The effect of 1-deamino-8-D-arginine vasopressin (DDAVP) on protein C was investigated in 10 uremics and 10 normal subjects. The protein C antigen was higher in the uremic patients than in the normal subjects. DDAVP had no influence on the level of protein C antigen. However, functional protein C in uremics was lower than in normals even before administration of DDAVP. Furthermore, there was a decrease in functional protein C in the uremics after administration of DDAVP. Further studies are needed to clarify the low functional protein C in uremics both before and during administration of DDAVP.

20 chronic hemodialysis patients were studied during two successive dialyses. Before the second dialysis patients ingested 320 mg acetylsalicylic acid (ASA). Hemodialysis was associated with a decrease in arterial oxygen tension, leukocyte and platelet counts. These changes were unaffected by pretreatment with ASA. In 8 of the patients platelet aggregate ratio (PAR) was measured during dialysis. As a reflection of an increase in circulating platelet aggregates PAR was found to decrease after 30 and 60 min of dialysis. This decrease was prevented by pretreatment with ASA. We conclude that circulating platelet aggregates do not seem to be a major contributing factor to hemodialysis-induced arterial hypoxemia.

Immunoreactive antithrombin III and antithrombin III activity was found to be significantly higher in 81 Greenland Eskimos than in 50 Caucasian Danes. Sixteen Eskimos who had emigrated to Denmark had significantly lower immunoreactive antithrombin III levels than the Greenland Eskimos, though higher than the Danes. The immunoreactive antithrombin III increased significantly while the increase in antithrombin III activity was insignificant in 20 male Caucasian Danes upon 3 weeks supplementation of the diet with 10 ml daily of a cod liver oil concentrate. The high antithrombin III level in the Eskimos may at least partly be a consequence of a high dietary intake of polyunsaturated fatty acids. It may also play a role for the low incidence of thrombosis apparently found in Greenland Eskimos.

The C3 phenotypes were determined by high-voltage agarose gel electrophoresis in 125 Greenland Eskimos. The frequency of the C3F gene was significantly lower than in a control group of Danes.

Hydrocortisone (HC) at concentrations above 0.5 mg/ml inhibited both ADP and thrombin induced aggregation as well as malondialdehyde (MDA) formation induced by thrombin in normal platelets, while even higher concentrations only produced minimal inhibition of aggregation of platelets with blocked prostaglandin synthesis. The inhibition produced by HC in normal platelets could easily be overcome by addition of small amounts of arachidonic acid and HC did not inhibit arachidonic acid induced platelet MDA formation. HC at concentrations above 0.4 mg/ml almost completely inhibited spontaneous prostacyclin release from pieces of rat aortic tissue. This inhibition could easily be overcome by addition of exogenous arachidonic acid. These results indicate an inhibitory effect of HC on the phospholipase enzymes in both platelets and endothelial cells.

The C3F gene has been associated with atherosclerotic vascular disease. Greenland Eskimos have a very low frequency of acute myocardial infarction (AMI). The C3 polymorphism phenotypes were therefore determined by high-voltage agarose gel electrophoresis in 125 Greenland Eskimos originating from different parts of Greenland and compared with a control group of 1,554 Caucasian Danes. p The C3F gene frequency in the Eskimos (0.056) was significantly lower (p <0.001) than in the control Danes (0.201). These results indicate that genetical factors may also play a role for the low AMI frequency seen in Greenland Eskimos.

