-induced onset of electrical silence in unanesthetized rats", PHARMAC RES, 42(3), 2000, pp. 261-268

Abstract

Pharmacological agents that delay the hypoxic arrest of neuronal electrical activity, as indicated by the suppression of electroencephalogram (EEG), have previously been thought to increase brain resistance to oxygen insufficiency. On the other hand, acceleration of the EEG suppression may offer some protection against severe hypoxia by reducing neuronal energy spending on electrogenesis. In unanesthetized rats we examined the effects of severalantihypoxic drugs on the time of appearance of isoelectric EEG (tiEEG), caused by normobaric hypoxia. In addition, alterations in cerebral blood flowinduced by hypoxia and by some drugs were monitored using polarographic techniques to determine if cerebrocirculatory changes play a significant rolein the drug effects on tiEEG. We also assessed drug effects on behavioral recovery after hypoxia by measuring the latency of restoration of the head-withdrawal reflex upon vibrissae stimulation. Pentobarbital (30 and 60 mg kg(-1) i.p.), chloralhydrate (400 mg kg(-1) i.p.) flunarizine (50-100 mg kg(-1) p.o.), hydergine (3-50 mg kg(-1) p.o.), nicergoline (50 mg kg(-1) and 85 mg kg(-1) p.o.), sabeluzole (3 and 7.5 mg kg(-1) i.p.) and vincamine (80 mg kg(-1) p.o.) reduced tiEEG (mean 27.1 +/- 3.3 min prior to drugs). In contrast, idebenone (29-85 mg kg(-1) p.o.) and vinpocetine (29-85 mg kg(-1) p.o.) had no significant effects on tiEEG. The divergent effects on cerebralblood how suggest an insignificant role fur cerebrocirculatory changes in the drug-induced reduction of tiEEG during severe hypoxia. The drug effectson recovery of the head-withdrawal reflex (mean 4.2 +/- 1.3 min prior to drugs) varied from a delay (sabeluzole) to acceleration (flunarizine) with no correlation to the effects on tiEEG, suggesting that EEG criteria alone may not predict the course of functional recovery. (C) 2000 Academic Press.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/09/20 alle ore 23:36:43