LIPOPROTEINS FROM NORMOLIPIDEMIC AND DYSLIPIDEMIC SUBJECTS MODIFY THE THROMBOXANE-A2 GENERATION BY PLATELETS IN CLOTTING HUMAN BLOOD

被引:7
作者
BEITZ, A
PEROVA, N
NIKITINA, N
BEITZ, J
SCHERBAKOVA, I
GIESSLER, C
MEST, HJ
机构
[1] MARTIN LUTHER UNIV HALLE WITTENBERG, SCH MED, DEPT PHARMACOL & TOXICOL, POB 302, O-4010 HALLE, GERMANY
[2] MOSCOW CTR PREVENT MED, MOSCOW 101953, RUSSIA
来源
PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS | 1993年 / 48卷 / 06期
关键词
D O I
10.1016/0952-3278(93)90054-Z
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The study was performed to investigate the influence of lipoproteins (LP) on the thromboxane (TX) A2 formation capacity of platelets in clotting whole blood in vitro. The different lipoprotein fractions VLDL, LDL, HDL2 and HDL3 Were isolated from blood of normo- or dyslipidemic volunteers by ultracentrifugation. These lipoproteins were incubated in blood with different levels of serum total cholesterol (TC) taken from normolipidemics (TC < 200 mg/dl), moderate hypercholesterolemics (TC: 200-250 mg/dl) or subjects with high cholesterol level (TC > 250 mg/dl), respectively. The amount of serum TXA2 formed within 60 min at 37-degrees-C was measured by enzyme immunoassay. The results obtained show that the efficacy of separate LP fractions to influence the TXA, production depends not only on the type of LP fraction but also on the source of plasma used for isolation of LP and on the cholesterol level in the blood for incubation: LDL taken from normolipidemics or moderate hyperlipidemics inhibited the TXA2 formation in blood from normolipidemics (P < 0.02, respectively), but enhanced it in blood from persons with moderate hypercholesterolemia (P < 0.05). LDL from hyperlipidemics enhanced TXA2 production in blood from hyperlipidemics (P < 0.05). The HDL2 fractions inhibited the TXA2 formation in blood from normo- and hypercholesterolemics (P < 0.02, resp.), but there was no effect of HDL2 in clotting blood from persons with moderate hypercholesterolemia. All HDL3 fractions tested inhibited the TXA2 formation in all types of blood used for clotting (P < 0.02, resp.), probably due to their great cholesterol accepting capacity.
引用
收藏
页码:475 / 479
页数:5
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