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Biomedical subjects

G Hornstra

Publications and source records attributed to G Hornstra.

At least 163 records · Page 9Linked to original sources
PubMed1985

Isolation and partial purification of a novel anticoagulant from arteries of human umbilical cord.

An anticoagulant fraction was isolated from the homogenate of human umbilical cord arteries, using Sephadex gel filtration and DEAE-Sephacel chromatography. Analysis with dodecyl sulfate/polyacrylamide gel electrophoresis and inactivation studies using proteolytic enzymes indicate that the anticoagulant activity is associated with a polypeptide with an apparent Mr of 32 000. The anticoagulant inhibits thromboplastin as well as factor Xa induced clotting but does not affect thrombin initiated fibrin formation. The anticoagulant inhibits the activation of prothrombin by the complete prothrombinase complex, by phospholipid bound factor Xa but not by free factor Xa. The inhibition is instantaneous and independent of the incubation time over the whole range of concentrations tested. Therefore, the anticoagulant is unlikely to be a phospholipase or a protease. Its action does not resemble that of the plasma protease inhibitors, but it probably interferes with the phospholipid--clotting factor interactions.

Blood Coagulation↗
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↗
PubMed1981

Platelet - vessel wall interaction: role of blood clotting.

Vascular damage initiates not only the adhesion and aggregation of blood platelets but also coagulation, which is of mixed (intrinsic and extrinsic) origin. Evidence is presented that thrombin, generated as a result of the injury, is a prerequisite for platelet aggregation. Platelets, after activation, in their turn promote coagulation. Prostaglandin I2 (PGI2 or prostacyclin) inhibits coagulation induced by damaged vascular tissue. This effect of PGI2 is mediated by the inhibition of platelets in their participation in the generation of factor Xa and thrombin. Dietary cod liver oil, by changing plasma coagulability, decreases the procoagulation activity of vessel walls, and arterial thrombosis. Another fish oil with similar effects on plasma coagulability and some other haemostatic parameters does not modify vessel wall-induced clotting, nor does it significantly lower arterial thrombosis tendency; this indicates the physiological relevance of vessel wall-induced clotting in arterial thrombus formation. Some evidence is also given for the importance of vessel wall-induced clotting in primary haemostasis.

Adenosine Diphosphate↗
PubMed1981

Fish oil feeding lowers thromboxane- and prostacyclin production by rat platelets and aorta and does not result in the formation of prostaglandin I3.

It is demonstrated that feeding cod-liver oil to rats leads to a considerable reduction in the formation of platelet TxA2 and of vascular PGI2. No appreciable formation of TxA3 and PGI3 is observed, although arterial thrombosis is depressed and bleeding time is prolonged. These findings contradict the suggested role of prostaglandins of the 3-series in thromboregulation.

Animals↗
PubMed1980

Dietary prevention of coronary heart disease. Effect of dietary fats on arterial thrombosis.

Epidemiological studies indicate that dietary saturated fats are implicated in coronary heart disease (CHD). Human prospective studies have shown that diets low in long chain saturated fatty acids and enriched in linoleic acid are beneficial in CHD-prevention. Experiments in animals have shown that such diets diminish atherosclerosis and the tendency to arterial thrombosis; they also lower the ability of platelets to aggregate in animals and in man. The mechanisms by which these diets produce these effects are not yet completely understood. Platelets and vascular prostaglandin-like substances may be involved as well as platelet membrane fluidity and platelet coagulant activities. On the basis of the available evidence, measures to decrease the intake of long chain saturated fatty acids (concomitant with an enhanced consumption of linoleic acid-rich products) are justified. Although certain marine oils may also have anti-thrombotic properties the possibility of undesirable side effects compels extensive investigation before their wide-spread use can be recommended.

Animals↗
PubMed1979

Clot-promoting effect of platelet-vessel wall interaction: influence of dietary fats and relation to arterial thrombus formation in rats.

A small piece of vascular tissue punched from a rat aorta is able to clot plasma. This coagulation process is promoted by blood platelets, especially after their activation. Thrombin, generated by this clotting process, plays a key role in vessel-wall induced platelet activation. Vascular prostacyclin inhibits vessel-wall-induced clotting of platelet-rich plasma, possibly by inhibiting platelet activation. Type and amount of dietary fats were shown to influence vessel-wall-induced clotting via at least four different mechanisms, namely: by modifying vascular prostacyclin formation; by affecting the clotting potency of the vascular tissue per sec; by an effect on some platelet property, probably connected with platelet activation; by influencing a plasma factor. Each of these mechanisms, as well as the nature of vessel-wall-induced coagulation, requires further investigation.

Animals↗