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Query: UNIPROT:P00750 (PLA)
16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The comparison of activator activity of blood, urine and pleural fluid in 55 patients suffering from chronic circulatory insufficiency, tuberculosis, pneumonia and lung cancer helped to determine pathognomonic signs for each of the exudates examined. Cardiac decompensation is associated with high activity of plasminogen activator in the transudate against low activator activity of the blood and urine. In tuberculous pleuritis there is low activator activity of the exudate in normal blood and urine parameters. Reduced activator activity of the blood, urine and pleural fluid is characteristic of parapneumonic pleuritis, while high activity of plasminogen activator in the blood and pleural exudate in its normal activity in the urine is seen in cancer pleuritis. The findings obtained can be used in clinical medicine for verification of pleural fluid nature.
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PMID:[Assessment of the activity of plasminogen activators in the differential diagnosis of pleural effusion]. 178 78

Substantial differences between mouse strains have been reported in the lesions present in the lung during the early phase of radiation injury. Some strains show only classical pneumonitis, while other strains develop substantial fibrosis and hyaline membranes which contribute appreciably to respiratory insufficiency, in addition to pneumonitis. Other strains are intermediate between these extremes. These differences correlate with intrinsic differences in activities of lung plasminogen activator and angiotensin converting enzyme. The genetic basis of these differences was assessed by examining histologically the early reaction in lungs of seven murine hybrids available commercially after whole-thorax irradiation. Crosses between fibrosing and nonfibrosing parents were uniformly nonfibrosing, and crosses between fibrosing and intermediate parents were uniformly intermediate. No evidence of sex linkage was seen. Thus the phenotype in which fibrosis is found is controlled by autosomal recessive determinants. Strains prone to radiation-induced pulmonary fibrosis and hyaline membranes exhibited intrinsically lower activities of lung plasminogen activator and angiotensin converting enzyme than either the nonfibrosing strains or the nonfibrosing hybrid crosses. The median time of death of the hybrids was genetically determined primarily by the longest-lived parent regardless of the types of lesions expressed.
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PMID:The genetic basis of strain-dependent differences in the early phase of radiation injury in mouse lung. 185 22

The peculiarly fibrinous nature of bovine acute lung injury due to infection with Pasteurella haemolytica A1 suggests an imbalance between leukocyte-directed procoagulant and profibrinolytic influences in the inflamed bovine lung. Calves with experimental pneumonia produced by intratracheal inoculation with P. haemolytica A1 developed acute locally extensive cranioventral fibrinopurulent bronchopneumonia. Pulmonary alveolar macrophages (PAM) recovered by segmental lavage from affected lung lobes were 30 times more procoagulant than PAM obtained from unaffected lung lobes and 37-fold more procoagulant than PAM from control calf lungs. Unlike the enhancement of procoagulant activity, profibrinolytic activity (plasminogen activator amidolysis) of total lung leukocytes (PAM and plasminogen activator neutrophils [PMN]) was decreased 23 times in cells obtained from affected lung lobes and also was decreased four times in cells obtained from unaffected lobes of infected animals. This marked imbalance in cellular procoagulant and fibrinolytic activity probably contributes significantly to enhanced fibrin deposition and retarded fibrin removal. In addition, PAM from inflamed lungs were strongly positive for bovine tissue factor antigen as demonstrated by immunocytochemistry. Intensely tissue factor-positive PAM enmeshed in fibrinocellular exudates and positive alveolar walls were situated such that they were likely to have, in concert, initiated extrinsic activation of coagulation in the acutely inflamed lung. These data collectively suggest that enhanced PAM-directed procoagulant activity and diminished PAM- and PMN-directed profibrinolytic activity represent important modifications of local leukocyte function in bovine acute lung injury that are central to the pathogenesis of lesion development with extensive fibrin deposition and retarded fibrin removal.
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PMID:The role of leukocytes in the pathogenesis of fibrin deposition in bovine acute lung injury. 202 7

