Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.7 (plasmin)
 9,023 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

The concentration of plasma antithrombin III (AT III) and the biological activity of plasma alpha2-plasmin inhibitor (alpha 2-PI) were measured in cases of mitral stenosis (MS) and rheumatic heart disease (RHD) without MS. Cases of MS showed the findings of the low levels of plasma AT III and normal or a little higher levels of plasma alpha 2-PI, that was not recognized in RHD without MS. This finding was interpreted to be hypercoagulable because of the acceleration of coagulation and of little or slight retardation of fibrinolysis. Besides, the influence of atrial fibrillation and chronic congestive heart failure on hypercoagulability in cases of MS was detected clearly, but the influence of them in cases of non-RHD was obscure. As the results, the severer the degree of MS, the clearer the hypercoagulable state. Therefore, the prethrombotic state existed in cases of MS, combined with blood flow disturbance due to atrial fibrillation or chronic congestive heart failure, endocardial damage resulted from rheumatic fever in an early stage and hypercoagulable state mentioned above in the present study. There was no significant difference between cases with and without thrombi in the degree of hypercoagulability in subjects with MS shown in the present work. It was concluded that the consumption of AT III caused the low levels of it in cases of MS, and that the low production of AT III in the liver rather than consumption caused the low levels of it in cases of non-RHD.
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PMID:Hypercoagulability in patients with mitral stenosis -- from the viewpoint of the behavior of plasma antithrombin III and alpha2-plasmin inhibitor. 743 47

Left ventricular (LV) remodeling after myocardial infarction (MI) results in LV dilation, a major cause of congestive heart failure and sudden cardiac death. Ischemic injury and the ensuing inflammatory response participate in LV remodeling, leading to myocardial rupture and LV dilation. Myeloperoxidase (MPO), which accumulates in the infarct zone, is released from neutrophils and monocytes leading to the formation of reactive chlorinating species capable of oxidizing proteins and altering biological function. We studied acute myocardial infarction (AMI) in a chronic coronary artery ligation model in MPO null mice (MPO(-/-)). MPO(-/-) demonstrated decreased leukocyte infiltration, significant reduction in LV dilation, and marked preservation of LV function. The mechanism appears to be due to decreased oxidative inactivation of plasminogen activator inhibitor 1 (PAI-1) in the MPO(-/-), leading to decreased tissue plasmin activity. MPO and PAI-1 are shown to have a critical role in the LV response immediately after MI, as demonstrated by markedly delayed myocardial rupture in the MPO(-/-) and accelerated rupture in the PAI-1(-/-). These data offer a mechanistic link between inflammation and LV remodeling by demonstrating a heretofore unrecognized role for MPO and PAI-1 in orchestrating the myocardial response to AMI.
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PMID:Myeloperoxidase and plasminogen activator inhibitor 1 play a central role in ventricular remodeling after myocardial infarction. 1261 2