Search PubMed⌕ Search

Biomedical subjects

D Ogston

Publications and source records attributed to D Ogston.

At least 37 records · Page 2Linked to original sources
PubMed1978

Familial thrombosis: inherited deficiency of antithrombin III.

Several members of a family living on the west coast of Scotland and on one of the islands off the coast had serious thrombotic disease. The plasma antithrombin III (ATIII) concentrations were measured by both functional and immunological assay in all available members of the family. Concentrations were 25% to 66% of normal in 12 people, including all seven with thrombotic disease. The inheritance pattern was characteristic of an autosomal dominant disorder. Thrombotic disease generally affected the leg, mesenteric, and axillary veins, although one man who had died before the study began had had severe arterial atheroma. In women the first thrombotic symptoms usually occurred during pregnancy. None of these patients have developed thrombotic symptoms until they were at least 18, so four younger members of the family who have ATIII deficiency but no thrombotic disease may eventually develop symptoms.

Adolescent↗
PubMed1978

Coagulation and fibrinolysis in thyroid disease.

The levels of components of the coagulation mechanism and fibrinolytic system in 20 hyperthyroid patients and 9 hypothyroid patients were compared with those of 20 euthyroid control subjects. The mean levels of fibrinolytic activity and plasminogen were significantly reduced in the hyperthyroid patients while mean levels of alpha1-antitrypsin and C1 inactivator were increased. Patients with hypothyroidism had significantly increased levels of fibrinolytic activity and alpha2-macroglobulin, a prolonged partial thromboplastin time, and reduced levels of factor XII and antithrombin III.

Adult↗
PubMed1977

Effect of local exercise and vessel occlusion on fibrinolytic activity.

Arterial occlusion of the upper limb did not affect the fibrinolytic activity in the venous blood of that limb; venous occlusion associated with venous distension resulted in a marked rise in activity. Local fibrinolytic activity was increased substantially by active exercise; passive exercise induced a smaller increase. Active exercise undertaken during arterial occlusion did not result in a rise in activator level. It is concluded from these results that blood flow into the venous system rather than accumulation of metabolites is responsible for the increased release of activator into the blood during local exercise and vessel occlusion.

Arm↗
PubMed1976

Platelet adhesiveness and fibrinolysis after recent cerebro-vascular accidents and their relationship with subsequent deep venous thrombosis of the legs.

In fifteen patients with a cerebro-vascular accident resulting in an acute hemiplegia there was a subsequent rise in the platelet count and plasma fibrinogen level. There were no significant alterations in platelet adhesiveness, plasminogen activator, plasminogen, FR-antigen and haematocrit. Patients diagnosed as developing deep venous thrombosis with the 125I-fibrinogen technique had a significantly lower platelet adhesiveness and plasminogen level than those who were not.

Aged↗
PubMed1976

Deep venous thrombosis of the legs after strokes. Part I--incidence and predisposing factors.

Forty out of 76 patients (53%) who had suffered a cerebrovascular accident developed deep venous thrombosis of the paralysed leg, as detected with the 125I-fibrinogen technique. A further five also had thrombosis in the non-paralysed leg. A study of many predisposing risk factors provided no help either in elucidating the cause of venous thromboembolism or in identifying patients at risk of DVT as a complication of cerebrovascular accidents.

Age Factors↗
PubMed1976

Deep venous thrombosis of the legs after strokes: Part 2-Natural history.

Seven out of 76 patients who had sustained a cerebrovascular accident suffered a pulmonary embolism as diagnosed at necropsy or by unequivocal antemortem criteria. A further five patients had probable embolisation diagnosed only by clinical and chest x-ray criteria. Eleven of these 12 patients had DVT as diagnosed by the 125I-fibrinogen technique. Though 125I-fibrinogen technique has its limitations, thrombosis seemed to be able to develop at several independent sites in the venous system of the leg.

Aged↗
PubMed1976

The contribution of plasma protease inhibitors to antiplasmin activity in man.

1. Human plasma contains a variety of proteins that are capable of inhibiting plasmin activity. Whole plasma possesses 'rapid' and 'progressive' plasmin-neutralizing activity: this study assesses the contribution of individual protease inhibitors to this plasmin-neutralizing property of plasma. 2. Rapid and progressive antiplasmin activities of human plasma correlate with alpha2-macroglobulin and alpha1-antitrypsin concentrations respectively. 3. Fluctuations in the amounts of the other measured inhibitors (antithrombin III, Cl in activator and inter-alpha-tryspin inhibitor) did not influence the measured antiplasmin activity.

Antithrombins↗
PubMed1976

Inhibitors of plasminogen activation in human blood.

