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Biomedical subjects

B Osterud

Publications and source records attributed to B Osterud.

At least 109 records · Page 6Linked to original sources
PubMed1984

Meningococcal septicaemia treated with combined plasmapheresis and leucapheresis or with blood exchange.

Mortality among patients suffering from meningococcal septicaemia has reached nearly 50% in parts of northern Norway despite intensive care. The activation of complement and blood cells by endotoxin is assumed to be the cause of most of the associated pathophysiological changes. Consequently, it would seem logical to remove such constituents either by combined plasmapheresis and leucapheresis or by blood exchange in patients with a fatal prognosis. Three patients were treated with plasmapheresis and leucapheresis and one with blood exchange. All recovered without sequelae, and no complications or serious problems caused by these procedures were observed. It is concluded that either combined leucapheresis and plasmapheresis or blood exchange is well tolerated and a valuable supplement to conventional intensive care in fulminant meningococcal septicaemia.

Adolescent↗
PubMed1984

Production and availability of thromboplastin in endothelial cells: the effects of thrombin, endotoxin and platelets.

Freshly prepared endothelial cells from umbilical cord veins were demonstrated to possess a weak but significant thromboplastin activity. Upon exposure of cultured endothelial cells to catalytically active thrombin (4.5 U/ml) or endotoxin (0.05 microgram/ml), the thromboplastin activity of the cells was increased 10-40-fold during 5 h incubation, and with the additional presence of washed, isolated platelets during the incubation, the activity was enchanced up to 170-fold. Platelets or catalytically inactivated thrombin added alone were largely ineffective as stimulants. 75-80% of the enhanced thromboplastin activity became available on the surface of the cultured cells as demonstrated by utilizing thromboplastin antibodies. Such exposed activity is suggested to be important in thrombotic situations where initial formation of thrombin may significantly accelerate the generation of thrombin by a positive feedback effect upon thromboplastin synthesis in the endothelial cells.

Blood Platelets↗
PubMed1984

The role of complement in the induction of thromboplastin synthesis.

Complement appears to be an important system for cell activation in circulating blood. It is established that granulocytes may be stimulated through complement activation. In the present paper we propose also a central role of complement in the induction of thromboplastin synthesis in blood monocytes and endothelial cells.

Antigen-Antibody Reactions↗
PubMed1984

Blood coagulation in patients with benign and malignant tumours before and after surgery. Special reference to thromboplastin generation in monocytes.

In this study we have looked for differences in coagulation parameters before and after surgical removal of benign or malignant tumours. A striking increase in thromboplastin activity of the blood monocytes was seen 1 d after surgery. This paralleled a fall in factor VII activity. At the same time, the sensitivity of the blood monocytes to stimulation by endotoxin increased significantly. We propose from this study that monocyte thromboplastin may be a postoperative thrombogenic factor. Increased levels of factor VIII and fibrinogen 2-3 d postoperatively were found, probably caused by inflammation reactions induced by the surgery. No difference in coagulation parameters could be demonstrated between patients with benign, noninvasive lesions and patients with invasive, carcinomatous lesions.

Blood Coagulation↗
PubMed1984

Controlled endotoxinemia in pigs. A suitable model for in vivo studies of some haemodynamic, humoral and cellular reactions.

To study the haemodynamic, cellular and humoral changes seen during septicemia-endotoxinemia a relatively large animal is needed. Pigs are satisfactory in size but have a tendency to develop malignant hyperthermia reaction to stress situations and certain anaesthetic agents. This problem was solved using a screening test of halothane exposure. When later used for experiments, the nonresponding pigs developed the typical hypokinetic low-flow state after endotoxin challenge seen in the advanced stage of septicemia in man. Decreased number of circulating leucocytes and platelets, increased tissue thromboplastin production in monocytes, and a significant coagulation disorder (DIC) were observed. Release of oxygen radicals and lysosomal enzymes from leucocytes could be estimated. Endotoxin levels in plasma were easily measured. This pig model of controlled endotoxinemia correlates well with some important haemodynamic, cellular and humoral reactions observed during human in vivo observations and in vitro studies. This model may thus be a valuable tool in clinical research of endotoxinemia and septicemia.

Animals↗
PubMed1983

Evidence for appearance of "lysis independent" procoagulant activities in collagen or thrombin stimulated platelets.

