Chinese tuina downregulates the elevated levels of tissue plasminogen activator in sciatic nerve injured Sprague-Dawley rats

2015 ◽  
Vol 23 (8) ◽  
pp. 617-624 ◽  
Author(s):  
Fan Pan ◽  
Tian-yuan Yu ◽  
Steven Wong ◽  
Si-tong Xian ◽  
Meng-qian Lu ◽  
...  
Keyword(s):  
Sciatic Nerve ◽  
Plasminogen Activator ◽  
Tissue Plasminogen Activator ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Tissue Plasminogen

The Effect of Alloxan-Induced Diabetes on Tissue Plasminogen Activator Activity of the Rat

1979 ◽  
Author(s):  
A.A. Smokovitis ◽  
B.R. Binder
Keyword(s):  
Plasminogen Activator ◽  
Tissue Plasminogen Activator ◽  
Vena Cava ◽  
Renal Medulla ◽  
Sprague Dawley ◽  
Plasminogen Activator Activity ◽  
Sprague Dawley Rats ◽  
Severe Diabetes ◽  
Tissue Plasminogen ◽  
Arteries And Veins

Subcutaneous injection of alloxan (10mg/100g)induced severe diabetes in Sprague-Dawley rats (hyperglycemia, glucosuria, weight loss, polydypsia, polyphagia and polyuria). The effect on tissue plasminogen activator activity (PAA) was studied histocheraically in key organs (heart, kidney, lung, aorta, and caudal vena cava) 4 days, 2, 3, 4, 6, and 8 weeks after induction of diabetes. After an initially increased vascular PAA (release reaction) seen in lung, kidney, aorta, and myocardium, but not in caudal vena cava, a decreased PAA was found in arteries of the renal medulla and particularly of the renal cortex and in arteries of the myocardium two bo eight weeks after the induction of diabetes. Compared to the normal PAA level, the intima of the aorta showed after the initial rise, a fall in two to three weeks, a second rise by four to six weeks, followed by a fall to the normal value at the eighth week. In the lung the initially increased PAA continued to be slightly elevated until the sixth week; by the eighth week it was normal. In the caudal vena cava no changes in the PAA were seen. Of interest are the observed differences in PAA patterns; (1) between arteries and veins, (2) large and small arteries, and (3) arteries in different tissues up to at least eight weeks post induction of diabetes.Supp-. by the Austrian Acad, of Sciences, Arteriosclerosis research group.

Ischemia–Reperfusion Injury of Sciatic Nerve in Rats: Protective Role of Combination of Vitamin C with E and Tissue Plasminogen Activator

2018 ◽  
Vol 43 (3) ◽  
pp. 650-658 ◽  
Author(s):  
Katerina Apostolopoulou ◽  
Dimitris Konstantinou ◽  
Rodoula Alataki ◽  
Ioannis Papapostolou ◽  
Dimitrios Zisimopoulos ◽  
...  
Keyword(s):  
Sciatic Nerve ◽  
Vitamin C ◽  
Reperfusion Injury ◽  
Plasminogen Activator ◽  
Tissue Plasminogen Activator ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Protective Role ◽  
Tissue Plasminogen

scholarly journals Tissue Plasminogen Activator–Mediated Fibrinolysis Protects against Axonal Degeneration and Demyelination after Sciatic Nerve Injury

2000 ◽  
Vol 149 (5) ◽  
pp. 1157-1166 ◽  
Author(s):  
Katerina Akassoglou ◽  
Keith W. Kombrinck ◽  
Jay L. Degen ◽  
Sidney Strickland
Keyword(s):  
Nervous System ◽  
Sciatic Nerve ◽  
Plasminogen Activator ◽  
Nerve Injury ◽  
Tissue Plasminogen Activator ◽  
Axonal Degeneration ◽  
Sciatic Nerve Injury ◽  
Axonal Damage ◽  
Protective Mechanism ◽  
Tissue Plasminogen

Tissue plasminogen activator (tPA) is a serine protease that converts plasminogen to plasmin and can trigger the degradation of extracellular matrix proteins. In the nervous system, under noninflammatory conditions, tPA contributes to excitotoxic neuronal death, probably through degradation of laminin. To evaluate the contribution of extracellular proteolysis in inflammatory neuronal degeneration, we performed sciatic nerve injury in mice. Proteolytic activity was increased in the nerve after injury, and this activity was primarily because of Schwann cell–produced tPA. To identify whether tPA release after nerve damage played a beneficial or deleterious role, we crushed the sciatic nerve of mice deficient for tPA. Axonal demyelination was exacerbated in the absence of tPA or plasminogen, indicating that tPA has a protective role in nerve injury, and that this protective effect is due to its proteolytic action on plasminogen. Axonal damage was correlated with increased fibrin(ogen) deposition, suggesting that this protein might play a role in neuronal injury. Consistent with this idea, the increased axonal degeneration phenotype in tPA- or plasminogen-deficient mice was ameliorated by genetic or pharmacological depletion of fibrinogen, identifying fibrin as the plasmin substrate in the nervous system under inflammatory axonal damage. This study shows that fibrin deposition exacerbates axonal injury, and that induction of an extracellular proteolytic cascade is a beneficial response of the tissue to remove fibrin. tPA/plasmin-mediated fibrinolysis may be a widespread protective mechanism in neuroinflammatory pathologies.

