摘要:

Changes in the types and concentrations of albumin-bound fatty acids in plasma have been related to subsequent changes in platelet and endothelial cell function both in vitro and in vivo. Fatty acids in the linoleate and linolenate sequences with the potential to act as prostaglandin and thromboxane precursors, seem to play a fundamental role in the homeostatic balance between platelets and endothelial cells. Variations in this balance may be directly related to the tendency to thrombosis.

ISSN:1424-8832    

DOI:10.1159/000214311

出版商:S. Karger AG    

年代:1979

数据来源: Karger

摘要:

Thrombin and low density lipoproteins (LDL) are capable of inducing damage to human endothelial cells in primary culture. These substances both induce endothelial contraction as first recognizable morphological change. However, the effect of thrombin appeared early, was reversible and prevented by hirudin, while LDL acted over hours and the injury was progressive. Addition and high density lipoprotein (HDL), together with LDL, inhibited the cellular injury induced by LDL.

ISSN:1424-8832    

DOI:10.1159/000214312

出版商:S. Karger AG    

年代:1979

数据来源: Karger

摘要:

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.

ISSN:1424-8832    

DOI:10.1159/000214313

出版商:S. Karger AG    

年代:1979

数据来源: Karger

摘要:

In Eskimos coronary heart disease is a rarity. This can partly be explained by their favorable plasma lipid levels. An additional factor seems, however, to be that in Eskimo food polyunsaturated fatty acids of the ω-3 series replace those of the ω-6 series. C20:5, ω-3 can be converted by the vessel wall to an antiaggregatory substance, whereas it has no proaggregatory effect on platelets. Consistent with these findings Eskimos were found to have a nearly 2-fold longer bleeding time than Danes. Platelet aggregability, too, was merkedly depressed when exposing platelets from Eskimos to ADP and collag

ISSN:1424-8832    

DOI:10.1159/000214314

出版商:S. Karger AG    

年代:1979

数据来源: Karger

摘要:

Results in animals and in man indicate that in many circumstances, lipemia is not closely related to the severity of atherosclerosis nor to the incidence of coronary heart disease (CHD) or the intake of saturated fats as observed in paired studies between farmers from Moselle and Var in France and from West and East Scotland. In rabbits, an increased response of platelets to thrombin occurs before any deposition of cholesterol, as a result of a saturated fat feeding. Under these conditions, the addition of alcohol to the drinking water decreases significantly both the platelet response to thrombin and the severity of atherosclerotic lesions without much affecting plasma cholesterol. In farmers from Moselle and Var (as well as from Scotland), platelet functions, namely the aggregation to thrombin and their clotting activity, i.e. PF3, are closely related to the intake of saturated fats, either as a result of the long-term feeding or of a 1 year change in the diet of Moselle farmers. Certain platelet functions appear to be the only blood parameter related to the incidence of CHD and significantly correlated on a group, as well as on an individual basis, with the intake of saturated fat, and inversely related with that of calcium. Saturated fats and calcium are known to be the two main dietary factors related to CHD. These results suggest that the intermediate link between dietary fats and CHD might be blood platelets rather than serum lipids, through an effect on both thrombosis and atherosclerosis.

ISSN:1424-8832    

DOI:10.1159/000214315

出版商:S. Karger AG    

年代:1979

数据来源: Karger

摘要:

Prostacyclin and thromboxane A2 are products of arachidonic acid which play a role in the regulation of haemostatic plug and thrombus formation. Aspirin inhibits the synthesis of both compounds but is more active in blocking TXA2 formation; based on this, aspirin is suggested to have an anti-thrombotic effect. Other possible approaches to the development of anti-thrombotic drugs are discussed.

