scholarly journals Erratum to : Thrombolytic Effect of Human Tissue-type Plasminogen Activator (t-PA, MMR 701) on a Canine Coronary Thrombosis Model

1996 ◽  
Vol 7 (3) ◽  
pp. 255-255
1987 ◽  
Vol 18 (3) ◽  
pp. 278-281
Author(s):  
Yoshikazu ASHIDA ◽  
Yoshifumi HORISAWA ◽  
Shuichi SHIRAKI ◽  
Yasuhiro HARADA ◽  
Masahiro NOBUHARA

1987 ◽  
Vol 18 (2) ◽  
pp. 164-167
Author(s):  
Yoshikazu ASHIDA ◽  
Yoshifumi HORISAWA ◽  
Shuichi SHIRAKI ◽  
Yasuhiro HARADA ◽  
Masahiro NOBUHARA

1998 ◽  
Vol 79 (03) ◽  
pp. 663-667 ◽  
Author(s):  
Kazuo Sato ◽  
Ken-ichi Suzuki ◽  
Yumiko Sakai ◽  
Yuta Taniuchi ◽  
Seiji Kaku ◽  
...  

SummaryWe examined the effect of a humanized anti-glycoprotein IIb/IIIa monoclonal antibody, YM337, on thrombolysis with tissue-type plasminogen activator in a copper coil-induced coronary thrombosis model in rhesus monkeys. Fifty minutes after the formation of an occlusive thrombus, a test drug was administered by either i.v. bolus injection followed by continuous infusion (YM337, 0.25 mg/kg + 1.5 μg/kg/min) or i.v. bolus injection (aspirin, 17 mg/kg). Sixty minutes after induction of the occlusive thrombus, thrombolysis was initiated with tPA at a total dose of 0.5 mg/kg intravenously administered over 60 min, with 10% given as an initial bolus. The median time to reperfusion was significantly shortened by YM337 [saline, 60 min (n = 5); aspirin, 45 min (n = 5); YM337, 30 min (n = 5)]. The incidence of reocclusion was significantly decreased by YM337 (saline, 4/4; aspirin, 5/5; YM337, 1/5), and the median time to reocclusion was significantly prolonged by YM337 [saline, 30 min (n = 4); aspirin, 30 min (n = 5); YM337, 180 min (n = 5)]. YM337 significantly reduced the thrombus protein content at the end of experiment. ADP-induced platelet aggregation was completely inhibited by YM337. These results suggest that YM337 may be of clinical value as an adjunctive agent in thrombolytic therapy for patients with acute myocardial infarction.


1995 ◽  
Vol 73 (03) ◽  
pp. 488-494 ◽  
Author(s):  
J L M Heeremans ◽  
R Prevost ◽  
M E A Bekkers ◽  
P Los ◽  
J J Emeis ◽  
...  

SummaryIn this study, we aimed at improving the therapeutic index of tissue- type Plasminogen Activator (t-PA) as thrombolytic agent in the treatment of myocardial infarction. Liposome-encapsulated t-PA was tested in a rabbit jugular vein thrombosis model: administration of free t-PA (t-PA) as a bolus injection in the ear vein was compared to a similar administration of liposomal t-PA (t-PA-lip), liposomal t-PA in plasminogen-coated liposomes (Plg-t-PA-lip), a mixture of free t-PA and empty liposomes (t-PA+empty lip) and a saline-blank (blank) in terms of thrombolytic activity and side effects.Liposomal t-PA (t-PA-lip/Plg-t-PA-lip) showed a significantly better thrombolysis efficiency than equimolar doses of free t-PA (t-PA/ t-PA+ empty lip): about 0.24 mg/kg of liposomal t-PA practically equalled the lysis-activity of a dose of free t-PA of 1.0 mg/kg (t-PAlmg/kg). On the other hand, liposome encapsulation did not affect the systemic activation of alpha2-antiplasmin and plasminogen by t-PA.We conclude that for this model an improvement in thrombolytic efficacy of t-PA is achieved by liposome encapsulation of t-PA. As t-PA-lip and Plg-t-PA-lip -treatment induced similar results, targeting of liposomal t-PA by coupled glu-Plg remains a topic to be optimized in future studies.


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