INFLUENCE OF A BRAIN PROTECTOR DRUG 21-AMINO STEROID ON THE EFFECTS OF EXPERIMENTAL EMBOLIC STROKE TREATED BY THROMBOLYSIS

Citation
J. Orozco et al., INFLUENCE OF A BRAIN PROTECTOR DRUG 21-AMINO STEROID ON THE EFFECTS OF EXPERIMENTAL EMBOLIC STROKE TREATED BY THROMBOLYSIS, Neurological research, 17(6), 1995, pp. 423-425
Citations number
19
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
01616412
Volume
17
Issue
6
Year of publication
1995
Pages
423 - 425
Database
ISI
SICI code
0161-6412(1995)17:6<423:IOABPD>2.0.ZU;2-7
Abstract
This study was designed to evaluate the effects of tissue-type plasmin ogen activator (tPA) and 21-amino steroid (U74006F) in experimental em bolic stroke in rabbits. The size of infarction from embolism was comp ared to controls with tPA alone, 21-amino steroid alone, and in combin ation. The middle cerebral artery of the rabbit was embolized by injec ting an arterial ('white') thrombus in the right internal carotid arte ry. The rabbit treatment was 2 mg kg(-1) of tissue-type plasminogen ac tivator and/or 3 mg kg of 21 amino steroid started at 2 h postemboliza tion. The animals were terminated 4 h post-treatment and brains were e xamined for evidence of ischemia and/or hemorrhage. Administration of tissue-type plasminogen activator and/or 21-amino steroid in the raw d ata show that there is a tendency for all treatments to reduce the isc hemic volume when compared to the control group, also it is evident th e standard deviation of these estimates is rather large when compared to the differences between treatments. The results of the analysis of variance shows that the differences expressed are not statistically si gnificant. (No statistical differences were found between the treatmen t groups and the control group.) The results show that administration of tissue-type plasminogen activator and/or 21 amino steroid at 2 h po st-embolization alone or in simultaneous administration does not signi ficantly reduce the volume of infarction. Further studies need to be a ddressed in regards to the region of viable brain in the peri-infarct area, and in reducing the time to treatment.