The availability of procoagulant activities in platelet suspensions lysed by sonication correlated directly with the degree of lysis (loss of LDH and 51Cr). Separate measurements of platelet factor 3 (PF3) and Factor V/Va activity revealed significant differences in appearance of these platelet activities in sonicated cell suspensions. Platelet factor 3 activity increased almost in parallel to the loss of 51Cr, whereas Factor V/Va activity became available at a significant slower rate. This might be explained by the localization of Factor V/Va activities inside the alpha-granules and therefore not immediately available on the surface of the partially lysed platelets. No increase in lactate dehydrogenase or 51Cr-loss was observed during 12 min incubation of platelet suspension with collagen or thrombin, whereas both PF3 and Factor V/Va activities increased. Thus, the high platelet factor 3 activity of 34% (lysed platelets 100%) measured in thrombin stimulated platelet suspensions probably represents "lysis-independent" activity.

Blood Coagulation Factors↗
PubMed1983

Increased tissue thromboplastin activity in monocytes of patients with meningococcal infection: related to an unfavourable prognosis.

In 16 patients, 13 with meningococcal infection and 3 suspected to have this infection, 8 patients were found to possess significant higher level of tissue thromboplastin activity of their monocytes isolated from the blood at the admission to the hospital than normal. Five of those 8 patients had an extremely high concentration, greater than 60-300 fold increase, and all these patients died. The exposed tissue thromboplastin activity on the surface of the endotoxin stimulated monocytes is probably the direct inducer of disseminated intravascular coagulation (DIC) in meningococcal infection.

Adolescent↗
PubMed1983

The clotting time of whole blood in plastic tubes: the influence of exercise, prostacyclin and acetylsalicylic acid.

An assay for detection of a hypercoagulable state was accomplished by measuring the clotting time of whole blood (without anticoagulant present) in plastic tubes. This assay appeared to be quite sensitive to the activation state of platelets. Thus, acetylsalicylic acid (ASA) or prostacyclin (PGI2) was found to prolong significantly the whole blood clotting time (WBCT), specially under conditions where the platelet might be hyperactive. When the WBCT was carried out before and after exercise, a mean value of 12.95 min was obtained before as compared to 7.48 min after exercise. In the presence of PGI2, the WBCT after exercise was prolonged to 13.91 min. The shorter clotting time after exercise, in the absence of inhibitor, might be explained by the observation in the present study that platelet factor 3 became more readily available upon consecutive stimuli. These results suggest that platelet release may be important for the initiation of prothrombin activation in situations without already available platelet factor 3 activity.

Adult↗
PubMed1983

Effects of cod liver oil on platelets and coagulation in familial hypercholesterolemia (type IIa).

Patients with familial hypercholesterolemia (type IIa) were given 30 ml cod liver oil (CLO) as dietary supplement daily for 6 weeks. The effects on platelets, bleeding time, coagulation and blood and platelet lipids were examined. The major findings were a reduced collagen-induced platelet aggregation and a decrease in thrombin-stimulated thromboxane B2 generation in platelets in vitro. The primary bleeding time was not significantly prolonged. Statistically significant increase in eicosapentaenoic acid/arachidonic acid ratios in the main platelet phospholipids were also observed. These changes did not correlate with any of the changes in platelet behavior observed after CLO intake. The serum total and HDL cholesterol and triglycerides were not altered during the trial.

Adult↗
PubMed1983

How to measure factor VII and factor VII activation.

This communication describes the different techniques that can be used to evaluate the activity state of factor VII in plasma samples. At the present time direct methods for quantitation of activated factor VII (factor alpha-VIIa) are not available. Combined methods are therefore used to measure the degree of factor VII activation. These methods can be summarized in the following way: a regular factor VII clotting assay measuring factor VII coagulant activity (factor VIIc) is carried out simultaneously with: (1) a factor VII antigen assay (factor VIIag): (2) a coupled amidolytic factor VII assay (factor VIIam), or (3) a factor VII clotting assay utilizing bovine tissue thromboplastin (VIIbt). The activity state of factor VII can then be calculated from either of the following ratios: f.VIIc/f.VIIag; f.VIIc/f.VIIam, or f.VIIbt/f.VIIc. A study of the potency of a 30-fold activated factor VII to activate factor X in the presence of phospholipids is also included. This experiment demonstrates that even a low factor VII concentration (0.01 U/ml in the coupled amidolytic assay and 0.30 U/ml in the factor VII clotting assay) causes a significant activation of factor X when incubated together in the presence of lipids and calcium ions. Activated factor VII may therefore possess potential thrombotic properties even in the absence of exposed tissue thromboplastin in the blood circulation.

Animals↗
PubMed1983

Heparin for infants and children with meningococcal septicemia. Results of a randomized therapeutic trial.

