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Biomedical subjects

J Dyerberg

Publications and source records attributed to J Dyerberg.

At least 109 records · Page 6Linked to original sources
PubMed1987

Defective protein C in uraemia.

Protein C activity and antigen levels were determined in 10 haemodialysis patients and 10 healthy controls matched for age and sex. Markedly decreased protein C activity was found whereas protein C antigen level was normal in uraemics. This finding, together with our recent observation that plasma protein C activity is partly normalised during haemodialysis, lead us to suggest the presence of one or more inhibitors of protein C activity in plasma from patients with uraemia.

Adult↗
PubMed1986

The prostacyclin/thromboxane balance is favourably shifted in Greenland Eskimos.

The rare incidence of cardiovascular disease in Eskimos has been ascribed to their diet rich in eicosapentaenoic acid (EPA, C20:5n-3) and hence a possible formation of trienoic prostanoids. In this study we compare endogenous formation of prostacyclin (PGI), which is formed by the endothelial cell, and thromboxane (TXA), which is formed by platelets in 20 Eskimos and 20 age and sex matched Danish controls by measurement of the main urinary metabolites. Considerable formation of bioactive PGI3 from dietary EPA was shown in Eskimos, which was barely detectable in the controls. Furthermore synthesis of PGI2 was significantly higher in Eskimos in spite of a markedly lower arachidonate content in membrane lipids. In contrast formation of TXA2,3 was lower in Eskimos as compared to the Danish controls. We conclude, that the balance between PGI and TXA, which may regulate the interaction of platelet and vessel wall, is favourably shifted in Greenland Eskimos to an antithrombotic state.

Adult↗
PubMed1986

Plasma prostaglandins: 6-keto-PGF1 alpha, TXB2 and PGE2 in juvenile-onset diabetes determined by high-pressure liquid chromatography and radio-immunoassay.

Some studies have recently reported increased production of platelet thromboxane and decreased vascular prostacyclin in patients with diabetes mellitus. The impact of these changes on platelet and vascular functions in vivo is still speculative. Using radio-immunoassay and high pressure liquid chromatography we have studied the plasma levels of 6-keto-PGF1 alpha, TXB2 and PGE2 in 23 juvenile-onset diabetics. There was no significant difference in these plasma prostaglandins between the diabetics and a control group. The prostaglandins were neither correlated to blood-glucose nor the degree of glycosylation (HbA1c). Our results can not support the hypothesis that decreased vascular prostacyclin and increased platelet production of TXB2 are important factors in diabetic patients.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Hemostatic factors and renin in Greenland Eskimos on a high eicosapentaenoic acid intake. Results of the Fifth UmanaK Expedition.

The Fifth UmanaK expedition compared the fatty acid composition of platelets, bleeding times before and after ingestion of acetylsalicylic acid, 24-hour urinary tetranorprostanedioate, creatinine and Na output, as well as plasma renin, serum electrolytes and antithrombin III in 20 Greenland Eskimos and 20 Danes. The results indicate that the prostaglandin production was not inhibited in the Eskimos, and that the antiaggregatory prostanoids predominate in Eskimos compared to Danes. Although blood pressure and 24-hour urinary Na output were similar, the plasma renin level was significantly higher in the Eskimos on a high eicosapentaenoic acid intake.

Adult↗
PubMed1985

Interactions between sodium salicylate and acetyl salicylic acid evaluated using ADP induced platelet aggregation and bleeding time.

1 g acetyl salicylic acid orally significantly enhanced the initial rate of platelet aggregation induced by 1 mumol/l and 2.5 mumol/l ADP. Sodium salicylate was without effects on the platelet aggregation and specifically it did not prevent acetylsalicylic acid from inhibiting the secondary aggregation. Sodium salicylate was without effect on the bleeding time and did not inhibit the prolongation induced by acetyl salicylic acid. Our study does not lend support to the concept of an important interaction in vivo between acetyl salicylic acid and its first metabolite salicylate in man.

Adenosine Diphosphate↗
PubMed1985

Protein C activity in renal disease.

Protein C activity was determined in 19 healthy controls and in 52 patients with renal diseases, clinically divided into three groups I) Nephrotic syndrome, II) Renal insufficiency, III) Terminal uremia, requiring maintenance dialysis. In the nephrotic syndrome protein C levels were found to be normal, but in renal insufficiency and terminal uremia the protein C activity was significantly decreased. A correlation between decreasing protein C and progressive renal failure is suggested. The reduced protein C activity may play an important role in the thrombotic tendency seen in renal diseases and uremia.

Adult↗
PubMed1985

Long term 'marine diet' in Eskimos is not associated with altered urinary excretion of total tetranor prostaglandin metabolites.

The total urinary excretion of tetranor prostaglandin metabolites, measured as tetranorprostanedioic acid (TPD), was quantified in traditionally living Greenland Eskimos (E) and compared with that in Caucasian Danes (D). TPD excretion (microgram/24h) was not significantly different between both groups, neither for males (331 +/- 62.4 (E) vs. 331 +/- 25.7 (D), mean +/- SEM, n = 9 and 10) nor for females (190 +/- 31.7 (E) vs. 264 +/- 27.4 (D), n = 11 and 10, P2 greater than 0.05). Since urinary prostaglandin metabolites are thought to reflect the total prostaglandin turnover in vivo, these results suggest that a long-term intake of relatively large amounts of polyunsaturated fatty acids of the (n-3) family does not alter total prostaglandin turnover in vivo. This is in contrast to stimulated prostanoid formation in vitro, and thus suggests a different regulatory role of dietary and tissue fatty acids for 'stimulated' and 'basal' prostaglandin production.