The potential importance of pleural fibrin deposition in the pathogenesis of pleural injury is supported by both clinical and experimental observations. We hypothesized that the local equilibrium between procoagulant and fibrinolytic activities is disrupted to favor fibrin deposition in exudative pleuritis. To test this hypothesis, we characterized procoagulant and fibrinolytic activities in pleural exudates from patients with pneumonia, lung cancer, or empyema and transudates from patients with congestive heart failure. Procoagulant activity was generally increased in exudative processes and was due mainly to tissue factor. All effusions contained antithrombin III and inhibited factor Xa and thrombin, but endogenous prothrombinase or thrombin activities were variably detected. Pleural fluid fibrinolytic activity was increased in congestive heart failure and was due to both tissue plasminogen activator and urokinase. Depressed fibrinolytic activity was found in pleural exudates despite increased concentrations of plasminogen, mainly glu-1-plasminogen, and was due to inhibition of plasminogen activation by plasminogen activator inhibitors 1 and 2 and of plasmin, in part by alpha 2-antiplasmin. Concentrations of PAI-1 in exudative pleural fluids were increased up to 913-fold, compared with normal pooled plasma. Exudative pleural effusions are characterized by increased procoagulant and depressed fibrinolytic activity, favoring fibrin deposition in the pleural space. The balance of these activities is reversed and favors fibrin clearance in congestive heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Abnormalities of pathways of fibrin turnover in the human pleural space. 206 28

Urokinase type plasminogen activator (u-PA) was purified from three different chest fluids obtained from patients with liver cirrhosis and pleuritis, aplastic anemia and pneumonia, and lung tumor, and the relationship between molecular weight and plasminogen activator (PA) activity was examined by zymography. The molecular weights of u-PAs from the chest fluids were 200 Kd, 150-180 Kd, 95 Kd, 55 Kd, 44 Kd, 33 Kd and 14 Kd, and PA activity was observed at molecular weights of 95 Kd, 55 Kd and 33 Kd. Fibrin binding of u-PA was observed at molecular weights of 55 Kd and 33 Kd.
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PMID:Properties of urokinase type-plasminogen activator found in chest fluid. 210 19

Hemostasis system and immune reactivity were studied in chronic alcoholics with (92 subjects) and without (65 subjects) acute pneumonia. Activation and antiplasmin activities of blood in the alcoholics were found reduced. In associated alcoholism and pneumonia the two diseases aggravate each other causing a sharp suppression of lymphocytic component of immunity and inhibition of plasminogen activator activity. The majority of patients respond with a compensatory rise in the number of monocytes with active receptors. In coupled lymphocytopenia and monocytopenia the favorable outcome is unlikely. The prognosis is more beneficial in enhanced systemic fibrinolysis observed in elevated count of mononuclears with active Fc-receptors suggesting laboratory evidence for convalescence.
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PMID:[Hemostasis system and immune reactivity in patients with acute pneumonia and chronic alcoholism]. 237 Jul 69

Extravascular coagulation and fibrinolysis is an integral part of inflammatory reactions. Disordered expression of procoagulant and profibrinolytic factors by mononuclear phagocytes of the lung (i.e. lung alveolar macrophages (LAM) and interstitial macrophages) may have important bearings on inflammatory lung tissue destruction and repair. Based on this hypothesis we have measured the presence of trigger molecules and activation products of the coagulation and fibrinolytic system in cell-free bronchoalveolar lavage fluid and in bronchoalveolar cells. Patient groups with chronic obstructive disease (COLD) (n = 76), idiopathic pulmonary fibrosis (IPF) (n = 29), sarcoidosis (n = 22), lung cancer (n = 36), pneumonia (n = 39), acquired immunodeficiency syndrome (AIDS) (n = 17) and a control group (n = 60) were studied by bronchoalveolar lavage (BAL). In all patient groups tissue thromboplastin (TPL) and fibrinopeptide A (FPA) were significantly increased compared to controls. Plasminogen activator (PA) activity was significantly lower in patients than in normals, and usually associated with high levels of antifibrinolytic activity. The level of PA inhibitor (PAI-2) was not significantly higher in any patient group compared to controls. The sensitivity of the method for fibrin degradation products (FDP) analysis was not high enough to detect FDP in BAL fluid of control individuals, whereas such products could be demonstrated in 25-53% of patients in various categories. We conclude that disordered expression of procoagulant and plasminogen activator activities in bronchoalveolar lavage fluid may reflect a milieu that favours accumulation of fibrin in inflammatory lung tissue and form the basis for the development of pulmonary fibrosis.
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PMID:Local activation of the coagulation and fibrinolysis systems in lung disease. 238 54

