Platelet hypersensitivity induced by cholesterol incorporation.

摘要: Platelets from individuals with familial hypercholesterolemia show increased sensitivity to the aggregating atents, epinephrine and ADP. Since mechanism of this abnormal is unknown, we examined, in vitro, influence plasma lipid environment on function platelets. The composition lipids was altered by addition sonicated cholesterol-dipalmitoyl lecithin liposomes which were "cholesterol normal" (cholesterol-phospholipid mole ratio [C/P] equals 1.0, rich" (C/P eauals 2.2), or poor" 0). Cholesterol-normal had no platelet function. In contrast, after incubation for 5 h at 37 degrees C cholesterol-rich liposomes, normal platelets acquired 39.2% excess cholesterol change phospholipids protein. percent increase membrane three-fold that granule fraction. acquisition associated a 35-fold epinephrine-induced aggregation (P less than 0.001) 15-fold ADP 0.001), as determined both aggregometry [13C]serotonin release. Response thrombin collagen unchanged. incubated cholesterol-poor underwent selective loss 21.4% an 18-fold reduction their epinephrine. These studies demonstrate content dependent milier. Cholesterol may exert its effect modification membrane.