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PubMed1983

Studies of the kallikrein-kinin system in patients with sickle cell anemia.

Eight patients with sickle cell anemia (SS hemoglobin) were found to have decreased plasma levels of prekallikrein compared to normal control subjects or patients with other types of anemia. The prekallikrein levels in the patients with sickle cell anemia were found to decrease further during a sickle cell crisis. These results suggest that components of the kallikrein-kinin system are profoundly affected in patients with sickle cell anemia, and during crises may play a role in the clinical presentation of patients.

Adolescent↗
PubMed1983

[Prothrombin--substrate for blood plasma kallikrein and factor XIIa].

A study was made of the interaction between prothrombin and enzymes: blood plasma kallikrein and factors alpha-XIIa and beta-XIIa immobilized on enzacryl-AH. Kallikrein-induced prothrombin proteolysis was accompanied by a decrease in prothrombin activity, appearance of BAME-esterase and poor clotting activity. As a result of fractionation of products on the column with DEAE-Sephadex A-50, some fractions that have thrombin amidase activity (splitting of the substrate S-2238) and high antithrombin activity were obtained. Antithrombin activity manifested in the inhibition of fibrinmonomer aggregation during fibrin formation. During incubation with prothrombin, factors alpha-XIIa and beta-XIIa also stimulated the appearance of BAME-esterase activity. None of the immobilized enzymes activated factor X.

Acrylic Resins↗
PubMed1984

Amino acid sequence and secondary structural analysis of the corn inhibitor of trypsin and activated Hageman Factor.

The amino acid sequence of a corn inhibitor for trypsin and activated Hageman Factor (Factor XIIa) was determined by automated Edman degradation from the intact inhibitor and two fragments generated by specific cleavage of the inhibitor. The 112-residue sequence is unique at each position except 91, where both Ala and Glu were found. The structural heterogeneity suggests the occurrence of two genes (possibly allelic) for the inhibitor. Based on analysis of fragments produced by the interaction of the inhibitor with trypsin-agarose, the reactive site peptide bond is identified as Arg 36-Leu 37. There is no strong similarity between the sequence of the corn inhibitor and the sequences published for other serine protease inhibitors. Thus, the corn inhibitor represents a new family of protease inhibitors. Circular dichroism measurements and a theoretical prediction of secondary structure indicate that the inhibitor has helix and beta sheet contents of approximately 40 and 20%, respectively.

Amino Acid Sequence↗
PubMed1983

Non-thrombogenicity of clean glass revealed by native whole blood assay in bead columns.

The previously described native whole blood assay for materials in solution or suspension has been adapted to materials in a bead column configuration. These experiments showed that the glass itself accounts for little or none of the high blood-reactivity observed with conventional glass bead columns. Columns composed solely of soft glass that was "cleaned" by heat treatment (500-595 degrees C 18 hr, electric oven) were benign toward flowing native whole blood for all variables measured (platelet count and platelet-free plasma [C14]-serotonin content, platelet factor 3 and factor XII activities, and recalcification time) with the standard contact protocol. In addition, the effluent successfully maintained perfusion of the isolated kidney, a measure of the ability of platelets to support vascular integrity. Prolonged (30 min) normothermic contact with citrated whole blood increased the subsequent reactivity of initially clean glass toward whole blood albeit to a level much less than that of conventional glass bead columns.

Animals↗
PubMed1984

[Secretion of the salivary glands of the medicinal leech Hirudo medicinalis inhibits ADP-induced aggregation of human platelets and platelet adhesion to a collagen-coated surface].

As was earlier demonstrated, secretion of medical leech exhibits high antithrombin activity of hirudin and inhibits contact activation of factor XII. Attempts were made to investigate the effects of the leech secretion on (i) the ADP-induced aggregation of platelets in suspension, registered by photometry according to Born, and (ii) platelet adhesion to the calf skin collagen-coated surface measured by scanning electron microscopy. The following results were obtained: 1) the secretion at doses of 0.13 vol % and 0.75 vol % inhibits the ADP-induced aggregation of gel-filtered human platelets by 50 and 97%, respectively; 2) the secretion inhibits the total adhesion and initial attachment of the gel-filtered platelets to the collagen substrate by 60-70% (dose 0.1-1.0 vol %) and 87-88% (dose 10 vol %); 3) platelet spreading on the collagen substrate and adhesion of the platelets from suspension to the upper surface of the spread platelets are inhibited by the secretion as well, but these effects are not statistically significant. The data obtained suggest that the secretion contains components which inhibit both the coagulating and platelet-vascular wall pathways of hemostasis.

Adenosine Diphosphate↗
PubMed1980

Prekallikrein activator levels and side effects with human albumin preparations.

