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Titolo:
ENDOGENOUS AND EXOGENOUS NITRIC-OXIDE PROTECT AGAINST INTRACORONARY THROMBOSIS AND REOCCLUSION AFTER THROMBOLYSIS
Autore:
YAO SK; AKHTAR S; SCOTTBURDEN T; OBER JC; GOLINO P; BUJA LM; CASSCELLS W; WILLERSON JT;
Indirizzi:
UNIV TEXAS,SCH MED,DEPT INTERNAL MED,POB 20708 HOUSTON TX 77225 UNIV TEXAS,SCH MED,DEPT INTERNAL MED HOUSTON TX 77225 UNIV TEXAS,SCH MED,TEXAS HEART INST,CULLEN CARDIOVASC RES LAB HOUSTONTX 00000 UNIV TEXAS,SCH MED,DEPT PATHOL HOUSTON TX 00000 UNIV TEXAS,SCH MED,MED LAB HOUSTON TX 00000 UNIV NAPLES,SCH MED 2,DIV CARDIOL I-80138 NAPLES ITALY
Titolo Testata:
Circulation
fascicolo: 4, volume: 92, anno: 1995,
pagine: 1005 - 1010
SICI:
0009-7322(1995)92:4<1005:EAENPA>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACUTE MYOCARDIAL-INFARCTION; TISSUE PLASMINOGEN-ACTIVATOR; CANINE CORONARY-ARTERIES; CYCLIC FLOW VARIATIONS; RELAXING FACTOR; PLATELET-AGGREGATION; SODIUM-NITROPRUSSIDE; DELAYS REOCCLUSION; ENDOTHELIUM; HEPARIN;
Keywords:
ENDOTHELIUM-DERIVED RELAXING FACTORS; PLATELETS; THROMBOLYSIS; THROMBOSIS; OCCLUSIONS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
50
Recensione:
Indirizzi per estratti:
Citazione:
S.K. Yao et al., "ENDOGENOUS AND EXOGENOUS NITRIC-OXIDE PROTECT AGAINST INTRACORONARY THROMBOSIS AND REOCCLUSION AFTER THROMBOLYSIS", Circulation, 92(4), 1995, pp. 1005-1010

Abstract

Background Nitric oxide (NO), an endothelium-derived relaxing factor,plays an important role in regulating platelet activation. We evaluated the effect of NO in a canine model of intracoronary thrombosis, thrombolysis, and reocclusion. Methods and Results Before thrombosis was induced, 34 anesthetized dogs were treated with a continuous intracoronary infusion of saline (n=8); N-G-nitro-L-arginine (L-NNA, n=8), an inhibitor of NO synthetase; L-arginine (n=7), the precursor for NO; or sodium nitroprusside (SNP, n=11), an NO donor. Ten minutes after the infusion was begun, an electric current of 150 mu A was applied to the endothelium of coronary arteries to induce thrombosis. Occlusive thrombi developed in all dogs in the saline group (38+/-4 minutes) and the L-NNA group (30+/-6 minutes), in 6 of 7 dogs in the L-arginine group (81+/-18 minutes), and in 6 of 11 dogs in the SNP group (102+/-21 minutes) (P<.01). The time to thrombus was prolonged by L-arginine (P<.05) and SNP (P<.01). After 3 hours of thrombus formation in coronary arteries, tissue plasminogen activator and heparin were administered intravenously. Thrombi were lysed in 4 (of 8) dogs in the saline group (71+/-8 minutes), in 4 (of 8) dogs in the L-NNA group (72+/-8 minutes), in 4 (of 6) dogs in the L-arginine group (50+/-14 minutes), and in 4 (of 6) dogs in the SNP group (49+/-11 minutes) (P>.05). After thrombolysis, coronary artery reocclusion developed in all reperfused dogs in the saline group (30+/-8 minutes) and in the L-NNA group (48+/-12 minutes), in 3 (of 4) reperfused dogs in the L-arginine group (123+/-26 minutes), and in 3 (of 4) reperfused dogs in the SNP group (128+/-19 minutes) (P<.01). The ex vivo platelet aggregation induced by collagen was inhibited after in vivo treatment with L-arginine or SNP. Conclusions Increasing NO production or giving an NO donor may inhibit platelet aggregation and delay intracoronary thrombus formation and reocclusion after thrombolysis.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/04/20 alle ore 02:11:21