Scandinavian Journal of HaematologyVolume 25, Issue 5 p. 445-447 Hydrocortisone, Platelet Aggregation and Platelet Prostaglandin Metabolism Kaj Anker Jørgensen, Corresponding Author Kaj Anker Jørgensen Coagulation Laboratory, Department of Clinical Chemistry, Aalborg Hospital, Section North, Aalborg, Denmark5Department of Clinical Chemistry, Aalborg Hospital, Section North, DK-9100 Aalborg, DenmarkSearch for more papers by this authorErik Stoffersen, Erik Stoffersen Coagulation Laboratory, Department of Clinical Chemistry, Aalborg Hospital, Section North, Aalborg, DenmarkSearch for more papers by this author Kaj Anker Jørgensen, Corresponding Author Kaj Anker Jørgensen Coagulation Laboratory, Department of Clinical Chemistry, Aalborg Hospital, Section North, Aalborg, Denmark5Department of Clinical Chemistry, Aalborg Hospital, Section North, DK-9100 Aalborg, DenmarkSearch for more papers by this authorErik Stoffersen, Erik Stoffersen Coagulation Laboratory, Department of Clinical Chemistry, Aalborg Hospital, Section North, Aalborg, DenmarkSearch for more papers by this author First published: December 1981 https://doi.org/10.1111/j.1600-0609.1981.tb01427.xCitations: 7AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat Citing Literature Volume25, Issue5December 1981Pages 445-447 RelatedInformation

Plasma C1q, C1 esterase inactivator, C4, C3 and C3 proactivator were measured in 20 chronic uremic patients on maintenance hemodialysis, in 10 conservatively treated chronic uremic patients and in 20 healthy volunteers. There was no statistical significant difference between the patient groups in any of the measured complement components. The C1q, C1 esterase inactivator and C4 concentration were found to be the same in the patient and the control groups. The C3 and C3 proactivator levels were equally and significantly lower in both patient groups compared with the healthy volunteers.

Antithrombin III activity and immunoreactive antithrombin III was determined in 31 patients before elective surgery and 3 h, 1, 3 and 7 d after. The values fell about 10--20% from 3 h to 3 d, but had returned to preoperative levels by the seventh day. A fall to 40% was seen. The fall in activity was a little smaller than the fall in immunoreactive protein.

Thrombin induced aggregation of washed aspirin and non-aspirin treated platelets was found to be inhibited by albumin, the inhibitory effect was most pronounced in non-aspirin treated platelets.

The case history of a patient with moderate factor XII deficiency and recurrent deep vein thrombosis is described. A decreased resting fibrinolytic capacity suggests that 'in vivo' Hageman factor acts mainly as a promotor of clot dissolution. It further indicates that the in vitro demonstration of factor XII as an activator for other biochemical pathways might be of minor importance in vivo, as alternative pathways for activation of these systems exist.

A family with a tendency to thrombosis and decreased antithrombin III (AT III) activity in plasma, but normal immunoreactive AT III is reported. 7 members of the family had the AT III defect, 4 of whom have had thrombotic episodes. The importance of biological determination of AT III when studying patients with recurrent thrombotic episodes is emphasized.

Bleeding time was determined before (BTo) and after ingestion of 1 (BT1), 3.5 (BT3.5) and 25 (BT25) mg acetyl-salicylic acid (ASA)/kg in 50 men and 20 women of varying age. It was found that BT falls with age in men maybe due to a reduction in PGI2/TXA2 ratio. The changes in bleeding time could be abolished by ASA ingestion. The index Ia = (BT25-BTo)/BT25 increased with age in both men and women. While all age groups increased bleeding time upon administration of a small dose of aspirin only in the younger age groups did the bleeding time thereafter fall significantly, when the dose was increased to 25 mg/kg.

The C3 polymorphism phenotypes were determined by high-voltage agarose gel electrophoresis in 83 patients with chronic uremia on maintenance hemodialysis. In 45 patients with chronic pyelonephritis, the frequency of C3F and C3FS was significantly lower than in 38 patients with chronic glomerulonephritis and in a large control group.

Changes in complement reactions are described in two patients exhibiting adverse reactions to Stesolid MR (diazepam with Cremophor as solvent). The recorded frequency of adverse reactions to Althesin, propandid and Stesolid MR suggests that the common solvent Cremophor is responsible for the adverse reactions.