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Fundamentals of fibrinolytic therapy.

The fibrinolytic system is activated by the conversion of plasminogen to plasmin by mediators such as tissue extract, plasma factor XII, or the exogenous activators urokinase (UK) and streptokinase (SK). The foreign protein composition of SK is responsible for the allergic response observed in some patients following administration. Clinical and investigational evidence has also shown a higher incidence of hemorrhagic complications with SK compared with UK. In general, thrombolytic therapy is a safe, effective way to resolve thrombotic obstruction in patients with such problems as acute pulmonary embolism, acute myocardial infarction, or occluded intravascular lines.

Fibrinolytic Agents↗

[Serine protease activity in blood plasma during the healing of aseptic and infected wounds under experimental conditions].

Activity of serine proteases--kallikrein-like activity (KLA) and plasmin-like activity (PLA)--were studied in the blood plasma of 220 sexually mature male Wistar rats with simulated aseptic and infected surface wounds in the time course before the operation, daily from the 1st to 10th day, as well as 12 and 15 days after the surgery. During the healing of aseptic and especially infected wound blood plasma KLA and PLA were found to be decreasing, thus indicating the active role of factor-XII-dependent systems in wound healing, reflecting the response of the body to operation-induced injury and wound infection, and dependent on the character and stage of wound healing course.

Animals↗

Deglycosylation of fibrinogen accelerates polymerization and increases lateral aggregation of fibrin fibers.

Fibrinogen, the major structural precursor of blood clots, was deglycosylated by peptide-N-(N-acetyl-beta-glucosaminyl)asparagine amidase without denaturation of the polypeptide chains. Deglycosylated fibrinogen behaved normally in clinical coagulation assays, although it is less soluble than normal fibrinogen. However, the turbidity of clots formed from deglycosylated fibrinogen always rose faster and higher than that of clots from normal fibrinogen. Scanning and transmission electron microscopy demonstrated that fibrin made from clots of deglycosylated fibrinogen consisted of thicker, less-branched fiber bundles in a more porous network. Moreover, the degree of lateral aggregation was directly related to clot turbidity and inversely related to branching. Deglycosylation promoted turbidity development, lateral aggregation, and porosity of clots under all conditions tested. All other steps in the coagulation pathways appeared to be unaffected by the absence of carbohydrate. These results suggest that carbohydrate constitutively affects the behavior of deglycosylated fibrinogens by 1) contributing a repulsive force that promotes fibrinogen solubility and limits fibrin assembly and 2) sensitizing fibrin to conditions that influence assembly and clot structure.

Factor XII↗

In vitro assay for prekallikrein activator (PKA).

The assay measures the action of prekallikrein in generating kallikrein. The prekallikrein activator is the limiting reagent. The product kallikrein is an esterase which can be quantitated using benzoyl arginine ethyl ester. The assay is reproducible and results are comparable with other methods. The large scale preparation of prekallikrein is described.

Blood Proteins↗

The assay of prekallikrein activator in human blood products.

An assay for the determination of prekallikrein activator (PKA) in human blood products is described. Kallikrein released from a prekallikrein substrate preparation by PKA in the sample is determined using the synthetic substrate S-2302 (H-D-Pro-Phe-Arg-pNA). The PKA content of the sample is quantitated by interpolation from a standard line obtained using a reference preparation of plasma protein fraction (PPF). Endogenous kallikrein is estimated and an adjustment made for its contribution to the apparent PKA content of the sample. The results of determinations on a number of PPF, immunoglobulin and coagulation factor preparations are presented and discussed.

Blood Proteins↗

[Monosomy 7qter (author's transl)].

A de novo terminal del (7)(q35) was found in a 3-month-old girl referred because of a peculiar cry. This observation, with seven others from the literature permit the delineation of a syndrome characterized by severe microcephaly with a flattened occiput, a bulbous nose, a "double chin", and a broad thorax with widely spaced nipples, without internal organ malformations. Assays of Hageman factor (XII) revealed normal values. The proposita is heterozygous Jk (a + b +). The parents and the proposita are iny-1.

Abnormalities, Multiple↗

Changes of contact phase proteins during haemodialysis.

Functional and immunological activities of factors XII and XI, Prekallikrein, high molecular weight kininogen and C-1-esterase inhibitor were studied in eight patients before, during and after haemodialysis. During and after dialysis sessions a significant decrease in the functional activities of Prekallikrein and high molecular weight kininogen (p less than 0.05) could be detected, whereas their immunological levels did not change. Furthermore C-1-esterase inhibitor increased after dialysis (p less than 0.05). These results indicate activation of the kinin system during haemodialysis.

Adult↗

The effect of C1 inhibitor upon Hageman factor autoactivation.

