P-selectin mediates the adhesion of sickle erythrocytes to the endothelium

Thromboembolic and ischemic complications frequently occur during and after endovascular procedures, because of associated arterial injury and the thrombogenic characteristics of arterial catheters, contrast agents, and implanted devices such as coils and stents. Platelet adhesion, activation, and aggregation occurring at the site of arterial injury are mediated by local factors, including thromboxane A2 (inhibited by aspirin) and adenosine diphosphate (inhibited by ticlopidine and clopidogrel). Concomitantly, thrombin is formed by serial activation of clotting factors via contact with subendothelial tissue factor. Thrombin cleaves fibrinogen into fibrin. Thrombin activation is indirectly blocked by heparin and its analogs. However, after thrombin is clot-bound (with fibrin), it is relatively protected from heparin and is effectively blocked only by direct thrombin inhibitors (hirudin and its analogs). The final common pathway in clot formation is the binding of fibrinogen to platelets via platelet glycoprotein IIb/IIIa receptors, which is inhibited by antibodies to platelet IIb/IIIa receptors. New treatment modalities, such as the use of direct thrombin inhibitors and antibodies to platelet glycoprotein IIb/IIIa, seem to be more effective for prophylaxis and treatment than conventional anticoagulation and antiplatelet therapies.

Prevention and treatment of thromboembolic and ischemic complications associated with endovascular procedures: Part I--Pathophysiological and pharmacological features.

Capillary hemangioma (infantile periocular hemangioma)

Deposition of thrombotic material on catheters was observed following more than 50% of 93 diagnostic catheterizations. The incidence of deposition of thrombotic material on catheters remaining in the body for more than 1 day was 100%. Polyethylene and siliconized polyurethane catheters were less thrombogenic than Teflon end-occluded catheters. A definite time relationship between the thrombus formation and the duration of the catheterization procedure was noted. The growth of thrombi on the outside of catheters does not appear to be linear since catheters can remain in place for 10 days or more. Postcatheterization thrombosis is believed to be due to thrombi stripped from the catheter by the arterial wall. The thrombus which originally encases the catheter will pile up at the puncture site as the catheter is withdrawn. The thrombus may remain attached at the puncture site or embolize peripherally.

Arterial Thrombus Formation During Clinical Percutaneous Catheterization

The role of platelets in thrombotic and vascular disease.

Vascular catheterisation is now widely used in diagnostic techniques (angiography, blood analysis, blood pressure recording) and in therapeutics (artificial cardiac pace-makers, intravenous and intraarterial drip). The most common serious complication of vascular catheterisation is thromboembolism. Though the causal mechanism is not properly understood, there is evidence that the risk varies with the area of the outer surface of the intravascular part of the catheter. This suggests thrombus formation to be stimulated by some reaction of the blood to the surface of the catheter (JACOBSSON & SCHLOSSMAN 1969a). I t has been demonstrated in vitro that platelets adhere to the surface of a catheter and aggregate (JACOBSSON 1969a). The initial phase of thrombus formation is characterised by a similar reaction of platelets to the vessel wall (HuGUES 1962, ZUCKER & BORRELLI 1962, HOVIG 1963, OWREN 1964, MUSTARD et colI. 1967). It was therefore thought worthwhile to investigate if platelets

Platelet adhesion and throms formation on vascular catheters in dogs.

SUMMARY Fibrinolytic split products (FSP) in the urine and the serum were determined by a quantitative immunoelectrophoretic method in 28 recipients of a kidney and in nine living donors. Twenty patients were examined for urokinase activity in the urine. FSP invariably occurred in both the serum and the urine during the first 2 postoperative weeks in the recipients but not in the donors. This finding in the urine is probably attributable to the ischaemic injury to the transplanted organ. During acute or chronic rejection, FSP occur in the urine and sometimes also in the serum. During severe and irreversible rejection, the concentration of FSP in the urine is much higher than that in the serum. Separation studies on Sephadex G-200 showed that the FSP consisted mainly of “high molecular weight substances.” The urokinase activity in the urine from patients with transplanted kidneys was abnormally low, indicating that FSP are probably not formed by the activity of urokinase but rather by the fibrinolytic activity in the vessel walls.

Kidney transplantation and fibrinolytic split products in serum and urine.

Analysis of platelet, red cell and fibrin content in experimental arterial and venous thrombi.

Platelets in shock and trauma

Summary

The mechanism of the coagulation disorder in an infant with a large haemangioma of the right arm has been studied. The disorder was characterised by thrombocytopenia, prolonged bleeding time and the occurrence of fibrinolytic split products in the blood. The levels of various coagulation factors were normal. The mechanism of the disorder was further investigated by injection of 51Cr labelled platelets, which disappeared very rapidly from the circulation owing to the uptake by the haemangioma. Injection of 125I labelled fibrinogen revealed a considerable increase in disappearance rate, which, however, was not as high as for 51Cr labelled platelets. Treatment with heparin in this case appeared inadvisable because the thrombocytopenia was found to be due mainly to mechanical destruction in the haemangioma while intravascular coagulation played only a subordinate role. On the other hand, the fibrinolytic activity in the tumour vessels was found to be high, which together with the occurrence of fibrinolytic split products in the blood was considered to indicate treatment with inhibitors of fibrinolysis (EACA). During this treatment the angioma decreased in size. It would therefore appear advisable to investigate the mechanisms of the coagulation disorders in these patients before deciding upon treatment.

Ulf Ljungqvist

Papers

Platelet adhesion and throms formation on vascular catheters in dogs.

Kidney transplantation and fibrinolytic split products in serum and urine.

Analysis of platelet, red cell and fibrin content in experimental arterial and venous thrombi.

Platelets in shock and trauma

Giant haemangioma with a disorder of coagulation