thromboxane-b2 and Hyperlipoproteinemia-Type-IV

Platelets play an essential role in the pathogenesis of atherosclerosis; by impedance method we valued in whole blood platelet aggregation induced by collagen in 40 healthy subjects and in 40 type II and type IV hyperlipemic subjects. Meanwhile by radioimmunoassay we dosed thromboxane B2, a stable product of thromboxane A2, released by platelets during activation, in 7 healthy subjects and 25 hyperlipemic subjects. The statistical investigation put in evidence that at higher plasmatic levels of cholesterol, triglycerides and LDL correspond a greater platelet sensitivity to the aggregating agent, while the opposite happens to higher levels of HDL. The dosage of thromboxane B2 put in evidence a moderate increase in hyperlipemic as to healthy subjects, probably pointing to a state of platelet activity.

Topics: Adult; Female; Humans; Hyperlipoproteinemia Type II; Hyperlipoproteinemia Type IV; Male; Middle Aged; Platelet Aggregation; Radioimmunoassay; Thromboxane B2

It is generally accepted that in hyperlipoproteinemia (HLP) the vascular prostacyclin formation is diminished. We wondered, whether HLP is also associated with changes in platelet sensitivity to antiaggregatory prostaglandins. Therefore, we examined the platelet sensitivity to the prostaglandins PGI2 and PGD2 as well as plasma thromboxane B2 (TXB2)-levels in 24 patients with HLP type IIa, IIb and IV. We found a marked decrease of platelet sensitivity to PGI2 in all the patients examined, which was more pronounced in type IIb than in types IIa and IV. Platelet sensitivity to PGD2 showed no difference in the hyperlipemic patients. Plasma TXB2-levels were significantly increased in comparison to a control group, the changes being most pronounced in patients with type IV HLP. Platelet half-life was significantly shortened in the HLP-patients. This in-vivo platelet function parameter was found to be reduced in patients with type IIa HLP to the greatest extent. Our findings suggest that platelet deposition in HLP is promoted not only by diminished vascular PGI2-formation, but also by decreased sensitivity of the platelets to antiaggregatory prostaglandins. The high TXB2-levels and the shortened platelet half-life reflect the in-vivo activated platelet population in these patients.

Topics: Adult; Aged; Blood Platelets; Epoprostenol; Female; Half-Life; Humans; Hyperlipoproteinemia Type II; Hyperlipoproteinemia Type IV; Hyperlipoproteinemias; In Vitro Techniques; Male; Middle Aged; Platelet Aggregation; Prostaglandin D2; Prostaglandins D; Thromboxane B2

In 13 type II hyperlipidemics (10 males and 3 females; mean age 50.2 +/- 10.6 years), in 10 type IV hyperlipidemics (7 males and 3 females; mean age 51 +/- 13.3 years) and in 23 healthy age- and sex-matched controls, the following parameters were measured: plasma cholesterol; plasma TG; plasma C-HDL; VLDL, separated in a preparative ultracentrifuge; C-LDL; Apo B, with immunoelectrophoretic method; platelet sensitivity to prostacyclin; TXB2 formation in PRP; TXB2 in serum. This study provides evidence for: 1. Reduced platelet sensitivity to prostacyclin, more evident in type II hyperlipidemia that provides an additional mechanism involved in increased platelet aggregation found in type II hyperlipidemia. 2. Enhanced TXB2 formation in PRP after thrombin stimulation (664.65 +/- 142.18 pmol/10(8) platelets) only in type II hyperlipidemics and such enhanced formation was positively correlated to C-LDL (r = 0.53; p less than 0.05) and to Apo B (r = 0.62; p less than 0.05); serum TXB2 formation rate was also increased in type II hyperlipidemia.

Topics: Adult; Aged; Blood Platelets; Cholesterol; Dose-Response Relationship, Drug; Epoprostenol; Female; Humans; Hyperlipoproteinemia Type II; Hyperlipoproteinemia Type IV; Male; Middle Aged; Platelet Aggregation; Prostaglandins; Thromboxane B2; Thromboxanes