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

Local and systemic coagulation and fibrin deposition occur in many types of alveolar injury and inflammation, but clotting factors capable of initiating the coagulation cascade in the alveolus have not been thoroughly identified and characterized. In the present studies, BAL (bronchoalveolar lavage) fluids obtained from rabbits were found to have procoagulant activity detectable in dilutions containing as little as 1.3 ng of protein. The specific activity of the procoagulant in these fluids was within 1 order of magnitude of that found in brain thromboplastin. The BAL procoagulant was shown to be associated with particles having a molecular weight greater than 15 X 10(6) daltons by gel filtration chromatography, and was characterized as tissue factor by showing specific requirements for factors VII, X, and II. Further experiments were performed using membranes purified from alveolar macrophages by sucrose density gradients and characterized by studies of alkaline phosphodiesterase I, a cytoplasmic membrane marker, and electron microscopy. These studies demonstrate that alveolar macrophages, especially low-density subpopulations, generate and release membrane material that is a source of tissue factor in BAL fluids.
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PMID:Tissue factor in bronchoalveolar lavage fluids. Evidence for an alveolar macrophage source. 397 71

The extrinsic pathway is probably the predominant pathway in initiating blood coagulation in inflammatory lung diseases. Tissue factor pathway inhibitor (TFPI) is a Kunitz-type protease inhibitor of factor VIIa/tissue factor in the presence of factor Xa. As it has been shown recently that TFPI plasma levels are increased under acute inflammatory conditions, we studied TFPI antigen plasma levels before and after injecting 20 IU/kg body weight of unfractionated heparin into 49 patients with different stages of sarcoidosis, into 9 with idiopathic pulmonary fibrosis, and into 15 normal controls. TFPI, before injecting heparin, was significantly increased in all sarcoidosis stages (stage I: 97.6 +/- 6.4 ng/mL; stage II: 116.2 +/- 11.9 ng/mL; stage III: 116.3 +/- 7.3 ng/mL) and in idiopathic pulmonary fibrosis (116.8 +/- 16.1 ng/mL), as compared to the control group (77.7 +/- 3.3 ng/mL). No correlation was found between the intensity of the activity of sarcoidosis, measured as BAL white cell count, and TFPI. Five minutes after heparin administration the rise in TFPI was lower, although not statistically significant, in all sarcoidosis stages than in controls. In contrast, idiopathic pulmonary fibrosis had a similar or even higher TFPI elevation than the control group. In sarcoidosis the elevated TFPI and the lower capacity by endothelial cells to release TFPI after heparin may represent a compensatory mechanism to prevent blood clotting and/or the endothelial cell dysfunction of the microvasculature in this condition. In contrast, the extensive mesenchymal cell proliferation present in idiopathic pulmonary fibrosis could explain our findings, as it has been shown that cultured human mesangial cells produce and release TFPI.
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PMID:Tissue factor pathway inhibitor (TFPI) antigen plasma level in patients with interstitial lung disease before and after heparin administration. 915 10