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PubMed1991

The acute effect of insulin on tissue plasminogen activator and plasminogen activator inhibitor in man.

The present study was performed to elucidate the acute effect of insulin on levels of tissue plasminogen activator (t-PA) and plasminogen activator inhibitor of endothelial cell type (PAI-1). Nine middle-aged, non-obese and non-smoking men were studied during a hyperinsulinemic, euglycemic glucose clamp for 2 h. Plasma insulin level during the clamp averaged 84 +/- 12 mU/l and euglycemia was maintained at 4.9 +/- 0.6 mmol/l. The t-PA activity gradually increased (75% mean increase after 2 h, p less than 0.001) and the PAI-1 activity decreased (49% mean decrease after 2 h, p less than 0.001) during the clamp. t-PA activity decreased and PAI-1 activity increased after the insulin infusion was ceased, but they were still 48% higher and 38% lower, respectively, after 60 min. PAI-1 and t-PA activities were not affected by saline infusion for 2 h. Thus, acute changes in the insulin levels lead to rapid alterations in the fibrinolytic system even when euglycemia is maintained. These effects may be induced by insulin itself or by the concomitant activation of the sympatho-adrenal system during the euglycemic clamp.

Blood Glucose↗
PubMed1991

[Plasma tissue-type plasminogen activator and plasminogen activator inhibitor activities and their ratio in patients with ischemic stroke associated with stagnation of blood during various stages].

The studies showed that t-PA activity was elevated during the acute phase, remained elevated during the recovery stage and declined during the sequelar stage. Lowering of PAI activity was found during the acute phase, which was reversed during the recovery phase and remained significantly elevated during the sequelar stage compared with the controls (P less than 0.001), F test showed that both t-PA and PAI activities changed significantly during various stages (t-PA, P less than 0.01; PAI, P less than 0.001). Because of these changes, the ratio of PAI and t-PA fluctuated during different stages of the disease. This ratio decreased during the acute stage and came close to the normal levels during the recovery phase. The ratio, however, elevated abnormally during the sequelar stage, compared with healthy controls (P less than 0.05), In addition, the result of correlation test and linear regression analysis of serum t-PA and PAI activities in 54 cases showed a significant negative correlation (P less than 0.001) existed between t-PA and PAI activities. The balance of plasma t-PA and PAI activities have the function in maintaining the normal bloodstream in human body. In the process of disease, the abnormality of plasma t-PA and PAI activities may be the different pathological characteristics involved in this stagnation process. If coordinated with differentiation of syndrome in TCM, it may have the important significance to follow-up, and determine prognosis and early diagnosis for certain potential clinical stagnation of blood.

Aged↗
PubMed1991

[The kinetics of plasma coagulation fibrinolysis levels in acute myocardial infarction before and after treatment with intravenous urokinase].

The levels of tissue-type plasminogen activator (t-PA), plasminogen activator inhibitor (PAI) and other substances of coagulation-fibrinolysis, such as fibronectin (Fn) and von willebrand factor (vWF) as well as the activity content of antithrombin-III(AT-III) in plasma were determined in 20 patients with acute myocardial infarction (AMI). In 11 of them these measurements were carried out before and after the treatment with urokinase (UK1000 000 IU). The results suggested that the function of coagulation-fibrinolytic system was disturbed in AMI. Thrombolytic treatment with UK could interfere and improve the stabilization of fibrinolytic activity in the body, but these actions last only short time. Some substances of coagulation showed change with UK treatment.

Aged↗
PubMed1991

[Evaluation of a new enzyme immunoassay method for determination of t-PA-PAI-1 complex].