Plasma contained two inhibitors of plasminogen activation by urokinase when fractioned by gel filtration on Sephadex G-200. The inhibitor in the lower molecular weight fractions was separate from the principal protease inhibitors of plasma: alpha1-antitrypsin, alpha2-macroglobulin, C1 inactivator and antithrombin III, and from factor XIII. This activation inhibitor was present in both plasma and serum and its recovery was not reduced by preincubating the serum for 6 h at 37 degrees C. Its inhibitory activity was stable for several days at 4 degrees C, and was enhanced in the presence of an increased saline concentration. Preparations of the inhibitor, active in a clot lysis system, failed to inhibit the esterase activity of urokinase on N-alpha-acetyl-glycyl-L-lysine methyl ester.

Chromatography, Gel↗
PubMed1976

Sequential studies on components of the haemostatic mechanism in pregnancy with particular reference to the development of pre-eclampsia.

Components of the haemostatic mechanism were studied at intervals in 60 primigravidae over the course of pregnancy and the puerperium; 12 of these developed pre-eclampsia. During pregnancy there was a fall in fibrinolytic activity and fibrinolytic capacity and a rise in fibrinogen, FR-antigen, alpha 1-antitrypsin and alpha 2-macroglobulin. The women who subsequently developed pre-eclampsia could not be identified on the basis of these measurements. Following delivery there was a more rapid return of fibrinolytic activity and capacity towards normal in the women who had not had pre-eclampsia. The urinary FR-antigen level was higher in the women with pre-eclampsia.

Adolescent↗
PubMed1976

Changes in protease inhibitors after acute myocardial infarction.

Plasma levels of fibrinogen, alpha1-antitrypsin, alpha2-macroglobulin, antithrombin III, and C1 inactivator were measured serially for 10 days in 11 patients after acute myocardial infarction. Both fibrinogen and alpha1-antitrypsin rose markedly to reach peak levels 5-7 days after infarction while C1 inactivator levels rose slowly with the highest observed mean level on the 10th postinfarction day. Neither antithrombin III nor alpha2-macroglobulin changed significantly after myocardial infarction. No relationship between C1 inactivator levels and either fibrinogen or alpha1-antitrypsin was found in a study of 30 patients with a variety of disorders while fibrinogen and alpha1-antitrypsin levels were significantly correlated.

Adult↗
PubMed1976

Interrelations between ABO blood group, plasminogen, alpha1-antitrypsin, alpha2-macroglobulin and the platelet count in blood donors.

The level of plasminogen alpha1-antitrypsin, alpha2-macroglobulin and the platelet count were measured in 511 blood donors. The mean level of alpha1-antitrypsin was significantly lower in men of group B compared with that of group O. No other differences between the blood groups reached statistical significance. Woman had higher mean levels of alpha1-antitrypsin and alpha2-macroglobulin and a higher platelet count than men. The levels of plasminogen and alpha1-antitrypsin were significantly higher in women using oral contraceptive compared with those who were not. The level of alpha2-marcoglobulin fell with age until the 60-64 year age-group in men and the 40-49 year age-group in women. A positive correlation existed between the alpha1-antitrypsin and the alpha2-macroglobulin level and between the platelet count and the plasminogen level.

ABO Blood-Group System↗
PubMed1976

The fibrinolytic enzyme system in anorexia nervosa.

The levels of components of the fibrinolytic enzyme system in 7 patients with anorexia nervosa were compared with those of healthy young women. Plasminogen activator levels were significantly higher and the mean fibrinogen concentration was lower in the anorexia nervosa patients.

Adolescent↗
PubMed1976

Platelet function after the administration of chlorpromazine to human subjects.

Chlorpromazine is known to inhibit platelet function in vitro. The intramuscular injection of 50 mg to human volunteers caused only minor changes in platelet function. There was a small, but significant, reduction in the platelet count, the second phase of the double-wave of adenosine diphosphate-induced aggregation and the rate of 5-hydroxytryptamine-induced aggregation. Patients on high doses of chlorpromazine had no demonstrable abnormality of platelet function. This suggests that chlorpromazine, despite its inhibitory effect on platelet function in vitro, is unlikely to interfere with either haemostasis or thrombogenesis after its administration to man.

Blood Cell Count↗
PubMed1976

Changes in coagulation factors following acute myocardial infarction in man.

The whole blood clotting time, plasma fibrinogen and individual coagulation factors II, V, VII, VIII, IX, X, XI, and XII were serially measured in 14 patients over a 10-day period following acute myocardial infarction. A further six patients with similar symptoms but without evidence of myocardial infarction were also studied. The whole blood clotting time was significantly shorter within the first 24 h after infarction than on subsequent days. There were significant increases in the levels of fibrinogen and of factors VIII, IX, and XI and a significant decrease in factor XII in the patients who had sustained a myocardial infarction. The patients without myocardial infarction had no significant change in any of the coagulation factors measured.

Acute Disease↗