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A cytochemical method for studying fibrinolytic (proteolytic) activity in specified white cells in blood and bone marrow smears has been developed and the spontaneous fibrinolytic activity at pH 6.0 and 7.65 as well as the activity of a plasminogen-like proenzyme were studied. These fibrinolytic enzymes appeared in the granulocytic and monocytic series; their activity depending upon the maturation stage. The enzymes appear in promyelocytes, reach the highest activity in metamyelocytes and in band cells and then gradually decrease during maturation. No significant differences between mature neutrophils, eosinophils and basophils were observed. Megakaryocytes, erythroblasts, erythrocytes and lymphocytes were devoid of significant fibrinolytic activity. Some implications of these findings are discussed.

Interactions of the dysfibrinogen Oslo I with platelets were investigated. This fibrinogen is a B beta-chain variant with faster than normal fibrin monomer polymerization. Fibrinogen Oslo I acted more efficiently in ADP-induced platelet aggregation, and bound to gel-filtered platelets with a higher affinity constant than did normal fibrinogen. At all concentrations more fibrinogen molecules became bound per platelet with the dysfibrinogen than with normal fibrinogen, both when the fibrinogens were tested separately or as a mixture using 125I or 131I to label the two types. At high concentrations this was probably due to ligand polymerization of the dysfibrinogen. These observations indicate that the increased cofactor function in platelet aggregation may be related to the increased affinity of the dysfibrinogen for the platelets.

A case of haemophilia A (Factor VIII deficiency) in a family of Samojed dogs is described. The Factor VIII activity was about 3 per cent of normal dog level. The dog died from a haematoma in the mediastinum. No other bleeders were recorded in its family.

Among 2014 apparently healthy men aged 40-59 years platelet function was studied with Hellem's retention method in 488 men. In 55 of these 488 men coronary heart disease (CHD) was strongly suspected and coronary angiography confirmed the diagnosis in 34 of 51 angiographied men. Platelet responsiveness was significantly lower among those who had angina pectoris than among their CHD-suspect counterparts without angina, regardless of coronary angiographic findings. Since angiopositive men without angina and 408 "normals" had similar retention values, it seems as if presenting symptoms, but not the development of CHD are linked to platelet function. During a near maximal bicycle exercise test significantly higher peak exercise blood pressure was found among men with very low retention values than among men with retention values in the middle and upper range. This could not be explained by differences in maximal heart rate or work performance. This indicates that blood pressure regulation during exercise may in part be linked to platelet function related mechanisms.

Two-thirds of osteogenesis imperfecta (OI) patients claimed that they bruised easily. We have studied haemostasis in 58 subjects with OI, tarda type. The most frequent abnormalities were increased capillary fragility (35%), decreased platelet retention (33%) and reduced factor VIII R:Ag (23%). Reduced ristocetin cofactor, deficient platelet aggregation induced by collagen and prolonged bleeding time were less common findings. The combination of vascular, platelet related and plasmatic defects may reflect that OI is a heterogeneous group of disorders with common clinical expression. The tourniquet test is the most valuable screening test of the haemostatic defects observed in OI.

A 17-year-old girl swallowed at least 50 Duroferon duretter. Each tablet contains ferrous sulphate equivalent to 0.1 g Fe2+. Thus, a total of 5 g Fe2+ was ingested. Vitamin K-dependent coagulation factors dropped within the next hours to very low levels. Thrombotest showed less than 3% of normal coagulation activity 8 h after oral intake. Recovery was uneventful except for laboratory evidence of transient liver damage. The rapidity by which the early coagulation deficiencies developed and the lack of evidence of disseminated intravascular coagulation suggested a direct effect of iron on coagulation factors. In vitro studies confirmed that iron in concentrations that may have been attained in vivo, altered the functional activity of several coagulation factors. Monitoring the vitamin K-dependent coagulation factors may be a simple and useful parameter in acute iron intoxication.

The subcellular distribution of platelet factor 3 and 4 (PF-3 and 4) activity has been determined in sucrose gradient fractions of platelet homogenates. The distribution patterns were influenced by the homogenization technique (blendor or pestle) and the method of calculation (total activity or per mg protein). The bulk PF-3 activity was present in membraneous fractions both from granular and plasma membranes with negligible amounts in the soluble fraction. In contrast, PF-4 activity appeared in small amounts in the membraneous fraction with a distribution of about one third in the soluble fraction and two thirds in the granule fraction, particularly the higher density fractions which fractions also contain the serotonin and the non-metabolic adenine nucleotides.