In retinal vein occlusion platelet response to thrombin is increased.

INTRODUCTION

Retinal vein occlusion is a major cause of ocular morbidity. The precise mechanism leading to thrombosis in retinal vein occlusion has not yet been clearly elucidated. Several risk factors have been identified, including hypertension diabetes, history of cardiovascular disease, hypercholesterolemia, hyperhomocysteinaemia, increased ocular pressure and glaucoma. Although thrombus formation in the vein plays a significant role in the onset of retinal vein occlusion, the relationship between platelet aggregation and retinal vein occlusion remains to be clarified.

MATERIALS AND

METHODS

In the present study the platelet response to thrombin in a selected group of retinal vein occlusion patients was investigated. Retinal vein occlusion patients were compared to a group of healthy subjects matched for age, sex, clinical and metabolic characteristics. In resting and activated platelets of both groups of subjects total protein tyrosine phosphorylation, p38MAPK and cytosolic phospholipase A(2) phosphorylation, arachidonic acid release, intracellular calcium levels, thromboxane B(2) and superoxide anion formation were measured.

RESULTS

Results show that platelets of patients were more responsive to thrombin than healthy subjects. In resting or in thrombin stimulated platelets of patients total protein tyrosine phosphorylation, p38MAPK and cytosolic phospholipase A(2) phosphorylation were increased. Also arachidonic acid release, thromboxane B(2) and superoxide anion formation were higher in patients than in healthy subjects. In addition intracellular calcium rise induced by thrombin was increased in patients.

CONCLUSIONS

Altogether data suggest that platelet hyperaggregability inducing thrombus formation might be an important factor in the onset and/or development of retinal vein occlusion.