Using components purified from human plasma, we have examined the effects of C1 inhibitor (C1 INH), the primary inhibitor of activated Hageman Factor (HFa) and Hageman factor fragment (HFf), on Hageman Factor (HF) autoactivation. When Hageman factor was exposed to a negatively charged surface, provided by either a glass cuvette or dextran sulfate, the addition of C1 INH gave a dose-dependent inhibition of the activity observed. The ability of C1 INH to decrease the maximal enzymatic activity generated was markedly temperature dependent with inhibition increasing as the temperature was raised from 4 degrees C to 37 degrees C. Although the rates of both autoactivation and inhibition were decreased at lower temperatures (4 degrees C), the latter rate was more sensitive to temperature modulation. When HF (final concentration 1 mumol/L) was incubated with C1 INH (0.54, 1.07, and 2.14 mumol/L) in the absence of an initiating surface, no increases in enzymatic activity were observed for up to 48 hours regardless of the C1 INH concentration. However, SDS polyacrylamide gel electrophoresis of the incubation mixture revealed that HF autodigestion had occurred by 48 hours despite the presence of C1 INH. In addition, the appearance of a new band suggested that a complex had been formed between the inhibitor and activated HF. Our findings indicate that C1 INH does not prevent HF autoactivation but rather inactivates the products of HF autodigestion.

Complement C1 Inactivator Proteins↗

Deficiency of the contact phase of intrinsic coagulation in a horse.

A 16-year-old gelding was examined because of weight loss, inappetence, and intermittent fever of 2 months' duration. Preliminary laboratory findings revealed anemia, hypoproteinemia, thrombocytopenia, and prolongation of the activated partial thromboplastin time. A deficiency or inhibition of coagulation factor XI, factor XII, or high molecular weight kininogen was diagnosed. This defect was not associated with a bleeding diathesis, but should be considered as a cause of prolongation of the activated partial thromboplastin time.

Animals↗

Rat plasma high-molecular-weight kininogen. A simple method for purification and its characterization.

High-molecular-weight kininogen has been isolated from rat plasma in three steps in a relatively high yield. The purified preparation gave a single band on sodium dodecyl sulfate-polyacrylamide gel electrophoresis in the absence and presence of 2-mercaptoethanol, and the apparent Mr was estimated as 100,000. On incubation with rat plasma kallikrein, rat high Mr kininogen yielded a kinin-free protein consisting of a heavy chain (Mr = 64,000) and a light chain (Mr = 46,000), liberating bradykinin. The kinin-free protein was S-alkylated, and its heavy and light chains were separated by a zinc-chelating Sepharose 6B column. The amino acid compositions of rat high Mr kininogen and its heavy and light chains were very similar to those of bovine high Mr kininogen and its heavy and fragment 1.2-light chains, respectively. A high histidine content in the light chain of rat high Mr kininogen indicated the presence of a histidine-rich region in this protein as in bovine high Mr kininogen, although this region was not cleaved by rat plasma kallikrein. Rat high Mr kininogen corrected to normal values the prolonged activated partial thromboplastin time of Brown-Norway Katholiek rat plasma known to be deficient in high Mr kininogen and of Fitzgerald trait plasma. The kinin-free protein had the same correcting activity as intact high Mr kininogen. Rat high Mr kininogen also accelerated approximately 10-fold the surface-dependent activation of rat factor XII and prekallikrein, which was mediated with kaolin, amylose sulfate, and sulfatide. These results indicate that rat high Mr kininogen is quite similar to human and bovine high Mr kininogens in terms of biochemical and functional properties.

Animals↗

Assessment of Hageman factor activation in human plasma: quantification of activated Hageman factor-C1 inactivator complexes by an enzyme-linked differential antibody immunosorbent assay.

An enzyme-linked immunosorbent assay has been developed for the quantitation of activated Hageman factor-C1 inactivator (HF-C1 INH) complexes. Addition of increasing quantities of either of the major forms of activated Hageman factor (HFa or HFf) to normal plasma or to Hageman factor-deficient plasma leads to a dose-dependent increase in activated HF-C1 INH complexes. As little as 0.5 micrograms/mL of activated HF added to plasma can be detected, corresponding to activation of approximately 2% of plasma HF. The sensitivity of the assay is increased at least tenfold when complexes are formed in HF-deficient plasma, indicating competition between unactivated HF and activated HF-C1 INH complexes for binding to the antibody. Specificity is demonstrated in that addition of activated HF to hereditary angioedema plasma yields less than 1% of the activated HF-C1 INH complex formation obtained with normal plasma. Kaolin activation of HF-deficient plasma yields no detectable complex formation. Kaolin activation of prekallikrein-deficient plasma demonstrates a time-dependent increase in formation of activated HF-C1 INH complex consistent with the ability of HF in this plasma to autoactivate as the time of incubation with the surface is increased. Kaolin treatment of high-molecular weight (HMW) kininogen-deficient plasma yields an even more profound abnormality in the rate of formation of activated HF-C1 INH complexes reflecting the complex role of HMW kininogen in the initiation of contact activation. Although addition of corn inhibitor to plasma prevents activated HF-C1 INH complex formation, it does not inhibit activated HF sufficiently fast to prevent prekallikrein activation.

Blood Coagulation↗