ISSN:1424-8832    

DOI:10.1159/000214301

出版商:S. Karger AG    

年代:1979

数据来源: Karger

ISSN:1424-8832    

DOI:10.1159/000214302

出版商:S. Karger AG    

年代:1979

数据来源: Karger

ISSN:1424-8832    

DOI:10.1159/000214303

出版商:S. Karger AG    

年代:1979

数据来源: Karger

ISSN:1424-8832    

DOI:10.1159/000214304

出版商:S. Karger AG    

年代:1979

数据来源: Karger

摘要:

This communication describes the morphological changes which result from the induction of experimental thrombi in the artery wall of the rabbit and pig. The role of the platelet as the initiator of neo-intimal proliferation is stressed and the genesis of the cells contributing to such proliferation discussed.

ISSN:1424-8832    

DOI:10.1159/000214305

出版商:S. Karger AG    

年代:1979

数据来源: Karger

摘要:

Vascular endothelial cells (EC) are non-thrombogenic. The basis for this property is still essentially unknown. This paper summarizes our previous studies on EC associated glycosaminoglycans and on the specific binding of heparin to EC and describes the preventive effect of heparin sulphate (HS) on platelet adhesion to collagen; attempts to affect the binding of platelets to EC by specific removal of endogenous HS were, however, unsuccessful. The possible importance of EC surface HS for interactions with coagulation factors is discussed.

ISSN:1424-8832    

DOI:10.1159/000214306

出版商:S. Karger AG    

年代:1979

数据来源: Karger

摘要:

Endothelial regeneration was studied in rabbit aorta after intra-arterial balloon catheterization. Most of the regenerated endothelium originated from existing branches which was assessed by the Evans-blue uptake pattern and confirmed by transmission and scanning electron microscopy. Glucocorticoid treatment enhanced re-endothelialization whereas hyperlipemic diet inhibited. Sera from minipigs fed an atherogenic diet consistently have less ability than sera from control pigs to stimulate in vitro the regeneration of wounded endothelium-like monolayers of 3T3-B cells. The deficiency is probably due to an inhibitor which appears and disappears with changes in the diet.

ISSN:1424-8832    

DOI:10.1159/000214307

出版商:S. Karger AG    

年代:1979

数据来源: Karger

摘要:

Collagens I and III, in fibrillar form, bound platelets equally well; both readily induced platelet aggregation. In contrast, collagens IV and V, although pretreated as collagens I and III to induce fibrillogenesis, failed to produce aggregation. No binding of platelets was detected. Lens capsule, containing collagen type IV in situ, was also inactive. Inactivity appears due to the lack of an appropriate quaternary structure since segment-long-spacing (SLS) aggregates of collagens IV and V, as of type I, induced aggregation. Elastin and its associated microfibrillar element did not aggregate platelets; some binding of platelets to elastin only was observed.

ISSN:1424-8832    

DOI:10.1159/000214308

出版商:S. Karger AG    

年代:1979

数据来源: Karger

摘要:

The simultaneous evaluation of platelet behaviour in vivo and of the accompanying bronchoconstriction in the guinea pig is described. Arachidonic acid induces bronchoconstriction, accompanied by, but independent from, thrombocytopenia, whereas collagen induces bronchoconstriction also accompanied by, but dependent from, thrombocytopenia. In both cases bronchoconstriction is due to cyclo-oxygenase metabolites of arachidonic acid. Use of potential inhibitors of thromboxane synthetase failed to reveal which of prostaglandin endoperoxides or thromboxane A2 is responsible for aspirin-inhibitive bronchoconstriction and thrombocytopenia. In contrast to PGE1 prostacyclin failed to interfere with bronchoconstriction by serotonin or by arachidonic acid, even though thrombocytopenia by the latter was suppressed. Bronchoconstriction by collagen, in contrast, was inhibited by nanogram doses of prostacyclin, confirming platelet-dependency. The combined bronchoconstriction/thrombocytopenia test in guinea pigs can discriminate sites of action of anti-inflammatory drugs, of agents which block specific platelet and/or bronchial receptors, which stimulate the cyclic AMP system, or generically which interfere with the mechanisms of bronchoconstriction and of thrombocytopenia.

ISSN:1424-8832    

DOI:10.1159/000214309

出版商:S. Karger AG    

年代:1979

数据来源: Karger

摘要:

The adherence of 51Cr-labeled platelets to rabbit aortae everted on probes rotated in platelet-red cell suspensions has been measured. Platelet adherence to the subendothelium exposed by passage of a balloon catheter before everting the aortae was inhibited by compounds that increase platelet cyclic AMP levels (PGE1, PGI2 or dipyridamole). These agents, however, did not abolish platelet adherence to the subendothelium. Aspirin treatment of the vessel wall was used to block PGI2 production; platelet adherence to the surface of the ‘undamaged’ aorta and the subendothelium was studied following this treatment. Since aspirin treatment of the ‘undamaged’ vessel wall did not cause platelets to adhere to it, it seems unlikely that PGI2 formation by the vessel wall is the mechanism that prevents platelet adherence to normal endothelium. In addition, PGI2 formation by the vessel wall does not appear to influence platelet adherence to the subendothelium, since adherence was not increased by aspirin treatment of the damaged wall. Thrombin treatment of the ‘undamaged’ vessel wall increased platelet adherence to the surface, but the adherent platelets were seen to be adherent only to small areas where the endothelium was lost or damaged. Heparin reversed the effect of thrombin. Similar results were found when the subendothelium was exposed to thrombin or thrombin

ISSN:1424-8832    

DOI:10.1159/000214310

出版商:S. Karger AG    

年代:1979

数据来源: Karger