Adult↗
PubMed1985

Exercise decreases the platelet sensitivity to prostacyclin in patients with angina pectoris.

Earlier reports have indicated, that the platelet sensitivity to prostacyclin (PGI2) is decreased in patients with coronary heart disease and that the onset of a spontaneous anginal attack is associated with a further decrease in platelet sensitivity to PGI2. We studied platelet function before and after bicycle exercise testing in 23 patients with angina pectoris and in 11 healthy males. We could not demonstrate any difference in platelet sensitivity to PGI2 between patients with angina pectoris and the controls neither before or after exercise testing. The platelet sensitivity to PGI2 decreased significantly after exercise, both in patients and in controls, but the decrease was not related to the development of myocardial ischemia. Our results could be interpreted in terms of different pathophysiological roles of platelets in spontaneous and in exercise-induced myocardial ischemia.

Angina Pectoris↗
PubMed1985

Platelets and antithrombin III in uraemia: the acute effect of haemodialysis.

In 14 haemodialysis patients, platelet count, secondary platelet aggregation rate, immunological antithrombin III and antithrombin III activity were lower and plasma beta-thromboglobulin higher than in 14 age- and sex-matched controls. In contrast, primary platelet aggregation, the degree of secondary aggregation and circulating platelet aggregates did not differ. Haemodialysis was associated with signs of platelet damage reflected by increase in plasma beta-thromboglobulin, extraction of platelets in the dialyser and decline in platelet count. Platelets in the dialyser effluent line were less aggregable than platelets in arterial blood. Circulating platelet aggregates and immunological antithrombin III were unchanged during dialysis whereas antithrombin III activity showed a minor rise. In conclusion, uraemics show a decreased rate of secondary platelet aggregation, and haemodialysis confers further platelet injury due to blood/surface interactions during extracorporeal circulation. The defective platelet function and low antithrombin III activity may help to explain the paradoxical occurrence of both haemorrhagic and thrombotic complications in uraemia.

Adenosine Diphosphate↗
PubMed1984

Eicosapentaenoic acid potentiates the production of prostacyclin-like material in the arachidonic acid perfused human umbilical vein.

The production of prostacyclin (PGI2)-like material in human umbilical veins perfused continuously at 37 degrees C with Hanks buffer solution with 1% human albumin (HBA) was studied by bioassay. Subsequent perfusion resulted in a time dependent significant decrease in production of PGI2-like material. After addition of 20 mumol/l arachidonic acid (HBA-AA) the production of PGI2-like material increased significantly. The production of PGI2-like material was significant greater when the vein was perfused with HBA-AA than when perfused with HBA with 20 mumol/l eicosapentaenoic acid (HBA-EPA). Examination of the HBA-EPA perfusate by thin layer chromatography showed that it contained a substance that comigrated with genuine 6-keto-PGF1 alpha and a substance that comigrated with delta 17-6-keto-PGF1 alpha. Finally, perfusion with HBA containing 10 mumol/l AA plus 10 mumol/l EPA resulted in a significant greater production of PGI2-like material than perfusion with HBA-AA alone. These results support the hypothesis that EPA has beneficial antithrombotic properties in human.

Arachidonic Acids↗
PubMed1984

Cigarette smoking and its effects on the platelet-vessel wall interaction.

The effect of smoking and of carbon monoxide on the platelet-vessel wall interaction was investigated. After smoking two high-nicotine content cigarettes (2.6 mg nicotine/cigarette) the mean bleeding time decreased 1.6 min (P less than 0.05) in five habitual smokers whereas the platelet aggregability was only moderately inhibited. After inhibiting the platelet cyclooxygenase by ingesting acetylsalicylic acid (ASA) 2 days prior to the study, smoking caused a markedly and significantly shortened bleeding time (-3.8 min; P less than 0.05). The bleeding time was unaffected by smoking when both the platelet cyclooxygenase and the vessel wall prostaglandin was inhibited by ASA 1 h prior to the study. When smoking two cigarettes with a low content of nicotine (0.25 mg nicotine/cigarette) no changes in the haemostatic mechanism were observed. Inhalation of carbon monoxide in high amounts in five non-smokers had a significant short-lasting effect on the bleeding time (-1.2 min, P less than 0.05). No changes in the bleeding time were observed after carbon monoxide inhalation when the platelet cyclooxygenase or when both the platelet cyclooxygenase and the vessel wall prostaglandin production were blocked. Based on the results it is concluded that the effect of smoking on the haemostasis is mainly mediated through an inhibitory effect on the prostacyclin production in the vessel wall by nicotine and that carbon monoxide only plays a minor role.

Bleeding Time↗
PubMed1983

Cigarette smoking shortens the bleeding time.

The cutaneous bleeding time was shortened after smoking high nicotine cigarettes while not after smoking nicotine free cigarettes. The ADP induced primary platelet aggregation was not enhanced. The number of circulating platelet aggregates did not change due to smoking.

Adult↗
PubMed1983

Verapamil does not alter platelet function in patients with recent myocardial infarction.

Reports concerning the influence of the calcium antagonist verapamil on platelet function are conflicting. In a randomized double blind trial including 52 patients with acute myocardial infarction the effect of verapamil 120 mg given perorally three times a day for three months was investigated. There were no alterations in cutaneous bleeding time, platelet aggregate ratio or platelet aggregation induced by ADP or collagen. Verapamil administered in therapeutic doses does not seem to affect platelet function in patients with ischaemic heart disease.

Aged↗