We evaluated a new enzyme immunoassay for determination of t-PA-PAI-1 complex (PAI-C) and studied the clinical utility of measuring PAI-C. This assay was performed by the capture/tag antibody technique using polystylene beads, in which the beads were coated with monoclonal antibody against PAI-1 and anti-t-PA polyclonal antibody was tagged (TDC-88, TEIJIN-LIMITED, Japan). The assay gave an excellent sensitivity with a detection limit of 0.1 ng/ml, and we were able to detect a trace amount of PAI-C in normal plasma. PAI-C in 6 volunteers showed significant daytime fluctuations. The normal value of PAI-C in plasma was below 13.8 ng/ml (n = 40). PAI-C levels in patients with accelerated fibrinolysis (n = 31) ranged from 2.9 to 66.4 ng/ml and 15 of them were outside the normal range. However, all of patients with DIC (n = 10) showed abnormally high PAI-C levels. In patients with accelerated fibrinolysis, PAI-C values correlated with t-PA antigen (r = 0.838), PAI-1 antigen (r = 0.519), ATIII activity (r = -0.669) (p less than 0.01) and D dimer levels (r = 0.391, p less than 0.05). However, PAI-C values did not correlate with plasminogen and alpha 2PI activity, alpha 2PI-plasmin complex or the FDP-E level in these patients. Our data suggests that PAI-C may be a new molecular marker that reflects t-PA release from endothelial cells and a useful indicator to study hypercoagulable states.

Fibrinolysis↗
PubMed1991

[A role of cultured bovine lens epithelial cells in the fibrinolytic system].

The release of plasminogen activators (PAs) and plasminogen activator inhibitor (PAI) from cultured bovine lens epithelial cells was investigated, in an attempt to study the effect of lens epithelial cells on the fibrin deposit and fibrinolytic process on the surface of IOL. Cultured bovine lens epithelial cells released tissue plasminogen activator (t-PA) and type 1 plasminogen activator inhibitor (PAI-1). t-PA activity was completely inhibited by PAI-1. These findings suggest that lens epithelial cells cause suppression of fibrinolysis in the anterior chamber of the eye.

Animals↗
PubMed1991

[Levels of tissue-type plasminogen activator and plasminogen activator inhibitor 1 in disseminated intravascular coagulation syndrome].

Since disseminated intravascular coagulation (DIC) may directly reflect the abnormal regulation of the fibrinolytic system by endothelial cells, we have measured the levels of tissue-type plasminogen activator (t-PA), type 1 PA inhibitor (PAI-1) and t-PA . PAI-1 complex which is formed as a result of interaction on the two factors, in the plasma of patients with DIC (n = 51) and healthy controls (n = 42). Antigens of t-PA, PAI-1 and t-PA . PAI-1 complex were significantly increased in the DIC plasma (36.4 +/- 25.1, 106.8 +/- 54.7 and 46.6 +/- 34.5 ng/ml, respectively) compared with those in normal plasma (8.5 +/- 4.3, 54.4 +/- 21.2 and 8.6 +/- 3.5 ng/ml, respectively). The molar ratio of t-PA to PAI-1 was much higher in the DIC plasma (1:3) than in normal plasma (1:6), which caused enhancement of the whole fibrinolytic activity in the DIC plasma. These changes resulted in significant consumption of plasminogen, alpha 2-plasmin inhibitor (alpha 2-PI) and a significant increase of plasmin . alpha 2-PI complex (PPI) and D-dimer. These results suggest that t-PA and its specific inhibitor PAI-1 both of which are secreted from endothelial cells into blood, play an important role on the progress of DIC.

Adult↗
PubMed1990

The effect of heparin and other glycosaminoglycans on levels of tissue plasminogen activator and plasminogen activator inhibitor in cultured human umbilical vein endothelial cells.

Human umbilical vein endothelial cells (HUVEC) were cultured in the presence of various glycosaminoglycans and the intracellular levels of tissue plasminogen activator (tPA) and plasminogen activator inhibitor-1 (PAI-1) measured by ELISA. 10 IU/ml heparin (90 micrograms/ml) brought about a significant (20-fold) increase in intracellular tPA levels over the 6-day culture period; intracellular PAI-1 levels were significantly decreased (by 60-70%) and culture growth rate promoted. The final cell density of heparin-containing cultures was 1.7 to 2.3 times greater than that of control cultures. Low molecular weight heparin (First International Standard) had similar effects but was less potent than unfractionated heparin. Chondroitin sulphate and heparan sulphate had no effect on tPA and PAI-1 levels but dermatan sulphate reduced PAI-1 significantly. The changes observed following exposure of HUVEC to heparin are consonant with the view that glycosaminoglycans may affect endothelial production of fibrinolytic components.