Recently the question has been raised whether the presence of prekallikrein activator (PKA) in human blood products for i.v. application could possibly cause adverse reactions in the recipient as observed now and then. Up to now a correlation between both properties is far from being established, even though in the U.S. there has been extensive discussion over some PPL batches containing elevated amounts of PKA, presumed to be causally related to an increased frequency of side reactions. As has been demonstrated in the past through wide clinical experience, human albumin is an exceptionally safe blood product. If at all, side effects sometimes seem to occur related to certain individual lots, the reason for which is still unrevealed. In the pursuit of eventually finding some association between PKA levels in and side reactions with albumin, we performed PKA measurements on a panel of commercial human albumin batches, a few of which had been reported occasionally to cause adverse reactions. The assay procedure was essentially that published (3). BOB PKA reference No 1 was included as a standard. PKA was detected in moderate amounts in huge series of albumin batches without any reported side reactions. We conclude, therefore, that PKA levels in the range of trace amounts cannot be related to side reactions with human albumin preparations.

Esterases↗
PubMed1982

Bradykinin-mediated hypotension after infusion of plasma-protein fraction.

In patients who required volume expansion during extracorporeal circulation, the plasma bradykinin concentration was monitored simultaneously with the mean arterial pressure during infusion of either albumin solution or PPF. The PKA content of the PPF and the albumin solution was 29 and 3 U/L, respectively, measured spectrophotometrically. In six patients receiving 250 ml of PPF, the mean arterial pressure decreased 22% to 54% within 1.5 min after infusion, whereas the plasma bradykinin concentration, measured by radioimmunoassay, increased significantly (p less than 0.0005) during the first minute. In six patients receiving 250 ml of 4% albumin solution, no blood pressure changes were found, and the plasma bradykinin concentration rose only slightly. In vitro, linear correlation (r = 0.94, p less than 0.0005) was observed between the level of PKA of 26 different lots of PPF and the concentrations of bradykinin that were generated in Hageman factor-deficient plasma after incubation with PPF. It is concluded that the hypotensive reactions observed after PPF infusion during extracorporeal circulation are caused by the PKA-induced bradykinin generation.

Adult↗
PubMed1982

Hypotensive effects of plasma protein fraction. The relation between prekallikrein activator, bradykinin generation, and blood pressure in an animal model.

In a rat model, the relationship between the activity of PKA in human PPFs, the changes in arterial BK concentration, and the changes in blood pressure on infusion of PPF was investigated. The rat was chosen as a model because it is reported to be one of the few animals sensitive to human PKA. However, hypotensive reactions after infusion of human PKA-containing PPF were observed only in the presence of a bradykinin-potentiating peptide (BPP9a). A correlation was found between the PKA content of the rapidly infused PPF, the BK generation in the rat, and the fall in arterial blood pressure. In control experiments, infusions of BK provoKed a similar fall in blood pressure at corresponding BK levels. After neutralization of the PKA activity in the PPF with C1-esterase inhibitor, neither a rise in BK level nor a fall in blood pressure was observed on infusion. We conclude therefore that the hypotensive reactions were caused by PKA-mediated generation of BK.

Animals↗
PubMed1981

Plasma prekallikrein and endotoxemia in liver cirrhosis.

In liver disease low prekallikrein levels may be found which has been suggested to be due to diminished synthesis. However, it may also be due to endotoxemia accompanying liver disease. To study the last possiblity prekallikrein, endotoxins and Normotest were determined in 18 cirrhosis patients. The relation between the prekallikrein concentration (after 15 min activation) and the Normotest was significant (r = + 0.72, P less than 0.001). Endotoxemia was only found in the more severe forms of liver disease (Normotest below 60%). During endotoxemia the prekallikrein levels were significantly lower than when no endotoxins were present in the blood of the same patients. The Normotest did not differ significantly in these patients in relation to the presence or absence of endotoxins. The activation of prekallikrein was slower in the more severe forms of liver disease. This might be due to reduced levels of factor XII and high molecular weight kininogen. In conclusion the reduced prekallikrein level in liver cirrhosis may be due to both diminished synthesis and endotoxemia. In the more severe forms of liver disease the time necessary to activate prekallikrein is increased.

Adult↗
PubMed1978

Effect of polyurethane morphology on blood coagulation.

A series of polyurethanes based on the hard segment MDI and soft segment PTMG were synthesized. The molecular weight of the PTMG was 730, 1000, and 2000, and ethylene diamine was used as chain extender. The fabrication process was varied so as to achieve the maximum disorder (nonequilibrium state) and maximum order, fully annealed. It was demostrated that the "quenched" non-equilibrium state reduces the rate of activation of the intrinsic systems, factor XII pathway, when compared to the fully annealed state. Platelet attachment is primarily affected by phase separation.

Blood Coagulation↗