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Titolo:
THROMBIN-INDUCED ENDOTHELIUM-DEPENDENT INHIBITION AND DIRECT ACTIVATION OF PLATELET-VESSEL WALL INTERACTION ROLE OF PROSTACYCLIN, NITRIC-OXIDE, AND THROMBOXANE A(2)
Autore:
YANG ZH; ARNET U; BAUER E; VONSEGESSER L; SIEBERMANN R; TURINA M; LUSCHER TF;
Indirizzi:
UNIV BERN,INSELSPITAL,DIV CARDIOL CH-3010 BERN SWITZERLAND UNIV BASEL HOSP,DEPT MED,DIV CLIN PHARMACOL CH-4031 BASEL SWITZERLAND UNIV BASEL HOSP,DEPT MED,DIV CARDIOL CH-4031 BASEL SWITZERLAND UNIV BASEL HOSP,DEPT RES,VASC RES LAB CH-4031 BASEL SWITZERLAND UNIV ZURICH HOSP,DEPT CARDIOVASC SURG CH-8091 ZURICH SWITZERLAND
Titolo Testata:
Circulation
fascicolo: 5, volume: 89, anno: 1994,
pagine: 2266 - 2272
SICI:
0009-7322(1994)89:5<2266:TEIADA>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
CORONARY-BYPASS GRAFTS; RELAXING FACTOR; L-ARGININE; SYNTHETASE INHIBITION; VASCULAR CONTRACTIONS; SAPHENOUS-VEIN; ONE MOLECULE; ARTERIES; RELAXATION; RECEPTOR;
Keywords:
ARTERIES; N-G-NITRO-L-ARGININE METHYL ESTER; RIDOGREL; SQ-30741;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
46
Recensione:
Indirizzi per estratti:
Citazione:
Z.H. Yang et al., "THROMBIN-INDUCED ENDOTHELIUM-DEPENDENT INHIBITION AND DIRECT ACTIVATION OF PLATELET-VESSEL WALL INTERACTION ROLE OF PROSTACYCLIN, NITRIC-OXIDE, AND THROMBOXANE A(2)", Circulation, 89(5), 1994, pp. 2266-2272

Abstract

Background Platelet-vessel wall interaction plays an important role in acute cardiovascular disorders. Thrombin is a potent platelet activator but also has profound effects on the endothelium. Endothelial cells possess antithrombotic activity by releasing nitric oxide and prostacyclin, both potent vasodilators and platelet inhibitors. We studied the role of thrombin as a regulator of platelet-vessel wall interactionin isolated human arteries suspended in organ chambers for isometric tension recording. Methods and Results In arteries with endothelium, thrombin (0.01 to 1 U/mL) induced endothelium-dependent relaxations, which were reduced by the nitric oxide synthase inhibitor N-G-nitro-L-arginine methyl ester (L-NAME; 10(-4) mol/L) and/or indomethacin (10(-5)mol/L). Human platelets (75 000/mu L) evoked only marginal contractions in arteries with endothelium (3+/-3% of the contraction to KCI 100 mmol/L; NS), which were markedly enhanced by endothelial removal (22+/-4%; P<.05). Thrombin (1 U/mL) did not affect the response to platelets in arteries with (6+/-5%; NS) but induced a huge contraction in rings without endothelium (53+/-6%; P<.01 versus control without endothelium). The potent contraction to thrombin-activated platelets (1000 to 75 000/mu L) in arteries without endothelium was markedly inhibited by the thromboxane A(2) synthetase/receptor antagonist ridogrel (10(-5) mol/L; P<.005 versus control) and the single-acting thromboxane receptor blocker SQ-30741 (10(-7) mol/L; P<.01 versus control). Conclusions Thus, thrombin directly stimulates platelets to release thromboxane A(2), inducing potent vasoconstriction, which is prevented by the simultaneous thrombin-induced release of prostacyclin and nitric oxide from endothelial cells. In arteries devoid of functional endothelial cells, as occurs in patients with coronary artery disease, a combined inhibition of thromboxane production and action provides a potent therapeutictool to interfere with the thrombin-induced activation of platelet-vessel wall interaction.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 12/07/20 alle ore 03:17:26