ISSN:1424-8832    

DOI:10.1159/000214316

出版商:S. Karger AG    

年代:1979

数据来源: Karger

摘要:

One of the earliest events in thrombus formation is the adherence of blood platelets to the exposed subendothelium. Under normal conditions no platelet adherence to the vascular endothelium occurs. To study a possible interaction between endothelial cells and blood platelets, endothelial cells were isolated from the umbilical cord vein. These isolated cells could be identified as endothelial cells by the presence of the so-called Weibel Palade bodies and the FVIII:AG. After incubation of monolayers of endothelial cells with blood platelets an unstable substance which inhibits platelet aggregation is released from the endothelial cell. This substance could be identified as prostacyclin according to the following criteria: (1) Its formation could be blocked by pretreatment of the endothelial monolayers with indomethacin or tranylcypromin. (2) After preincubation of endothelial cells with [14C]-endoperoxide, chemically detectable amounts of [14C]-6-keto PGF1α, the stable end product of prostacyclin could be detected. (3) In incubation supernatants the presence of 6-keto PGF1α could be shown by means of gas chromatography. Monolayers of endothelial cells only synthesize prostacyclin when the cells are stimulated for example by mechanical stress or after addition of substances like arachidonic acid or thrombin. It has been suggested that apart from the aforementioned endogenous production of prostacyclin the endothelial cell may also synthesize prostacyclin using endoperoxides provided by platelets. In these studies the production of prostacyclin was measured as the inhibition of platelet aggregation. Comparison of the amount produced in the presence of buffer alone, with the amount formed in the presence of platelets, led to the suggestion that endoperoxides liberated by platelets were used by endothelial cells to synthesize prostacyclin. If, however, the retainment of the biological activity in these two systems is compared, then it appears that in the presence of plasma or platelets, prostacyclin is stabilized to

ISSN:1424-8832    

DOI:10.1159/000214317

出版商:S. Karger AG    

年代:1979

数据来源: Karger

摘要:

The effects of PGG2 and PGH2 on platelets are mimicked by synthetic PG analogues in which the nature and specificity of the substituents on carbons 11 and 15 (or 16) are important determinants of reactivity. Arachidonic acid and stimulatory PGs induce secretion of platelet dense granule and alpha granule constituents, but not lysomal constituents, although arachidonate metabolism is necessary for collagen-induced release of lysosomal enzymes. N0164 acts on platelets as an endoperoxide antagonist: Trimethoquinol acts as an endoperoxide and TxA2 antagonist. PGs induce platelet aggregation by combining with a specific (endoperoxide) receptor.

ISSN:1424-8832    

DOI:10.1159/000214318

出版商:S. Karger AG    

年代:1979

数据来源: Karger

摘要:

When infused intravenously into anaesthetized cats angiotensin II (1–4 μg/ kg) released into the circulation an unstable substance that caused de-aggregation of platelet clumps, relaxed a strip of bovine coronary artery, and its release was blocked by aspirin and indomethacin. Because of these characteristics this substance is likely to be prostacyclin. Catecholamines and phenylephrine did not induce the release of prostacyclin. It is suggested that a chemical modification of the molecule of angiotensin II may render a peptide with little hypertensive properties which will be an activator of prostacyclin biosynthes

ISSN:1424-8832    

DOI:10.1159/000214319

出版商:S. Karger AG    

年代:1979

数据来源: Karger

摘要:

In several experimental and clinical conditions associated with thrombotic tendency, or complicated by thrombotic episodes, either prostacyclin (which inhibits platelet aggregation) or plasminogen activator (which promotes fibrinolysis), or both, appear to be decreased in the vessel wall. In other conditions, however, either activity may not change or even be increased. Possibly, vascular damage is followed by an early stimulation of both activities (a defence mechanism?) which may be subsequently reduced or exhausted. While the role of vascular plasminogen activator in haemorrhagic conditions is apparently unknown, prostacyclin activity appears to be markedly enhanced both in experimental animals and in patients with uraemia and bleeding complications. There is a suggestive evidence that uraemic plasma powerfully stimulates vascular prostacyclin generation.

ISSN:1424-8832    

DOI:10.1159/000214320

出版商:S. Karger AG    

年代:1979

数据来源: Karger