Heparin has been given intravenously, as part of a prospective study, to 11 of 26 infants and children with severe meningococcal septicemia. This therapy was started as early as possible following admission to hospital, and continued for two days. The age and sex distributions were roughly similar for the two treatment groups, but the prognostic signs on admission were somewhat less favourable for the group that did not receive heparin. Two boys who received heparin and two girls who did not, died. The clinical courses of the surviving patients in the two groups were also roughly similar, except that the tendency to cutaneous necroses was slightly more prominent in those who had not received heparin. We have thus no evidence that heparin has any great influence on the final outcome of meningococcal septicemia, even when given so early that shock had not developed.

Child↗
PubMed1982

The mandatory role of complement in the endotoxin-induced synthesis of tissue thromboplastin in blood monocytes.

Fresh isolated blood cells recombined with normal heparinized plasma and then incubated with endotoxin, induced a 100-fold increase in monocyte tissue thromboplastin synthesis. In contrast, recombination of these cells with heat inactivated plasma, cobra venom factor-treated plasma, Ca2+-free plasma, or BioRex 70-treated plasma (plasma free of Clq and D) before incubation with endotoxin, failed to induce monocyte synthesis of tissue thromboplastin. These results strongly support the hypothesis that complement is required for endotoxin stimulation of blood monocyte synthesis of tissue thromboplastin.

Complement Pathway, Alternative↗
PubMed1982

Studies, with a luminogenic peptide substrate, on blood coagulation factor X/Xa produced by mouse peritoneal macrophages.

The formation and secretion of coagulation Factor X/Xa by mouse peritoneal macrophages was studied with a luminogenic peptide substrate (S-2613; t-butyloxycarbonylisoleucylglutamyl-gamma-piperidylglycylarginylisoluminol). Amidolysis was quantified by measuring the light emitted during oxidation of isoluminol, released by Factor Xa. A lower detection limit of about 0.5ng of Factor Xa was established; the assay was linear with enzyme concentration up to at least 100ng/ml. Factor X was determined after treatment with the Factor X-activating component of Russell's-viper (Vipera russelli) venom. Macrophages, cultured in the absence of serum, released Factor X/Xa into the culture medium. The concentration of coagulation enzyme in the medium increased in an essentially linear fashion over a period of at least 3 days, at a rate corresponding to 6-8ng produced/24h per 10(6) cells. The ratio of Factor Xa/X+Xa varied from about 60 to 100%, showing that activation of Factor X to Xa is not prerequisite to release of the enzyme from the cells. Factor Xa activity was suppressed in the presence of warfarin [3-(alpha-acetonylbenzyl)-4-hydroxycoumarin; 12.5mug/ml of medium], but could be restored by adding vitamin K (0.1mug/ml) along with the warfarin. Cultures to which Sepharose beads containing covalently bound anti-(Factor X) antibodies had been added showed decreased amounts of free Factor X/Xa in the culture medium. The missing activity could be demonstrated by incubating the recovered conjugate with the substrate peptide S-2613. Factor Xa produced by the macrophages was efficiently inactivated by heparin in the presence of antithrombin, heparin with high affinity for antithrombin being more effective than the corresponding low-affinity species.

Animals↗
PubMed1982

The production and availability of tissue thromboplastin in cellular populations of whole blood exposed to various concentrations of endotoxin. An assay for detection of endotoxin.

These studies were undertaken to determine the type and availability of the procoagulant activities generated in blood incubated with endotoxin. The shortening of the recalcification time of blood incubated with endotoxin was directly correlated with the increase in synthesis of tissue thromboplastin in the monocytes. The procoagulant activity which resulted in the shortening of the clotting time was shown to be almost totally blocked by tissue thromboplastin antibodies. Thus, no additional procoagulant activity was generated in platelets during the 5 h incubation of blood with endotoxin. However, lysed platelets enhanced the synthesis of tissue thromboplastin in blood monocytes in the presence of endotoxin. Lysed red blood cells or granulocytes had no such effect. In endotoxin stimulated monocytes the main part of the newly synthesized tissue thromboplastin appeared to be exposed on the cellular surface. Thus, only 25% of the tissue thromboplastin activity was recovered when tissue thromboplastin antibodies had been present during the stimulation. Unstimulated monocytes were also found to possess tissue thromboplastin activity, but this low activity was not affected by tissue thromboplastin antibodies unless the monocytes were disrupted by sonication. The high percentage of tissue thromboplastin exposed on the surface of the endotoxin stimulated monocytes in whole blood may contribute significantly to the rapid induction of disseminated intravascular coagulation in gram negative sepsis.

Animals↗