Lucio F J, Puyol M R, Marques L D, Escribano C G, Duarte A M
Department of Physiology and Pharmacology, University of Alcalá de Henares, Madrid, Spain.
Biomed Biochim Acta. 1991;50(7):893-9.
Compensatory responses tending to prevent a thrombotic state in rats fed a high lipid diet have been investigated. Platelet membranes from these animals had an increased cholesterol content but the membrane fluidity was found to be within values nearly normal. A decrease in phosphatidylethanolamine was noted. These changes may maintain normal platelet sensitivity to aggregating agents. In fact, platelets from hyperlipidemic rats were hypersensitive to thrombin, but not to adenosine diphosphate. In addition, platelets were apparently able to correct, at least in part, the stated hyperactivity of hyperlipidemic plasma to coagulate, as shown by thrombelastographic tests in both platelet-rich plasma and plasma from hyperlipidemic rats. Finally, thrombelastographic features of whole blood from these animals were found to be normal. This suggests an important role of blood cells in compensating plasma hyperactivity to coagulate during hyperlipidemia.
对喂食高脂饮食的大鼠中倾向于预防血栓形成状态的代偿反应进行了研究。这些动物的血小板膜胆固醇含量增加,但发现膜流动性在接近正常的值范围内。观察到磷脂酰乙醇胺减少。这些变化可能维持血小板对聚集剂的正常敏感性。事实上,高脂血症大鼠的血小板对凝血酶高度敏感,但对二磷酸腺苷不敏感。此外,如在富含血小板血浆和高脂血症大鼠血浆中的血栓弹性图测试所示,血小板显然能够至少部分纠正高脂血症血浆所述的高凝活性。最后,发现这些动物全血的血栓弹性图特征正常。这表明血细胞在高脂血症期间补偿血浆高凝活性方面发挥重要作用。