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Titolo:
THROMBOLYTIC ACTIVITY OF BETA-ADRENOLYTIC DRUG, SOTALOL
Autore:
KORBUT R; SWIES J; MARCINKIEWICZ E; GRYGLEWSKI RJ;
Indirizzi:
JAGIELLONIAN UNIV,SCH MED,CHAIR PHARMACOL,GRZEGORZECKA 16 PL-31531 KRAKOW POLAND
Titolo Testata:
Journal of Physiology and Pharmacology
fascicolo: 1, volume: 49, anno: 1998,
pagine: 51 - 60
SICI:
0867-5910(1998)49:1<51:TAOBDS>2.0.ZU;2-K
Fonte:
ISI
Lingua:
ENG
Soggetto:
NITRIC-OXIDE; FIBRINOLYTIC-ACTIVITY; SODIUM-NITROPRUSSIDE; ENDOTHELIAL-CELLS; PROSTACYCLIN; PLATELETS; RELAXATION; INVIVO;
Keywords:
SOTALOL; BETA-ADRENORECEPTOR BLOCKING DRUGS; PROSTACYCLIN (PGI(2)); NITRIC OXIDE (NO); THROMBOLYSIS; FIBRINOLYSIS; THROMBORESISTANCE; EUGLOBULIN CLOT LYSIS TIME (ECLT); N-G-NITRO-L-ARGININE (L-NNA);
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
24
Recensione:
Indirizzi per estratti:
Citazione:
R. Korbut et al., "THROMBOLYTIC ACTIVITY OF BETA-ADRENOLYTIC DRUG, SOTALOL", Journal of Physiology and Pharmacology, 49(1), 1998, pp. 51-60

Abstract

Sotalol is a beta-adrenoreceptor blocking drug, the clinical efficacyof which has been linked up to its negative chrono-and inotropic effects and its hypotensive action. In addition, beta-adrenolytic drugs are known to inhibit platelet aggregation in vitro possibly through lowering of calcium ions level. Here, we report that in rats sotalol at a dose of 10-20 mg/kg i.v., apart from hypotension, evokes instantaneousthrombolytic effect. This is associated with an increase in plasma level of tissue plasminogen activator (t-PA). In vitro, sotalol at a concentration of 1-100 mu M inhibits thrombogenesis on surface of rabbit aorta endothelium superfused with blood. Sotalol also has a weak anti-aggregatory activity (IC50 similar to 500-1000 mu M) in human plateletrich plasma (PRP). Since the thrombolytic and fibrinolytic but not hypotensive effects of sotalol were inhibited by cyclooxygenase inhibitor, indomethacin, while its hypotensive but not thrombolytic potency was dimished by an inhibitor of nitric oxide synthase, N-G-nitro-L-arginine (L-NNA), we have linked up the sotalol-induced effects in vivo with the release of prostacyclin and nitric oxide. Our data point out to a possibility that prostacyclin and nitric oxide concomitantly released from endothelium and/or from other blood cells after administration of sotalol, may play different roles: prostacyclin may be responsible for fibrinolytic, thrombolytic and antithrombotic properties, while nitric oxide may take part in the mechanism of sotalol-induced hypotension.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 19/09/20 alle ore 08:48:58