Alpha 2-plasmin inhibitor.

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Evaluation of fibrinolytic therapy by measuring cross-linked fibrin derivatives and plasmin-alpha 2-plasmin inhibitor complex in plasma.

Plasma levels of alpha 2-plasmin inhibitor (alpha 2PI), plasmin-alpha 2PI complex and cross-linked fibrin derivatives (XDP) were measured in 8 patients (12 episodes) with thromboembolic disorders on the initial administration of urokinase. In conjunction with a decrease in plasma alpha 2PI activity and antigen, plasmin-alpha 2PI complex increased following urokinase infusion in all cases except...

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Acceleration of fibrinolysis by the N-terminal peptide of alpha 2-plasmin inhibitor.

When blood plasma containing the NH2-terminal 12-residue peptide (N-peptide) of alpha 2-plasmin inhibitor (alpha 2PI; alpha 2-antiplasmin) was clotted in the presence of calcium ions, the N-peptide and alpha 2PI were cross-linked to fibrin by activated coagulation factor XIII. The amount of N-peptide cross-linked to fibrin was proportional to the concentration of N-peptide present in plasma. On...

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Synthesis and secretion of alpha 2-plasmin inhibitor by established human liver cell lines.

The site of synthesis of alpha 2-plasmin inhibitor (alpha 2-PI), a physiologic inhibitor of plasmin, is not known with certainty. We have studied the production and secretion of alpha 2-PI by three established human liver cell lines derived from hepatocellular carcinoma and hepatoblastoma (Hep G2, Hep 3B, and PLC/PRF/5). As measured by a specific radioimmunoassay, the titer of alpha 2-PI increa...

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Fibrinolytic states in a patient with congenital deficiency of alpha 2-plasmin inhibitor.

The fibrinolytic system of a patient with congenital deficiency of a2-proteinase (plasmin) inhibitor (a2Pl) was studied. The patient’s whole blood clot formed in vitro was lysed rapidly in several hours on incubation. This accelerated in vitro fibrinolysis was suppressed by an addition of purified a2Pl. The degree of suppression was proportional to the amount of a2PI added. In spite of the acce...

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Formation of C 8 - CI - Inhibitor , Kallikrein - CI - Inhibitor , and Plasmin - a 2 - Plasmin - Inhibitor Complexes During Cardiopulmonary Bypass

Stimulation of platelets and neutrophils occurs during clinical cardiopulmonary bypass. We investigated whether the classical complement. contact. or fibrinolytic pathways are activated as potential sources of neutrophil agonists. Using enzyme-linked immunosorbent “sandwich” assays specific for Cl 8-C1 -and kallikrein-C1 -inhibitor complexes respectively. we found that there was a modest increa...

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ژورنال

عنوان ژورنال: Nihon Naika Gakkai Zasshi

سال: 1991

ISSN: 0021-5384,1883-2083

DOI: 10.2169/naika.80.1339