scholarly journals Dependence of fibrinolytic activity on the concentration of free rather than total tissue-type plasminogen activator in plasma after pharmacologic administration.

Circulation ◽  
1989 ◽  
Vol 79 (6) ◽  
pp. 1204-1213 ◽  
Author(s):  
C L Lucore ◽  
S Fujii ◽  
B E Sobel
Keyword(s):  
Plasminogen Activator ◽  
Fibrinolytic Activity ◽  
Tissue Type ◽  
Tissue Type Plasminogen Activator ◽  
Type Plasminogen Activator ◽  
Total Tissue

On the Fibrinolytic System in Aged Rats, and Its Reactivity to Endotoxin and Cytokines

1992 ◽  
Vol 67 (06) ◽  
pp. 697-701 ◽  
Author(s):  
J J Emeis ◽  
A Brouwer ◽  
R J Barelds ◽  
M A Horan ◽  
S K Durham ◽  
...  
Keyword(s):  
Plasminogen Activator ◽  
Fibrinolytic Activity ◽  
Fibrinolytic System ◽  
Tissue Type ◽  
High Dose ◽  
Base Line ◽  
Aged Rats ◽  
Tissue Type Plasminogen Activator ◽  
Young Rats ◽  
Type Plasminogen Activator

SummaryAged rats are more susceptible to endotoxin-induced effects, including microthrombosis and platelet aggregation, than are young rats. To investigate whether changes in the fibrinolytic system might be involved, we investigated the fibrinolytic activity in plasma euglobulin fractions and tissues (lung and heart) of young (6-months old) and aged (24-months old) rats under baseline conditions and after challenge with endotoxin. Aged rats had lower plasma levels of tissue-type plasminogen activator (t-PA) and of urokinase-type PA (u-PA) activity. PA inhibitor (PAI) activity was higher in the plasma of aged rats, as was t-PA activity in lung and heart.Rats were treated with either a low dose (1 μg/kg) or a high dose (10 mg/kg) of endotoxin. Both treatments induced a transient phase of increased blood fibrinolytic activity, as evidenced by higher levels of tissue-type plasminogen activator (t-PA) activity and decreased levels of PA inhibitor (PAI) activity. Over time, the fibrinolytic activity decreased, probably due to increased levels of PA inhibitor.Both the early increase in t-PA activity, and the subsequent increase in PAI activity, were more pronounced in the aged rats, as compared with the younger rats, after the high dose of endotoxin. The aged rats also responded to an injection of interleukin-1β or tumor necrosis factor-α with a larger increase of PAI activity than did the younger rats.Together the data suggest that, compared to young rats, aged rats have a decreased base-line plasma fibrinolytic activity, while their fibrinolytic system is more responsive to challenge by endotoxin and cytokines.

FIBRINOLYSIS AFTER HEART TRANSPLANTATION

1987 ◽  
Author(s):  
J A Páramo ◽  
R Arcas ◽  
J Fernández ◽  
J Herreros ◽  
R Llorens ◽  
...  
Keyword(s):  
Plasminogen Activator ◽  
Fibrinolytic Activity ◽  
Cardiac Transplantation ◽  
Degradation Products ◽  
Plasminogen Activator Inhibitor ◽  
Tissue Type ◽  
Inhibitor Activity ◽  
Tissue Type Plasminogen Activator ◽  
Type Plasminogen Activator ◽  
Activator Inhibitor

Some aspects of the function of the fibrinolytic system were investigated in 12 patients undergoing cardiac transplantation. Plasminogen, euglobulin fibrinolytic activity (EFA), tissue-type plasminogen activator (t-PA), plasminogen activator inhibitor activity (PAI),α2-antiplasmin (α2-Ap) and fibrinogen degradation products (FDP) were determined preo-peratively and on postoperative days 1 and 5. Results showed a significant decrease of plasminogen (p <0.005), EFA (p <0.0001) and t-PA (p ^.0.001) on postoperative day 1 as compared to the baseline value, followed by recovery on day 5. There was a significant increase of PAI (p < 0 . 005) , α2-AP (p <0.0001) and FDP (p < 0.02) on postoperative day 1 as compared to the preoperative value. PAI and FDP reached the baseline value on postoperative day 5, but α2AP also increased on postoperative day 5. Our data show that there is an impairment in blood fibrinolytic activity early after cardiac transplantation, mainly related to a decrease of plasminogen and t-PA and a increase of PAI and α2AP. The clinical relevance of these data needs further evaluation.

scholarly journals Arsenite Inhibits Tissue-Type Plasminogen Activator Synthesis through NRF2 Activation in Cultured Human Vascular Endothelial EA.hy926 Cells

2021 ◽  
Vol 22 (2) ◽  
pp. 739
Author(s):  
Tsuyoshi Nakano ◽  
Tsutomu Takahashi ◽  
Chika Yamamoto ◽  
Eiko Yoshida ◽  
Toshiyuki Kaji ◽  
...  
Keyword(s):  
Plasminogen Activator ◽  
Fibrinolytic Activity ◽  
Vascular Endothelial Cells ◽  
Tissue Type ◽  
Vascular Endothelial ◽  
Tissue Type Plasminogen Activator ◽  
Nrf2 Pathway ◽  
Type Plasminogen Activator ◽  
Ea.Hy926 Cells ◽  
Pai 1

Chronic arsenic exposure is known to be related to the progression of atherosclerosis. However, the pathogenic mechanisms of arsenic-induced atherosclerosis have not been fully elucidated. Because disruption of the blood coagulation/fibrinolytic system is involved in the development of arteriosclerosis, we investigated the effect of arsenite on fibrinolytic activity in human vascular endothelial EA.hy926 cells in the present study. Fibrinolysis depends on the balance between tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor 1 (PAI-1) secreted from vascular endothelial cells. We found that arsenite reduced fibrinolytic t-PA activity by inhibiting its synthesis without affecting PAI-1 production. The inhibitory effect of arsenite on t-PA expression was partially recovered by the reactive oxygen species (ROS) scavenger Trolox. The nuclear factor erythroid 2 related factor 2 (NRF2) pathway is known to be activated by arsenite via ROS production. We confirmed that arsenite activated the NRF2 pathway, and arsenite-induced inhibition of fibrinolytic t-PA activity was abrogated in NRF2-knockdown EA.hy926 cells. These results suggest that arsenite inhibits the fibrinolytic activity of t-PA by selectively suppressing its synthesis via activation of the NRF2 pathway in vascular endothelial cells.

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