Molecular mechanism underlying impaired platelet responsiveness in liver cirrhosis.
We have studied platelet function in 10 patients with severe liver cirrhosis, compared to healthy subjects. Using washed platelets, we have investigated the molecular mechanism underlying the defect in platelet aggregation frequently observed in these patients. We have found that platelets from cirrhotic patients have a reduced responsiveness to thrombin and collagen in terms of aggregation, and receptor-dependent activation of phospholipase C, A2 and cyclooxygenase/thromboxane synthetase. We thus suggest that this impairment in transmembrane signalling is responsible for the defective platelet function observed in cirrhosis.
D000328:Adult; D003094:Collagen / Q000494:pharmacology; D004789:Enzyme Activation / Q000187:drug effects; D005260:Female; D006801:Humans; D008103:Liver Cirrhosis / Q000097:blood* / Q000201:enzymology; D008297:Male; D008875:Middle Aged; D010741:Phospholipases A / Q000378:metabolism; D010974:Platelet Aggregation / Q000187:drug effects*; D013917:Thrombin / Q000494:pharmacology; D013929:Thromboxane B2 / Q000096:biosynthesis; D010738:Type C Phospholipases / Q000378:metabolism
D013929:Thromboxane B2; D003094:Collagen; D010741:Phospholipases A; D010738:Type C Phospholipases; D013917:Thrombin