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Biomedical subjects

D A Lane

Publications and source records attributed to D A Lane.

At least 199 records · Page 11Linked to original sources
PubMed1980

An abnormal fibrinogen with delayed fibrinopeptide A release.

Investigation of the family of a patient presenting with haematuria revealed seven cases in three generations showing a prolonged thrombin clotting time. A dysfibrinogenaemia was confirmed when purified fibrinogen from an affected member of the family was shown to also exhibit a prolonged thrombin clotting time. No molecular abnormality could be demonstrated using electrophoretic and immunological techniques. However, using a specific radioimmunoassay to fibrinopeptide A a major defect has been localized to a delay in the rate of release of this peptide by thrombin when the abnormal fibrinogen is converted to fibrin. This case of dysfibrinogenaemia has been tentatively designated fibrinogen Manchester.

Blood Coagulation Disorders↗
PubMed1980

In vivo platelet release reaction in patients with heart valve prosthesis.

Platelets play an important role in the genesis of thromboembolic episodes frequently observed in patients following cardiac valve replacement. No simple and reliable method as yet exists for quantitating platelet function in vivo. Platelet-specific proteins, serum beta-thromboglobulin related antigen and platelet factor 4 as well as thromboxane B2 were measured in 50 healthy subjects and in 100 patients who had cardiac valve replacement at least 6 months previously; these were related to the type, site and number of valves replaced. Highly significant differences were observed in the mean plasma beta-thromboglobulin related antigen, platelet factor 4 and thromboxane B2 levels in patients compared with healthy controls. The elevated levels of platelet release products observed 6 months after cardiac valve replacement suggest a continuous activation by the prosthesis. No significant differences were observed in patients with different types and site of valve prosthesis.

Adult↗
PubMed1980

Platelet function during haemoperfusion in acute liver failure.

The changes in platelet-related haemostatic parameters have been studied during haemoperfusion of eleven patients with acute liver failure. Five patients were treated by haemoperfusion with an albumin-coated resin column and six with a polymer-coated charcoal column. The platelet and white cell losses over four hours' haemoperfusion were small in both groups. Significant increases in beta-thromboglobulin (mean 341 +/- SE 145 ng/ml) were seen after one hour in the patients treated by charcoal haemoperfusion. One patient in the charcoal group with the greatest rises in beta-thromboglobulin (860 ng/ml) and screen filtration pressure (205 mmHg) developed severe hypotension and haemoperfusion was terminated after 1 hour. One patient in the resin group showed rapid consumption of heparin after 2 hours. Measurement of beta-thromboglobulin is a sensitive assay of platelet activation during haemoperfusion. Albumin-coated resin haemoperfusion appears to be a more blood-compatible procedure with respect to platelets than charcoal haemoperfusion.

Acrylic Resins↗
PubMed1979

Evidence for a plasma inhibitor of the heparin accelerated inhibition of factor Xa by antithrombin III.

The ability of heparin fractions of different molecular weight to potentiate the action of antithrombin III against the coagulation factors thrombin and Xa has been examined in purified reaction mixtures and in plasma. Residual thrombin and Xa have been determined by their peptidase activities against the synthetic peptide substrates H-D-Phe-Pip-Arg-pNA and Bz-Ile-Gly-Arg-pNA. High molecular weight heparin fractions were found to have higher anticoagulant activities than low molecular weight heparin when studied with both thrombin and Xa incubation mixtures in purified mixtures and in plasma. The inhibition of thrombin by heparin fractions and antithrombin III was unaffected by other plasma components. However, normal human plasma contained a component that inhibited the heparin and antithrombin III inhibition of Xa particularly when the high molecular weight heparin fraction was used. Experiments using a purified preparation of platelet factor 4 suggested that the platelet-derived heparin-neutralizing protein was not responsible for the inhibition.

Animals↗
PubMed1978

Characterization of serum fibrinogen and fibrin fragments produced during disseminated intravascular coagulation.

The fibrinogen and fibrin degradation products (FDP) in serum samples taken from nine patients with suspected disseminated intravascular coagulation have been characterized using a method of immunoprecipitation followed by sodium dodecyl sulphate polyacrylamide gel electrophoresis. Aall of the serum samples contained a fragment with the same electrophoretic mobility as fibrinogen fragment X, while the majority also had evidence of fragments with similar mobility to fibrinogen fragments Y and D. In eight of the nine serum samples there was strong evidence of the D-dimer fragment that is released by plasmin lysis of crosslinked fibrin. Also present in all but one of the samples were fragments of higher molecular weight than fibrinogen which were probably soluble, non-clottable, factor XIIIa induced crosslinked derivatives of fibrinogen. These results suggest that during disseminated intravascular coagulation thrombin and activated factor XIII act upon fibrin(ogen) to form complexes that are subsequently lysed by plasmin to produce soluble crosslinked derivatives of fibrin.

