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Biomedical subjects

A Nordoy

Publications and source records attributed to A Nordoy.

8 recordsLinked to original sources

The inhibitory effect of aspirin on human endothelial cells.

Human endothelial cell monolayers prepared from umbilical veins have been incubated with aspirin (1--2 mM) dissolved in Hepes modified solution and in platelet-rich plasma. They have also been incubated with plasma prepared from subjects before and after intake of aspirin giving a mean plasma concentration of 0.5 mM. The effects of the endothelial cells on ADP and collagen-induced platelet aggregation and malondialdehyde production in platelet-rich plasma have been tested. The endothelial cells had a spontaneous inhibitory effect on all three parameters. This effect was abolished when the cells were incubated with aspirin dissolved in MHS for 20 min and the increase in effect observed when platelet-rich plasma was incubated with endothelial cells for a period of 30 min was similarly inhibited when aspirin was dissolved in plasma or when plasma prepared from subjects who had taken aspirin were used. Aspirin had no inhibitory effect on prostacyclin (PGI2) with regard to the effect of PGI2 on platelets. On the contrary, the two compounds had an additive inhibitory effect on platelet aggregation induced by ADP and collagen. These findings should be considered with regard to the use of aspirin as an antithrombotic agent.

Aspirin

Transitory IgA-deficiency, persistent IgE deficiency and recurrent respiratory tract infectious disease after splenectomy.

In a 14 year old boy, a ruptured spleen was removed. Two months after the splenectomy he developed recurrent infections of the respiratory tract. A deficiency of IgA and IgE in his blood serum was found. His impaired resistance to respiratory tract infections responded well to substitution therapy with IgA. Spontaneous clinical recovery occurred during 3 years after the splenectomy, and was parallelled by a slow return of IgA to normal levels, whereas the absence of IgE persisted. The identical twin brother of the patient, who had his spleen intact, had normal levels of serum IgA and did not suffer from frequent respiratory tract inflammations.

Adolescent

Effects of fasting on plasma and platelet-free fatty acids and platelet function in healthy males.

10 healthy male volunteers fasted for 72 hours. Their plasma concentration of free fatty acid increased more than two-fold, to 1.8 mmol/l. The number of reversible venous "in vivo" platelet aggregates increased significantly (p less than 0.01); this figure correlated with the concentration of long-chain saturated free fatty acid in plasma (p less than 0.02). The correlation with the amount of long-chain saturated free fatty acid plus oleic acid (18:1) was even better (p less than 0.01). Plasma PF-4 concentration increased, suggesting increased platelet release reaction. In spite of the plasma increase, total platelet FFA concentration was reduced and there was a change in the distribution of platelet free fatty acid which correlated with the degree of aggregation.

Adult

Lipids as triggering factors in thrombosis.

An association has been established between acute and more persistent changes in lipid metabolism as reflected in plasma lipids, and platelet lipid metabolism. Platelet function is affected, particularly the activity and availability of platelet factor 3, however, also other changes making the platelets more sensitive to aggregating substances without interfering with the lipid part of platelet factor 3, have been documented. Experimental studies have demonstrated an increased tendency to thrombosis in animals given a diet with a high fat content with a high ratio of saturated to polyunsaturated fatty acids. Studies in man have mainly established a connection between dietary fats, plasma lipid abnormalities and frequency of coronary heart disease and clinical studies more directly relating thrombosis to lipid metabolism is highly warranted. Many open questions remain to be answered. Probably most relevant would be to understand how the antithrombotic mechanisms in the body are affected by changes in lipid metabolism. Even if thrombotic lesions are very common events in the western world our knowledge based on laboratory and experimental studies should indicate a much higher incidence, solely based on interactions between lipids and platelets in subjects exposed to our dietary habits and our way of life.

Animals

Haemostatic and lipid abnormalities in hypothyroidism.

10 patients with hypothyroidism were examined before and 3 months after initiation of thyroxin treatment. All patients had high levels of plasma total cholesterol and total phospholipids, and 5 had an additional hypertriglyceridaemia. 1 patient had a prolonged primary bleeding time and all had a prolonged activated partial thromboplastin time and recalcification time in plasma. Platelet factor 3 activity in platelet rich plasma was reduced and total phospholipid and protein concentration in platelets were low. No significant correlation could be estiblished between the observed lipid, protein and haemostatic parameters, and it is suggested that they represent independent phenomena. All abnormalities were corrected by thyroxin replacement.

Adult

Tocopherol in human platelets.

A spectrophotometric method was used to determine the total tocopherol levels in platelets, plasma, and erythrocytes from human subjects. The platelets contained about three times as much total tocopherol per cell as erythrocytes. This difference was not related to the content of polyunsaturated fatty acids in platelets and erythrocytes. In vitro incubation resulted in significant uptake of tocopherol by plasma and RBC, whereas no uptake was observed into platelets. A 3-month period of tocopherol treatment increased the level of tocopherol in plasma and erythrocytes, whereas the platelet level was unchanged. Tocopherol treatment did not interfere with platelet function or platelet lipid metabolism. The tocopherol fractions of platelets, red cells, and plasma were similar, and alpha-tocopherol was the main fraction.

Arteriosclerosis