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Titolo:
THE MECHANISM OF ANTITHROMBOTIC, THROMBOL YTIC AND FIBRINOLYTIC ACTIONS OF CAMONAGREL - A NEW THROMBOXANE SYNTHASE INHIBITOR
Autore:
GRYGLEWSKI RJ; SZCZEKLIK A; KORBUT R; SWIES J; MUSIAL J; KRZANOWSKI M; MAGA P;
Indirizzi:
JAGIELLONIAN UNIV,COLL MED,DEPT PHARMACOL,16 GRZEGORZECKA PL-31531 KRAKOW POLAND JAGIELLONIAN UNIV,COLL MED,DEPT MED KRAKOW POLAND
Titolo Testata:
Wiener Klinische Wochenschrift
fascicolo: 9, volume: 107, anno: 1995,
pagine: 283 - 289
SICI:
0043-5325(1995)107:9<283:TMOATY>2.0.ZU;2-L
Fonte:
ISI
Lingua:
GER
Soggetto:
BETA-PYRIDYLCARBINOL RONICOL; NITRIC-OXIDE; ARTERIOSCLEROSIS OBLITERANS; VASCULAR-DISEASE; RELAXING FACTOR; PROSTACYCLIN; ENDOTHELIUM; PLATELETS; ILOPROST; RELEASE;
Keywords:
CAMONAGREL; THROMBOXANE SYNTHASE INHIBITION; THROMBOXANE A(2) (TXA(2)); THROMBOXANE B-2 (TXB(2)); PROSTACYCLIN (PGI(2)); 6-KETO-PROSTAGLANDIN F1-ALPHA (6-KETO-PGF(1-ALPHA)); NITRIC OXIDE (NO); THROMBORESISTANCE IN VITRO; T-PA; PAI-1; EUGLOBULIN CLOT LYSIS TIME (ECLT); THROMBIN-ANTITHROMBIN III COMPLEX (TAT); N-G-NITRO-L-ARGININE METHYL ESTER (L-NAME);
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
26
Recensione:
Indirizzi per estratti:
Citazione:
R.J. Gryglewski et al., "THE MECHANISM OF ANTITHROMBOTIC, THROMBOL YTIC AND FIBRINOLYTIC ACTIONS OF CAMONAGREL - A NEW THROMBOXANE SYNTHASE INHIBITOR", Wiener Klinische Wochenschrift, 107(9), 1995, pp. 283-289

Abstract

So far pharmacological consequences of inhibition of thromboxane A(2)(TXA(2)) synthase by imidazole derivatives (e.g., camonagrel or dazoxiben) were linked to suppression of platelet activity. Here we report that in patients with peripheral atherosclerosis or in cats with extracorporeal thrombogenesis treatment with camonagrel is associated with activation of fibrinolysis or thrombolysis. These phenomena seem to berelated to the camonagrel-induced shift in metabolism of prostaglandin endoperoxides from TXA(2) to prostacyclin (PGI(2)), although in an in vitro model the involvement of the L-arginine/nitric oxide pathway cannot be excluded. In cats camonagrel (10 mg/kg i.v.) produced not only a fall in TXB(2) but also a rise in 6-keto-PGF(1 alpha), and no change in cyclic-GMP plasma levels. This points to PGI(2) rather than to nitric oxide as an in vivo mediator of camonagrel-induced thrombolysis. The crucial role of endogenous PGI(2) in the thrombolytic response tocamonagrel in cats was evidenced by its blockade following pretreatment of animals with a megadose of aspirin (50 mg/kg i.v.) and lack of any effect on pretreatment with L-NAME (100 mu g/kg/min, i.v.). Obviously TXA(2) synthase inhibitors (e.g., camonagrel) and cyclo-oxygenase inhibitors (e.g., aspirin) antagonize each other in their anti-thrombotic actions and must not be administered at the same time. Furthermore,in patients camonagrel (800 mg orally) suppressed TXA(2) generation by 99.5% and doubled the plasma level of 6-keto-PGF(1 alpha). This was accompanied by lowering of PAI-1 antigen concentration and a rise in plasma t-PA activity. Euglobulin clot lysis time (ECLT) was also shortened. In conclusion, in men and cats camonagrel activates fibrinolysis and thrombolysis through the release of endogenous PGI(2).

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 19/09/20 alle ore 08:01:20