Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:6.2.1.7 (BAL)
 1,977 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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)
 ...
PMID:Tissue fibrin deposition during acute lung injury in rabbits and its relationship to local expression of procoagulant and fibrinolytic activities. 356 41

The function of a newly devised bioartificial liver (AMC-BAL) based on viable, freshly isolated porcine hepatocytes has been evaluated in anhepatic pigs. The aim of this study was to assess the contribution of BAL treatment on blood coagulation parameters. Pigs were anesthetized and a total hepatectomy was performed (n = 15). The infrahepatic caval vein and the portal vein were connected to the subdiaphragmatic caval vein using a three-way prosthesis. Animals received standard intensive care (control, n= 5), treatment with an empty BAL (device control, n= 5) or with a cell-loaded BAL (BAL-treatment, n= 5) for a period of 24 h starting 24 h after hepatectomy. Coagulation parameters studied concerned prothrombin time (PT), platelet count, the procoagulant system (factors (F)II, FV, FVII, FVIII and fibrinogen), anticoagulant system (AT III), fibrinolytic system (t-PA, PAI-1) as well as markers of coagulation factor activation (TAT complexes, prothrombin fragment F1 + 2). FII, FV, FVII, AT III and fibrinogen rapidly decreased after total hepatectomy in pigs in accordance with the anhepatic state of the animals. FVIII levels were not influenced by the hepatectomy. A mild drop in platelet count was seen in all groups. Treatment of anhepatic pigs with the cell-loaded BAL did not restore PT or clotting factor levels. TAT and F1 + 2 complexes, however, were significantly increased in this group. Levels of t-PA and PAI-1 were not influenced by cell-loaded BAL treatment. Treatment of anhepatic pigs with the AMC-BAL based on freshly isolated porcine hepatocytes does not result in an improved coagulation state due to extensive consumption of clotting factors. However, increased levels of TAT complexes and prothrombin fragments F1 + 2 during treatment of anhepatic pigs indicate synthesis and direct activation of coagulation factors, leading to thrombin generation. This demonstrates that this bioartificial liver is capable of synthesizing coagulation factors.
 ...
PMID:Blood coagulation in anhepatic pigs: effects of treatment with the AMC-bioartificial liver. 1287 59

Histidine-rich glycoprotein (HRG) is an enigmatic glycoprotein able to interact with a variety of ligands such as IgG, complement components, heparan sulfate, thrombospondin, fibrinogen and plasminogen. HRG is present at high concentrations in plasma and there is evidence indicating that it is able to modulate the course of biological processes such as angiogenesis, fibroblast proliferation, complement activation, coagulation and fibrinolysis. Because these processes are involved in the pathogeneses of lung fibrosis we here analyzed a possible link between HRG and idiopathic pulmonary fibrosis (IPF). We found that plasma concentrations of HRG are significantly diminished in IPF patients compared to healthy subjects. Moreover, we found a positive correlation between HRG plasma levels and forced vital capacity (FVC) values, suggesting that plasma concentration of HRG would be a useful indicator of disease activity in IPF. HRG has been described as a negative acute phase reactant able to accumulate at sites of tissue injury. Hence, we also measured the concentrations of HRG in BAL samples from IPF patients. We found that the concentrations of HRG in samples from IPF patients were significantly higher compared to controls, suggesting that the reduced concentration of HRG in plasma from IPF patients could be due, at least in part, to an enhanced uptake of this protein in the lung.
...
PMID:Histidine-rich glycoprotein and idiopathic pulmonary fibrosis. 2652 73