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Biomedical subjects

K W Denson

Publications and source records attributed to K W Denson.

9 recordsLinked to original sources
PubMed1977

Factor-VIII consumption in pre-eclampsia.

In 50 women with high-risk pregnancies, increased factor-VII consumption, as estimated by the difference between the levels of factor-VIII-related antigen and factor-VIII clotting activity, correlated with the severity of pre-eclampsia, particularly when measured by increases in plasma-urate. Longitudinal studies of the evolution of pre-eclampsia demonstrated that increased factor-VIII consumption usually but not always developed before hyperuricaemia. The earliest time that abnormal factor-VIII consumption was demonstrated was at 18 weeks' gestation in a woman who had had two previous stillbirths. Subcutaneous heparin and oral dipyridamole failed to reverse the coagulation abnormality, and the fetus died in utero at 28 weeks' gestation. The renal and coagulation changes characteristic of pre-eclampsia were also seen in a patient without hypertension. This suggests that the concept of pre-eclampsia may need to be widened to include a non-hypertensive syndrome characterised by these changes in clotting and renal function.

Adult↗
PubMed1977

Factor-VIII activity and antigen, platelet count and biochemical changes after adrenoceptor stimulation.

Adrenaline, isoprenaline and salbutamol were administered by intravenous infusion to human subjects. Isoprenaline was covered with practolol in an attempt to reduce the unpleasantness of the circulatory effects. Changes were recorded in pulse rate and blood pressure, and in blood levels of factors V, VIII, X, XI, and XII, platelet count, lactate, pyruvate, potassium and free fatty acids. Factor VIII was studied by clotting assays, by reactions with two rabbit antisera and two human antibodies, and by desulphated agarose chromatography. At the rate at which they were adiminstered, all three drugs increased the pulse rate by 20-40 beats/min. Factor VIII rose c. 2.5 X with adrenaline but only c. 1.5 X with isoprenaline and salbutamol; but other clotting factors did not alter. Chromatography provided no evidence of a change in the size of the molecule carrying factor-VIII clotting activity. The rate of clearance of the heightened plasma activity could not be shown to differ from that of "ordinary" factor VIII infused into haemophiliacs. The platelet count rose after adrenaline, fell after salbutamol and did not change significantly after isoprenaline. Among the biochemical responses, the only significant difference between the drugs was that lactate rose after adrenaline and salbutamol but did not change after isoprenaline. The rise in factor-VIII clotting activity after adrenaline is considered to represent a real increase in blood concentration, presumably by release of additional factor VIII from stores. The evidence suggests that this could be classified as a beta2 effect; and that the quantity which can be released is unrelated to the current plasma level. The rise in platelet count produced by adrenaline may be the resultant of an alpha-mediated rise due to contraction of the exchangeable splenic pool and a beta2-mediated fall, the alpha effect predominating.

Adult↗
PubMed1976

The clotting of a snake (Crotalus viridis Helleri) plasma and its interaction with various snake venoms.

The clotting of C. V. Helleri plasma is not accelerated by the factor X activator or thrombin-like enzymes from its own venom. Clotting of the plasma is accelerated by the factor Xactivator from Russell's viper venom, but not by the thrombin-like enzyme from Agkistrodon Rhodostoma venom ("Arvin"). The prothrombin activator from the Taipan venom clots C.V. Helleri plasma equally well as human plasma, but the thrombin which is produced has a marked specificity for its own fibrinogen, and clots bovine fibrinogen more slowly. C.V. Helleri plasma contains an inhibitor which progressively inactivates bovine factor Xa and thrombin, but the inhibitor is not potentiated by heparin. The slow, protracted clotting of the snake plasma either alone or when mixed with human plasma or bovine fibrinogen suggests that this inhibitor may interfere with the polymerisation of fibrin monomer.

Ancrod↗
PubMed1976

The role of coagulation and fibrinolysis in preeclampsia.

The coagulation and fibrinolytic systems play a key role in maintaining the integrity and patency of the vascular compartment. Pregnancy induces extensive physiological changes in these systems, thus creating an enhanced capacity to produce fibrin and a diminished ability to remove it. Fibrin deposition localized to the uteroplacental circulation is a feature of normal pregnancy. In women with fatal eclampsia, disseminated intravascular coagulation with fibrin deposition in the renal glomeruli is well documented. The condition of preeclampsia is not well defined. Nonetheless, evidence of intravascular coagulation, as shown by elevated levels of fibrin degradation products and reduced platelet counts, has been found in many women with preeclampsia. Serial studies showed that thrombin generation, as indicated by the ratio of factor VIII-related antigen to factor VIII coagulant activity, is considerably in excess of that which occurs in normal pregnancy, and its appearance coincides with the development of the clinical features of preeclampsia. Heparin therapy has bot been proven of value in established preeclampsia, but this fact does not disprove that role that intravascular coagulation may play in the pathogenesis of the disease. A controlled trial ina high-risk group of low-dose he;arin and an antiplatelet agent from the 16th to the 18th weeks of pregnancy onwards is required to elucidate the role of intravascular coagulation in preeclapmsia and its effect on the fetus.

Blood Cell Count↗
PubMed1975

Measurement of heparin in patients receiving subcutaneous heparin therapy.

Heparin assays based on four different tests of clotting function have been compared with a heparin assay utilizing the potentiating effect of heparin on anti-factor Xa in a group of patients receiving subcutaneous heparin therapy during late pregnancy. It is considered that the anti-factor Xa method is a better indication of the antithrombotic effect of heparin. In the presence of high levels of clotting factors, heparin assays based on tests of clotting function can be misleading.

Blood Coagulation Tests↗