PLATELET HYPOAGGREGABILITY IN HEREDITARY HYPERTRIGLYCERIDEMIC RATS - RELATION TO PLASMA TRIGLYCERIDES

To define better the relationships between lipid metabolism disturbanc es and platelet aggregation we have examined these parameters in hered itary hypertriglyceridemic and control Lewis rats, Hereditary hypertri glyceridemic rats are hypertensive and have high plasma triglycerides but not elevated plasma total cholesterol. In the present study, we ha ve demonstrated that platelets from hereditary hypertriglyceridemic ra ts have lowered initial rate and maximal aggregation after stimulation with thrombin or ADP in comparison with controls. These two strains d id not differ significantly in the inhibition of platelet aggregation by the thromboxane A(2) receptor inhibitor, SQ 29 548. In hereditary h ypertriglyceridemic rats, the thrombin response, as well as the contri bution of the thromboxane A(2)-sensitive pathway, were positively asso ciated with the plasma level of triglycerides. Similar trend was found in Lewis rats. However, the slopes of these relationships were reduce d in hereditary hypertriglyceridemic rats, These alterations of the ag gregatory responses in hereditary hypertriglyceridemic rats were indep endent of blood pressure and plasma cholesterol level. In conclusion, our results showed a clear-cut platelet hypoaggregability to both thro mbin and ADP in hypertensive hypertriglyceridemic rats. This hypoaggre gability was not due to an impaired function of the thromboxane A(2) p athway but could be connected with disturbances of lipid metabolism, ( C) 1998 Elsevier Science Ltd.