Cell Division↗
PubMed1990

Plasminogen activator inhibitor 1 in renal fibrin deposits of human nephropathies.

The persistency of fibrin deposits in the kidney during renal diseases could reflect either a defective release of plasminogen activators (PA) or a local excess of PAI. In order to investigate this question, we studied human renal biopsies by immunofluorescence technique with specific antibodies for fibrin, tissue-type plasminogen activator (t-PA), urokinase (u-PA), PAI-1 and PAI-2. By this technique t-PA could be detected in the glomerular flocculus and the endothelium of small arteries of the normal control kidneys. We failed to detect significant fluorescence with other antibodies in normal kidneys. Conversely, in cases of vascular nephropathy with thrombosis the positive fluorescence obtained with anti-fibrin antibodies at the site of thrombosis was associated with a positive fluorescence with anti-PAI-1 and to a lesser extent with anti-t-PA antibodies. u-PA and PAI-2 were not detected in these lesions. Similarly in the most severe forms of crescentic glomerulonephritis, extracapillary fibrin deposits were associated with PAI-1. In one case u-PA was also detected. This is in agreement with our previous findings that glomerular epithelial cells release both PAI-1 and the inactive form of u-PA (pro u-PA). Thus, our results support the hypothesis that PAI-1, which is able to inhibit both t-PA and u-PA, may play a major role in the persistency of fibrin deposits in the human kidneys during pathological conditions.

Female↗
PubMed1990

Relationships between euglobulin clot lysis time and the plasma levels of tissue plasminogen activator and plasminogen activator inhibitor 1.

The relationships between tissue plasminogen activator (tPA), its fast acting inhibitor (PAI-1) and euglobulin clot lysis time (ELT) were investigated with healthy volunteers' plasma. Turbidimetric clot lysis assay by the microtiter plate reader was utilized for ELT with a slight modification. Both tPA and PAI-1 showed the significant correlation with ELT. tPA had a significantly positive, not negative, correlation with ELT (R = 0.387, p less than 0.001). Higher correlation coefficients (R = 0.580, p less than 0.001 and R = 0.599, p less than 0.001) were obtained between ELT and total PAI-1 or free PAI-1 than tPA or tPA-PAI-1 complex (R = 0.427, p less than 0.001). The positive correlation was also obtained between tPA and PAI-1. These data suggest that PAI-1 is a highly important factor for ELT, especially, the amounts of free PAI-1 being the key factor to determine the ELT, which can represent the potential activity of the fibrinolytic system.

Adult↗
PubMed1990

[t-PA activity, antigen and PAI-1 antigen levels in blood obtained from the patients with cerebral infarction].

Tissue plasminogen activator (t-PA) produced by endothelial cells exerts a powerful effect on the course of thrombosis, embolism, or arteriosclerosis. However, the fluctuations of fibrinolytic system in the patients with cerebral infarction (CI), have yet to be demonstrated. This study was designed to investigate t-PA activity, t-PA antigen and plasminogen activator inhibitor-1 (PAI-1) antigen levels in the CI patients. The mean t-PA activity, t-PA antigen and PAI-1 levels in patients were 0.53 +/- 0.64 IU/ml, 10.9 +/- 5.2 ng/ml and 23.0 +/- 14.9 ng/ml, and the normal ranges were 0.02-0.28 IU/ml, 1.0-7.0 ng/ml and 5.3-45.0 ng/ml, respectively. Almost all the patients were plotted out to the abnormal range by scattergrams relating t-PA activity to t-PA antigen, and no daytime fluctuations of the above three parameters in the patients differed from those in normal controls. When CI patients were followed up to the 8th hospital day, abnormal fluctuations were also observed. Consequently we suggest that this information may help to attain the more progressive treatment or the preventive therapy of CI.