Blood Coagulation Tests↗
PubMed1977

Intermittent plasminogen-streptokinase treatment of deep vein thrombosis.

The fibrinolytic response of 12 patients receiving single daily infusions of 600,000 units of streptokinase (SK) and 90 mg of plasminogen for the treatment of DVT has been studied. The mean plasminogen concentration was maintained throughout the treatment period (4-6 days) at between 20-40% the initial value, while mean circulating plasmin concentration rose to only about twice initial plasma levels. The degradation of fibrinogen as indicated by a fall in clottable fibrinogen did not fall below 1 mg/ml and serum FDP rose to greater than 1 mg/ml. Limited fibrinogenolysis occurred in 2 patients, while in another patient who bled there was immediate and extensive depletion to below 0.5 mg/ml. The beneficial clinical results obtained with this regimen (Kakkar et al. 1975), which produces only limited systemic plasminaemia, suggest that thrombolysis may be facilitated by higher levels of plasminogen than those maintained during conventional SK treatment.

Fibrin Fibrinogen Degradation Products↗
PubMed1977

A heparin analogue with specific action on antithrombin III.

The effects of heparin and a semi-synthetic heparin analogue were compared in vivo and in vitro. The two drugs differed strikingly in their in-vitro behaviour: unlike heparin, the heparin analogue had little effect in a specific heparin assay or on overall clotting, as measured by the kaolin-cephalin clotting time (K.C.C.T.). When given by parenteral injection, the heparin analogue had almost the same potentiating effect on antithrombin III as mucous heparin, but without a comparable effect on the K.C.C.T. These observations suggest that the heparin analogue may have desirable characteristics for the prophylaxis of venous thrombosis, since it selectively potentiates antithrombin III in vivo while having little effect on overall clotting.

Adult↗
PubMed1977

Acquired dysfibrinogenaemia in acute and chronic liver disease.

Plasma from patients with both acute and chronic liver disease has been examined for evidence of acquired dysfibrinogenaemia, using electrophoretic methods and coagulation tests. An examination of isolated fibrins upon SDS polyacryamide gel electrophoresis failed to demonstrate any molecular or structural defect associated with the polypeptide chains of the patients' fibrinogen or fibrinogen derivatives produced by thrombin or plasmin. However, purified fibrin monomers isolated from plasma using both Reptilase and thrombin exhibited delayed polymerization rates and the occurrence of acquired dysfibrinogenaemia in liver disease is therefore confirmed.

Acute Disease↗
PubMed1977

Comparison of heparin and a semi-synthetic heparin analogue, A73025. I. Kinetics of clearance from the circulation of man following intravenous injection.

A study has been made of a low molecular weight semi-synthetic heparin analogue, A73025, that may be clinically useful as an antithrombotic agent because of its reported high specificity for antithrombin III. The clearance from the circulation of both heparin and the analogue has been studied in man following intravenous injection. Heparin obeyed almost first order kinetics when assayed using a specific anti-Xa assay and first order kinetics when measured with KCCT. At high concentrations the heparin analogue was cleared with first order kinetics when assayed both with the anti-Xa assay and with KCCT. At low concentrations the analogue produced between one half and two-thirds of the anti-Xa activity of an equal dose of heparin, producing only a small prolongation of KCCT. With increasing dose, the more specific anti-Xa potentiating effect of A73025 decreased because of a flattening of its anti-Xa dose-response curve. These results suggest that the analogue might be useful as an antithrombotic agent when it is used as a prophylactic agent.

Adult↗
PubMed1977

Comparison of heparin and a semi-synthetic heparin analogue, A73025. II. Some effects on platelet function.

A comparison has been made of some effects of a semi-synthetic heparin analogue, A73025, and heparin upon platelet function. In several of the in vitro tests performed, such as their potentiating effects on ADP and adrenaline induced aggregation and their effects on the aggregation of washed platelets by activated factor X, heparin proved to be more potent than A73025. Following intravenous injection of twice the quantity of A73025, an equivalent anti-factor Xa activity was obtained, in the agreement with our previous studies. However, it was found that PRP containing heparin and A73025 with comparable anti-Factor Xa acitvity responded differently to the addition of thrombin, as A73025 barely inhibited thrombin induced aggregation. Similarly, A73025 had little effect on the dilute thrombin clotting time of plasma, following intravenous injection. Heparin and A73025 were neutralized to approximately the same degree by a crude PF4 preparation.

Adenosine Diphosphate↗