scholarly journals Tissue-type plasminogen activator improves neurological functions in a rat model of thromboembolic stroke.

Stroke ◽  
1994 ◽  
Vol 25 (2) ◽  
pp. 451-456 ◽  
Author(s):  
T Sakurama ◽  
R Kitamura ◽  
M Kaneko
Keyword(s):  
Plasminogen Activator ◽  
Rat Model ◽  
Tissue Type ◽  
Thromboembolic Stroke ◽  
Tissue Type Plasminogen Activator ◽  
Type Plasminogen Activator

scholarly journals Iron Overload Exacerbates the Risk of Hemorrhagic Transformation After tPA (Tissue-Type Plasminogen Activator) Administration in Thromboembolic Stroke Mice

Stroke ◽  
2018 ◽  
Vol 49 (9) ◽  
pp. 2163-2172 ◽  
Author(s):  
Isaac García-Yébenes ◽  
Alicia García-Culebras ◽  
Carolina Peña-Martínez ◽  
David Fernández-López ◽  
Jaime Díaz-Guzmán ◽  
...  
Keyword(s):  
Iron Overload ◽  
Plasminogen Activator ◽  
Hemorrhagic Transformation ◽  
Tissue Type ◽  
Thromboembolic Stroke ◽  
Tissue Type Plasminogen Activator ◽  
Type Plasminogen Activator

Microvascular repair following a modified crush-avulsion injury in a rat model: Effect of recombinant human tissue-type plasminogen activator on the patency rate

Microsurgery ◽  
2000 ◽  
Vol 20 (2) ◽  
pp. 52-58 ◽  
Author(s):  
Efstathios G. Lykoudis ◽  
Petros N. Panayotou ◽  
Constantinos N. Stamatopoulos ◽  
Konstantina B. Frangia ◽  
Apostolos E. Papalois ◽  
...  
Keyword(s):  
Plasminogen Activator ◽  
Rat Model ◽  
Human Tissue ◽  
Patency Rate ◽  
Tissue Type ◽  
Tissue Type Plasminogen Activator ◽  
Avulsion Injury ◽  
Type Plasminogen Activator

scholarly journals A Rat Model of Studying Tissue-Type Plasminogen Activator Thrombolysis in Ischemic Stroke With Diabetes

Stroke ◽  
2012 ◽  
Vol 43 (2) ◽  
pp. 567-570 ◽  
Author(s):  
Xiang Fan ◽  
Jianhua Qiu ◽  
Zhanyang Yu ◽  
Haibin Dai ◽  
Aneesh B. Singhal ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Plasminogen Activator ◽  
Rat Model ◽  
Tissue Type ◽  
Tissue Type Plasminogen Activator ◽  
Type Plasminogen Activator

scholarly journals A combined therapy of rtPA-loaded thermoresponsive gels and ultrasound on hematoma in a rat model of intracerebral hemorrhage

RSC Advances ◽  
2017 ◽  
Vol 7 (26) ◽  
pp. 15809-15816 ◽  
Author(s):  
Wei Sun ◽  
Zhongxin Qian ◽  
Mingzhu Zhao ◽  
Ming Shen ◽  
Yourong Duan ◽  
...  
Keyword(s):  
Intracerebral Hemorrhage ◽  
Plasminogen Activator ◽  
Rat Model ◽  
Combined Therapy ◽  
Pluronic F127 ◽  
Tissue Type ◽  
Intracerebral Hematoma ◽  
Tissue Type Plasminogen Activator ◽  
Type Plasminogen Activator ◽  
Neurological Response

To develop and validate an effective method for the removal of residual intracerebral hematoma, we prepared a recombinant tissue-type plasminogen activator (rtPA)-loaded Pluronic F127 (NP-rtPA) delivery system to evaluate the neurological response of the ICH rat model.

scholarly journals Pinocembrin Protects Blood-Brain Barrier Function and Expands the Therapeutic Time Window for Tissue-Type Plasminogen Activator Treatment in a Rat Thromboembolic Stroke Model

2018 ◽  
Vol 2018 ◽  
pp. 1-13 ◽  
Author(s):  
YinZhong Ma ◽  
Li Li ◽  
LingLei Kong ◽  
ZhiMei Zhu ◽  
Wen Zhang ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Plasminogen Activator ◽  
Blood Brain Barrier ◽  
Time Window ◽  
Tissue Type ◽  
Stroke Model ◽  
Thromboembolic Stroke ◽  
Tissue Type Plasminogen Activator ◽  
Type Plasminogen Activator ◽  
Therapeutic Time Window

Tissue-type plasminogen activator (t-PA) remains the only approved therapy for acute ischemic stroke but has a restrictive treatment time window of 4.5 hr. Prolonged ischemia causes blood-brain barrier (BBB) damage and increases the incidence of hemorrhagic transformation (HT) secondary to reperfusion. In this study, we sought to determine the effect of pinocembrin (PCB; a pleiotropic neuroprotective agent) on t-PA administration-induced BBB damage in a novel rat thromboembolic stroke model. By assessing the leakage of Evans blue into the ischemic hemisphere, we demonstrated that PCB pretreatment 5 min before t-PA administration significantly reduced BBB damage following 2 hr, 4 hr, 6 hr, and even 8 hr ischemia. Consistently, PCB pretreatment significantly decreased t-PA infusion-resulting brain edema and infarction volume and improved the behavioral outcomes following 6 hr ischemia. Mechanistically, PCB pretreatment inhibited the activation of MMP-2 and MMP-9 and degradation of tight junction proteins (TJPs) occludin and claudin-5 in the ischemic hemisphere. Moreover, PCB pretreatment significantly reduced phosphorylation of platelet-derived growth factor receptor α (PDGFRα) as compared with t-PA alone. In an in vitro BBB model, PCB decreased transendothelial permeability upon hypoxia/aglycemia through inhibiting PDGF-CC secretion. In conclusion, we demonstrated that PCB pretreatment shortly before t-PA infusion significantly protects BBB function and improves neurological outcomes following prolonged ischemia beyond the regular 4.5 hr t-PA time window. PCB pretreatment may represent a novel means of increasing the safety and the therapeutic time window of t-PA following ischemic stroke.

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