Tissue plasminogen activator as a novel diagnostic aid in acute pulmonary embolism

VASA ◽  
2014 ◽  
Vol 43 (6) ◽  
pp. 450-458 ◽  
Author(s):  
Julio Flores ◽  
Ángel García-Avello ◽  
Esther Alonso ◽  
Antonio Ruíz ◽  
Olga Navarrete ◽  
...  
Keyword(s):  
Pulmonary Embolism ◽  
Negative Predictive Value ◽  
Plasminogen Activator ◽  
Tissue Plasminogen Activator ◽  
Predictive Value ◽  
Acute Pulmonary Embolism ◽  
Enzyme Linked Immunosorbent Assay ◽  
Diagnostic Utility ◽  
Tissue Plasminogen ◽  
D Dimer

Background: We evaluated the diagnostic efficacy of tissue plasminogen activator (tPA), using an enzyme-linked immunosorbent assay (ELISA) and compared it with an ELISA D-dimer (VIDAS D-dimer) in acute pulmonary embolism (PE). Patients and methods: We studied 127 consecutive outpatients with clinically suspected PE. The diagnosis of PE was based on a clinical probability pretest for PE and a strict protocol of imaging studies. A plasma sample to measure the levels of tPA and D-dimer was obtained at enrollment. Diagnostic accuracy for tPA and D-dimer was determined by the area under the receiver operating characteristic (ROC) curve. Sensitivity, specificity, predictive values, and the diagnostic utility of tPA with a cutoff of 8.5 ng/mL and D-dimer with a cutoff of 500 ng/mL, were calculated for PE diagnosis. Results: PE was confirmed in 41 patients (32 %). Areas under ROC curves were 0.86 for D-dimer and 0.71 for tPA. The sensitivity/negative predictive value for D-dimer using a cutoff of 500 ng/mL, and tPA using a cutoff of 8.5 ng/mL, were 95 % (95 % CI, 88–100 %)/95 % (95 % CI, 88–100 %) and 95 % (95 % CI, 88–100 %)/94 %), respectively. The diagnostic utility to exclude PE was 28.3 % (95 % CI, 21–37 %) for D-dimer and 24.4 % (95 % CI, 17–33 %) for tPA. Conclusions: The tPA with a cutoff of 8.5 ng/mL has a high sensitivity and negative predictive value for exclusion of PE, similar to those observed for the VIDAS D-dimer with a cutoff of 500 ng/mL, although the diagnostic utility was slightly higher for the D-dimer.

Desmopressin Stimulates Parallel Norepinephrine and Tissue Plasminogen Activator Release in Normal Subjects and Patients with Diabetes Mellitus

1988 ◽  
Vol 59 (02) ◽  
pp. 269-272 ◽  
Author(s):  
M B Grant ◽  
C Guay ◽  
R Lottenberg
Keyword(s):  
Diabetes Mellitus ◽  
Plasminogen Activator ◽  
Tissue Plasminogen Activator ◽  
Time Course ◽  
Vascular Endothelial Cells ◽  
Normal Subjects ◽  
Plasma Norepinephrine ◽  
Endogenous Catecholamine ◽  
Tissue Plasminogen ◽  
Patients With Diabetes

SummaryDesmopressin acetate administration markedly stimulates release of tissue plasminogen activator (t-PA) from vascular endothelial cells. The mechanism for this effect is unknown. Because infusion of epinephrine has been shown to increase t-PA levels, we examined the role of endogenous catecholamine mediation of t-PA release by desmopressin. Intravenous desmopressin acetate (0.3 μg/kg) was infused over 30 min in 9 controls and 11 subjects with diabetes mellitus, a condition associated with abnormalities of the fibrinolytic system. Plasma was collected in the supine, overnight fasted state at 15 min intervals (0-60 min) for measurement of t-PA activity, t-PA antigen and fractionated catecholamines. t-PA activity peaked at 30-45 min and subsequently decreased. The norepinephrine levels paralleled the t-PA activity. t-PA activity increased 10-fold from 0.14 ± .12 to 1.49 ± 0.79 IU/ml (Mean ± SD) and plasma norepinephrine increased 2- fold from 426 ± 90 to 780 ± 292 pg/ml. However, epinephrine and dopamine levels did not change significantly. The response to desmopressin of control and diabetic subjects was not shown to differ and their data were combined. We conclude that desmopressin increases plasma norepinephrine in addition to t-PA and that the parallel time course of change suggests a possible role for norepinephrine in mediating endothelial cell t-PA release.

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