Urokinase receptors on lymphocytes described in the paper link immune system of the body with fibrinolytic one, play a biological role in sano-++- and pathogenesis in aggravation of chronic purulent bronchitis, of focal and croupous pneumonia. A correlation between the trend in the expression of urokinase receptors on lymphocytes and changes in activity of plasminogen activator in the blood and urine was established: the more the expression, the more the activity. The method can serve a criterion of the treatment effectiveness+ in nonspecific inflammatory bronchial and pulmonary diseases and be helpful in designing methods of their treatment improvement.
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PMID:[Regulation of fibrinolysis by lymphocytes in inflammatory diseases of the bronchopulmonary system]. 256 May 7

Parenchymal fibrin deposition is well recognized in many forms of acute lung injury. Proteins derived from the actions of the coagulation and fibrinolytic systems may potentiate these inflammatory reactions as well as influence the subsequent repair process. However, the factors regulating fibrin formation and dissolution in acute pneumonitis have not been defined. In this study, we characterized the procoagulant (PC) and fibrinolytic activities simultaneously present in the alveolar space during the course of acute lung injury induced in rabbits by an intravenous injection of phorbol myristate acetate (PMA). Within 6 h of PMA injection, this injury was characterized histologically by extensive intra-alveolar fibrin formation and marked accumulation in pulmonary parenchyma of intravenously administered 125I-fibrinogen. Clearance of fibrin ensued over the remainder of the 72-h study period. Normal BAL fluid contained high levels of procoagulant activity which did not vary after the onset of inflammation. The procoagulant activity was attributed to particle-bound tissue thromboplastin as well as other factors of the extrinsic coagulation pathway. There were low levels of plasminogen activator (PA) activity in normal BAL fluid, but the mean activity increased 9.3-fold over control values by 12 h after PMA injection (p less than 0.01). When plasminogen activator activity in BAL fluid was referenced to the concomitant procoagulant activity, this ratio (PA/PC) increased 17.8-fold over controls, peaking 24 h after PMA injection (p less than 0.01). The levels of both procoagulant and plasminogen activator activities associated with alveolar macrophages were stable during the study period. Compared to alveolar macrophages, granulocytes expressed similar levels of plasminogen activator but negligible procoagulant activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tissue fibrin deposition during acute lung injury in rabbits and its relationship to local expression of procoagulant and fibrinolytic activities. 356 41

Low dose intra-arterial thrombolysis is too slow for many patients with severe acute limb ischaemia. Accelerated thrombolysis with high dose bolus t-PA was used in a consecutive series of 43 patients. Complete or clinically useful lysis was achieved in 39 patients, with a median duration of 7 h. Lysis occurred in 46% in under 4 h. Fifty-six per cent of patients required further procedures after lysis. Eleven per cent suffered a major bleed. The limb salvage rate at 30 days was 56%. Amputation was required in 22% and 22% died. Most deaths were due to associated thrombotic conditions: myocardial infarction (5), pulmonary embolism (1) and malignant thrombosis (1). One patient died from pneumonia two weeks after lysis and two died from renal failure within a week of thrombolysis. The high mortality rate was not associated with bleeding but may reflect the high risks involved in treating this group of patients. High dose bolus t-PA infusion appears to predict immediate outcome of thrombolysis as well as reducing infusion times. It may expand the indications for the non-surgical treatment of acute limb ischaemia to include most patients with the condition. Careful case selection is still necessary for optimal results.
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PMID:Accelerated thrombolysis with high dose bolus t-PA extends the role of peripheral thrombolysis but may increase the risks. 748 22


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