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Titolo:
DELAYED PROTECTION AGAINST ISCHEMIA-INDUCED VENTRICULAR ARRHYTHMIAS AND INFARCT SIZE LIMITATION BY THE PRIOR ADMINISTRATION OF ESCHERICHIA-COLI ENDOTOXIN
Autore:
SONG W; FURMAN BL; PARRATT JR;
Indirizzi:
UNIV STRATHCLYDE,DEPT PHYSIOL & PHARMACOL GLASGOW G1 1XW LANARK SCOTLAND UNIV STRATHCLYDE,DEPT PHYSIOL & PHARMACOL GLASGOW G1 1XW LANARK SCOTLAND
Titolo Testata:
British Journal of Pharmacology
fascicolo: 8, volume: 118, anno: 1996,
pagine: 2157 - 2163
SICI:
0007-1188(1996)118:8<2157:DPAIVA>2.0.ZU;2-P
Fonte:
ISI
Lingua:
ENG
Soggetto:
ISCHEMIA-REPERFUSION INJURY; TUMOR-NECROSIS-FACTOR; NITRIC-OXIDE SYNTHASE; CORONARY-ARTERY LIGATION; MYOCARDIAL ISCHEMIA; L-ARGININE; OXYGEN-CONSUMPTION; ANESTHETIZED RATS; STRESS PROTEIN; FACTOR-ALPHA;
Keywords:
ENDOTOXIN; CARDIAC ARRHYTHMIAS; INFARCT SIZE LIMITATION; DEXAMETHASONE; MYOCARDIAL ISCHEMIA;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
58
Recensione:
Indirizzi per estratti:
Citazione:
W. Song et al., "DELAYED PROTECTION AGAINST ISCHEMIA-INDUCED VENTRICULAR ARRHYTHMIAS AND INFARCT SIZE LIMITATION BY THE PRIOR ADMINISTRATION OF ESCHERICHIA-COLI ENDOTOXIN", British Journal of Pharmacology, 118(8), 1996, pp. 2157-2163

Abstract

1 Bacterial endotoxin (lipopolysaccharide derived from Escherichia coli) was injected intraperitoneally in conscious rats in doses ranging from 0.5 to 2.5 mg kg(-1). At various times afterwards the animals were anaesthetized and subjected to a 30 min period of left coronary artery occlusion. 2 Under these conditions the severity of ventricular arrhythmias was markedly suppressed, in comparison with saline-injected controls, but this was particularly marked with the higher doses (1.5 and 2.5 mg kg(-1)); the number of ventricular premature beats was reduced from 1687+/-227 over the 0.5 h coronary artery occlusion period to 190+/-46 in those rats administered 2.5 mg kg(-1) endotoxin 8 h previously (P <0.05). The duration of ventricular tachycardia was also significantly reduced (138+/-26 s to 8.9+/-4.2 s; P <0.01) and there was a reduction in the incidence of ventricular fibrillation (from 56% to 10%). 3 The time course of this protection was studied following the administration of a single dose of 2.5 mg kg(-1) of endotoxin by anaesthetizing rats 4, 8 or 24 h later. Protection was apparent at each time but was particularly marked at 8 h. 4 No rat given the highest dose of endotoxin (32 in all) died as a result of ventricular fibrillation, orfrom any other cause, during an occlusion, in contrast to a 26% mortality in the controls (P <0.01). 5 Infarct size, measured following a 30 min period of coronary artery occlusion followed by a 3 h reperfusion period, was reduced both 8 and 24 h after the administration of 2.5 mg kg(-1) endotoxin (reductions of 24.3 and 23.1% respectively; P <0.05). Endotoxin had no significant effect on the area at risk. 6 The beneficial effects of endotoxin infarct size and on ventricular arrhythmias were markedly attenuated by the prior administration of dexamethasone, 3 mg kg(-1) given 1 h prior to endotoxin administration. Dexamethasone itself reduced infarct size (P <0.05) but had no direct effect onarrhythmia severity following coronary artery occlusion. 7 The mechanisms of this 'cross-tolerance' induced by bacterial endotoxin against ischaemia-reperfusion injury remain to be elucidated but the most likely mechanisms appear to be the induction of protective enzymes or proteins (e.g. nitric oxide synthase, cyclo-oxygenase (COX) 2) probably mediated by cytokine release.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 11/07/20 alle ore 20:53:51