摘要:

The adhesion of human platelets to the human arterial subendothelium was investigated using everted postmortem renal arteries after the first bifurcation and reconstituted blood containing 51Cr-labelled, aspirin-treated platelets in a perfusion chamber according to Baumgartner. The accumulation of 51Cr on the arterial segment was a reliable reflection of the number of platelets that adhered. The dependence of platelet adhesion on platelet number, perfusion time, haematocrit and perfusion rate were found to be similar to what was observed with rabbit aorta previously, notwithstanding the essentially different nature of the human subendothelium, with its layers of smooth muscle cells above the internal elastic lamina. The system was used to study the role of factor VIII-von Willebrand factor (VIII-VWF). VIII-VWF was found to be the only plasma factor enhancing adhesion of platelets to the vessel wall. No suggestion of an inhibitory substance in plasma was found. Double perfusion experiments indicated that VIII-VWF binding to subendothelium supported subsequent platelet adhesion. A good correlation was found between the amount of VIII-VWF bound and platelet adhesion. Comparison of binding of albumin, fibrinogen, 7-globulin and VIII-VWF showed that VIII-VWF bound less. This suggests that VIII-VWF does penetrate less easily in the subendothelium, which is in agreement with immunofluorescence studies of tissues. Studies with washed platelets not treated with aspirin showed parallelism between accumulation of VIII-VWF and platelet deposition in thrombi. These data may be explained by assuming a non-easily exchangeable pool of VIII-VWF on the platelet surface and increased binding of VIII-VWF to platelets in thrombi.

ISSN:1424-8832    

DOI:10.1159/000214321

出版商:S. Karger AG    

年代:1979

数据来源: Karger

摘要:

The effect of collagen on isolated platelets, platelet-rich plasma and whole blood has been studied. Collagen failed to generate factor XIa-like activity in mixtures of isolated platelets, collagen and Ca++. Moreover, collagen added to whole blood or platelet-rich plasma containing 125I-factor IX and Ca++, also failed to form cleaved (activated) factor IX. In preliminary studies, lysed endothelial cells were found to enhance the formation of factor Xa and thrombin and to induce cleavage of 125I-factor IX in normal plasma, factor XII and factor-XI-deficient plasma even in the presence of antibody to tissue factor.

ISSN:1424-8832    

DOI:10.1159/000214322

出版商:S. Karger AG    

年代:1979

数据来源: Karger

摘要:

A survey is given of recent data pertaining to the presence of components of the fibrinolytic system in the vascular wall. Activators and inhibitors of fibrinolysis were shown to be present in the vessel wall, while activators were mainly found in the endothelial cells, and inhibitors in the media. Activators will be released into the circulation by a variety of stimuli. Among these stimuli are compounds formed or released during coagulation and thrombus formation, thus indicating how coagulation or thrombosis might induce increased fibrinolysis. Abnormal fibrinolytic activity in the vessel wall in relation to thrombosis is discussed.

ISSN:1424-8832    

DOI:10.1159/000214323

出版商:S. Karger AG    

年代:1979

数据来源: Karger

摘要:

The interaction of rabbit platelets with subendothelium of rabbit aorta was investigated under controlled blood flow conditions. Platelet adhesion and thrombus formation were compared after perfusion of native blood and of blood anticoagulated with citrate, heparin or heparin plus citrate. 15 mM citrate in plasma caused significant reduction of aggregation, thrombus volume and thrombus height; adhesion was concomitantly increased. Heparin (500 U/kg) had no significant effect on adhesion and thrombus dimensions. Treatment of rabbits with acetylsalicylic acid or sulfinpyrazone caused a significant reduction of thrombus volume and thrombus height in the presence of citrate. However, no significant effects were observed in native or heparinized blood. It is concluded that low citrate concentrations: (1) inhibit thrombus growth; (2) enhance thrombus breakdown; (3) therefore increase adhesion, and (4) strongly enhance a possible inhibitory effect of acetylsalicylic acid and sulfinpyrazone on thrombus growth.

ISSN:1424-8832    

DOI:10.1159/000214324

出版商:S. Karger AG    

年代:1979

数据来源: Karger

摘要:

In guinea pigs, sodium arachidonate-induced platelet aggregation ex vivo proved a more sensitive method for detecting drug-related effects after the administration of sulphinpyrazone than collagen-induced platelet aggregation. It was possible to detect inhibition of platelet aggregation after giving sulphinpyrazone orally in a single dose of 3 mg/kg. Excellent correlation was achieved between ex vivo and in vivo inhibition of platelet function with sulphinpyrazone using the Arthus reaction. The results are consistent with the formation, in the guinea pig of metabolites more potent than the parent molecule.

ISSN:1424-8832    

DOI:10.1159/000214325

出版商:S. Karger AG    

年代:1979

数据来源: Karger