Adult↗
PubMed1990

Impaired fibrinolytic capacity in patients with inflammatory bowel disease.

The venous occlusion test was applied to 17 patients with inflammatory bowel disease (IBD; 7 cases of Crohn's disease, 10 cases of ulcerative colitis). Results were compared to those obtained in 20 healthy matched control subjects. Patients with IBD had significantly decreased t-PA Ag release (p less than 0.001) and had no significant vWF Ag release. Residual PAI activity was evidenced after venous stasis in the IBD group but not in the control group. Hypofibrinolysis was more important in patients with an evolutive IBD than in patients with IBD in remission. Impaired systemic fibrinolytic capacity might contribute to an increased risk for thromboembolic complications and to the pathogenesis of inflammatory bowel disease.

Adult↗
PubMed1990

Changes in plasma levels of tissue plasminogen activator and its inhibitor in aged myocardial infarction patients.

Plasma levels of tissue plasminogen activator (tPA) antigen, tPA activity and plasminogen activator inhibitor (PAI) activity were determined in 40 cases of acute myocardial infarction (AMI) at the onset and 2-4 weeks after the onset of the disease. 24 healthy subjects served as controls. At the onset of AMI, mean plasma level of tPA antigen was significantly higher than that of control subjects (13.5 +/- 4.8 ng/ml vs 6.4 +/- 2.0 ng/ml), with the highest elevation in the group greater than 65 years of age. Mean plasma level of tPA activity was significantly lower than in the controls (1.1 +/- 0.4 IU/ml vs 1.6 +/- 0.4 IU/ml), especially in patients over 65 years of age. Mean plasma level of PAI activity was significantly higher than in the controls (17.5 +/- 12.0 AU/ml vs 9.0 +/- 4.6 AU/ml), especially in patients over 65 years of age. At 2-4 weeks, mean plasma levels of tPA and PAI activities of AMI patients had dropped to 1.5 +/- 0.6 IU/ml and 9.5 +/- 8.9 AU/ml, respectively, not significantly different from controls. The tPA antigen had come down to 11.0 +/- 5.4 ng/ml, but still higher than in the controls. The possible mechanism of these phenomena was discussed.

Aged↗
PubMed1990

Heparin stimulates fibrinolysis in mesothelial cells by selective induction of tissue-plasminogen activator but not plasminogen activator inhibitor-1 synthesis.

The regulation of tissue-plasminogen activator (tPA) and plasminogen activator inhibitor 1 (PAI-1) synthesis was studied in cultured human mesothelial cells derived from omentum (HOMC). Heparin (100 U/ml) as well as pentosan polysulfate (300 micrograms/ml) stimulated tPA synthesis by HOMC 2.9-4.5-fold. Heparin-induced tPA production was dose- and time-dependent and was inhibited by cycloheximide. tPA production by HOMC was also stimulated by phorbol 12-myristate 13-acetate (2.6-fold), fibrin clots (1.9-fold), or batroxobin (1.9-fold). Heparin and pentosan polysulfate did not stimulate PAI-1 production by HOMC, while phorbol 12-myristate 13-acetate (100 nM) increased the concentration of PAI-1 in the conditioned medium by 2.6-fold over 24 h. The interaction of heparin with HOMC was studied by direct binding experiments. Dose-dependent specific binding of biotinylated heparin to HOMC was saturable at about 10 micrograms/ml, the KD was estimated to about 0.15 microM. Biotinylated heparin bound rapidly to HOMC and reached a plateau within 60 min. Unlabeled heparin as well as pentosan polysulfate inhibited binding of biotinylated heparin in a dose-dependent fashion. These data demonstrate that heparin interacts with HOMC, and increases the fibrinolytic capacity in these cells by selectively increasing the production of tPA.

Biotin↗