ISSN:0001-6101    

DOI:10.1111/j.0954-6820.1980.tb10928.x

出版商:Blackwell Publishing Ltd    

年代:1980

数据来源: WILEY

ISSN:0001-6101    

DOI:10.1111/j.0954-6820.1980.tb10929.x

出版商:Blackwell Publishing Ltd    

年代:1980

数据来源: WILEY

ISSN:0001-6101    

DOI:10.1111/j.0954-6820.1980.tb10930.x

出版商:Blackwell Publishing Ltd    

年代:1980

数据来源: WILEY

摘要:

ABSTRACT.Platelet aggregation is a complex event, and no single pathway for release and/or activity of mediators can be postulated. Three mechanisms at least operate for aggregation: release of ADP, formation of thromboxane A2, and a third process in which PAF appears to be centrally involved. In every case the adenylate cyclase system is likely to control aggregation, after appropriate stimuli have been provided and potential aggregating substances have been released. Any approach which involves inhibiting the release of the mediators must be based on a knowledge of the mechanism of this release. Phospholipase A2appears to be a reasonably critical point at which to attempt inhibition of platelet aggregation and activation in general, particularly since doing so should at the same time reduce the synthesis of thromboxane A2(which is dependent upon the availability of AA hydro‐lysed from phospholipids) and also that of PAF.Platelet aggregation is essential for arterial thrombosis. Even though the insidious vascular lesion precedes the platelet alteration, and thus appears to be the critical step where prophylaxis against coronary thrombosis should be applied, attempts to inhibit platelet responsiveness during acute myocardial infarction or during the post‐infarction stages appear justified. This is true for two reasons, first precisely because of the insidious and relatively uncontrolled nature of the vascular disease, and secondly because the clinician has to deal with established atherosclerotic patients who are statistically likely to undergo myocardial reinfarction. The understanding of the mechanisms of platelet aggregation is thus important for the biologist, as well as for the physiopathologist and the clinician. This paper attempts to summarize the presently available knowledge on these mechani

ISSN:0001-6101    

DOI:10.1111/j.0954-6820.1980.tb10931.x

出版商:Blackwell Publishing Ltd    

年代:1980

数据来源: WILEY

摘要:

ABSTRACT.A study has been performed on the effects of alternating pressure on the functional state of circulating platelets. Platelet aggregation, changes in platelet shape and the time of shape recovery after deformation have been measured, as well as plasma adenine nucleotide concentrations. A pressure impulse of 60–80 Torr applied for 1 min causes a 50°% decrease in the extent of platelet aggregation, but if 110–120 Torr is applied, the amplitude of platelet aggregation is increased by 50°%. With pressure impulses increasing to 350 Torr, the peak of aggregation process was recorded, with subsequent inhibition as the alternating pressure grew further. The possible physiological significance of these findings is disc

ISSN:0001-6101    

DOI:10.1111/j.0954-6820.1980.tb10932.x

出版商:Blackwell Publishing Ltd    

年代:1980

数据来源: WILEY

摘要:

ABSTRACT.In view of the supposed importance of prostacyclin (PGI2) and thromboxane A2(TXA2) in coronary regulation and platelet aggregation, the hypothesis has been proposed that anti‐anginal drugs might increase the blood supply to the heart not only by vasodilation and diminution of cardiac work but also by inhibition of formation or dissolution of platelet aggregates. Anti‐anginal drugs, especially dipyridamole and nitroglycerin were investigated to establish whether they increase the biosynthesis or anti‐platelet effect of PGI2and inhibit TXA2synthesis. In various in vitro models, dipyridamole showed an enhancement of PGI2, synthetase and cyclo‐oxygenase activity and increased PGI2, release, whereas it had only a weak inhibiting effect on TXA2synthesis. There was a stimulating effect on PGI2, formation by some other anti‐anginal drugs. In contrast, nitroglycerin did not stimulate the biosynthesis of PGI2, in rabbits or guinea pigs, but strongly inhibited TXA2, formation in platelets. It showed an additional inhibiting effect on platelet aggregation and increased additively or more than additively the antiplatelet effect of small doses of PGI2, in ADP‐induced, arachidonic acid‐induced, and thrombin‐induced platelet aggregation. A hypothesis is discussed in which the action of nitroglycerin could be brought about by a vasodilating effect, as well as by its antiplatelet action on reversible plat

ISSN:0001-6101    

DOI:10.1111/j.0954-6820.1980.tb10933.x

出版商:Blackwell Publishing Ltd    

年代:1980

数据来源: WILEY

ISSN:0001-6101    

DOI:10.1111/j.0954-6820.1980.tb10934.x

出版商:Blackwell Publishing Ltd    

年代:1980

数据来源: WILEY

ISSN:0001-6101    

DOI:10.1111/j.0954-6820.1980.tb10935.x

出版商:Blackwell Publishing Ltd    

年代:1980

数据来源: WILEY

摘要:

ABSTRACT.The incorporation of [3H] thymidine and the synthesis of glycosaminoglycans (GAG) by cultured human aortic smooth muscle cells were studied in the presence of human sera with high HDL cholesterol concentration, high LDL cholesterol concentration or with normal serum lipoprotein concentrations. The sera were prepared either conventionally (CPS, platelet factor present) or from platelet poor plasma by recalcification (PPPS). As compared to normolipidaemic sera, HDL‐aemic CPS decreased the incorporation of thymidine but LDL‐aemic sera had no effect. HDL‐aemic sera decreased markedly the synthesis of sulphated GAG but had no effect on the synthesis of hyaluronic acid (HA). Therefore, the sulphated GAG/HA ratio was decreased. The decrease in sulphated GAG was observed only in the presence of CPS, not in the presence of PPPS. LDL‐aemic sera decreased the synthesis of hyaluronic acid causing an increase in the sulphated GAG/HA ratio. This effect was observed in the presence of both CPS and PPPS.The results suggest that determination of the sulphated GAG/HA ratio in aortic smooth muscle cell cultures provides a useful method for estimating the atherogeneity of various sera. The anti‐atherogenic effect of HDL‐aemic sera seems to be dependent on the platelet factor while the atherogenic effect of LDL‐aemic sera may be independent of the pl

ISSN:0001-6101    

DOI:10.1111/j.0954-6820.1980.tb10936.x

出版商:Blackwell Publishing Ltd    

年代:1980

数据来源: WILEY

ISSN:0001-6101    

DOI:10.1111/j.0954-6820.1980.tb10937.x

出版商:Blackwell Publishing Ltd    

年代:1980

数据来源: WILEY