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Titolo:
Comparison of TNK with wild-type tissue plasminogen activator in a rabbit embolic stroke model
Autore:
Chapman, DF; Lyden, P; Lapchak, PA; Nunez, S; Thibodeaux, H; Zivin, J;
Indirizzi:
Vet Adm Med Ctr, Dept Neurol, San Diego, CA 92161 USA Vet Adm Med Ctr SanDiego CA USA 92161 pt Neurol, San Diego, CA 92161 USA Univ Calif San Diego, Sch Med, Dept Neurosci, San Diego, CA 92103 USA UnivCalif San Diego San Diego CA USA 92103 osci, San Diego, CA 92103 USA
Titolo Testata:
STROKE
fascicolo: 3, volume: 32, anno: 2001,
pagine: 748 - 752
SICI:
0039-2499(200103)32:3<748:COTWWT>2.0.ZU;2-D
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACUTE MYOCARDIAL-INFARCTION; HEMORRHAGIC TRANSFORMATION; INTRACEREBRAL HEMORRHAGE; VENOUS THROMBOSIS; THROMBOLYSIS; VARIANT; TRIAL; TIMI; TPA; THERAPY;
Keywords:
cerebral embolism; hematoma; hemorrhage; thrombolysis; thrombolytic therapy; rabbits;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
28
Recensione:
Indirizzi per estratti:
Indirizzo: Lyden, P 127,3350 La Jolla Village Dr, San Diego, CA 92161 USA 127,3350 La Jolla Village Dr San Diego CA USA 92161 CA 92161 USA
Citazione:
D.F. Chapman et al., "Comparison of TNK with wild-type tissue plasminogen activator in a rabbit embolic stroke model", STROKE, 32(3), 2001, pp. 748-752

Abstract

Background and Purpose-Tissue plasminogen activator (tPA) is an effective treatment for stroke, but its utility is limited by fear of cerebral hemorrhage. Tenecteplase (TNK), a genetically modified form of wild-type tPA, exhibits a longer biological half-life and greater fibrin specificity, features that could lead to fewer cerebral hemorrhages than wild-type tPA in stroke patients. Methods-We injected radiolabeled blood clots into the cerebral circulationof New Zealand White rabbits, One hour later, we administered tPA (n=57), 0.6 mg/kg TNK (n=43), 1.5 mg/kg TNK (n=27), or vehicle control (n=37). A blinded observer examined the brains for macroscopic hemorrhage using a semiquantitative score. We estimated thrombolysis by assessing the amount of radiolabel remaining in the cerebral vessels postmortem. Results-Both wild-type tPA and TNK caused thrombolysis in most subjects. Hemorrhage was detected in 26% (6/23) of the control group, 66% (27/41) of the wild-type tPA group, 55% (16/29) in the 0.6-mg/kg TNK group, and 53% (9/17) in the 1.5-mg/kg TNK group (P<0.05, <chi>(2) test). The tPA group was statistically significantly different from the control group, but the TNK and tPA groups did not differ from each other. Neither TNK nor tPA affected the size of the hemorrhages. Conclusions-TNK shows comparable rates of recanalization compared with wild-type tPA in a model of embolic stroke. While tPA increases hemorrhage rate, the hemorrhage associated with TNK treatment is not statistically different compared with controls or the tPA group. These findings suggest that TNK shows promise as an alternative thrombolytic treatment for stroke, but wecould not demonstrate improved safety compared with wild-type tPA.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/04/20 alle ore 11:59:45