Balance of prostacyclin and thromboxane in offspring of parents with premature coronary arterial disease.

6-keto-prostaglandin F1a and thromboxane B2 were determined in order to obtain more information about the prostacyclin synthesis and thromboxane A2 release in 3- to 18-year-old healthy children and in offspring of parents who have had an acute myocardial infarction before the age of 45. The authors demonstrated a reduction of plasma prostacyclin synthesis in children with a positive family history of premature coronary arterial disease. Thromboxane levels in the affected adolescent boys were significantly lower compared with the controls. The ratio of thromboxane:prostacyclin in endangered children did not show a significant difference from that of healthy controls. These data indicate that prostaglandins are a definitive marker for identifying cardiovascular risk children. It must be supposed that in adolescence, only in boys, with a positive family history of premature coronary arterial disease, a compensatory mechanism exists to protect them from developing an imbalance in the regulation of prostaglandins.

Inhibition of ACAT activity after 7-oxo-PGI2 treatment in cholesterol-fed rabbits.

It has been supposed that prostacyclin (PGI2) and its analogues have important antiatherogenic effects. The aim of this work was to test the effect of PGI2 and 7-oxo-PGI2- (a stable analogue of PGI2) (6) treatment on the acyl CoA: cholesterol-acyltransferase (ACAT) activity in the aortic wall of rabbits. The rabbits had been previously fed with cholesterol and treated with PGI2 and 7-oxo-PGI2 intravenously. Cholesterol feeding increased ACAT activity compared to the control group which was not fed with cholesterol: 16.84 nmol/mg prot./h and 10.03 nmol/mg prot./h, respectively. PGI2 treatment of the cholesterol fed group did not cause a significant decrease, while 7-oxo-PGI2 treatment significantly decreased aortic ACAT activity compared to the cholesterol-fed control group; 14.31 nmol/mg prot./h; 11.53 nmol/mg prot./h and 16.84 nmol/mg prot./h, respectively. The decrease found in the ACAT activity after PGI2 and 7-oxo-PGI2 treatment are new data for the protective effect of these agents against atherosclerosis.

[Plasma prostacyclin and thromboxane concentration in healthy children and in offspring of parents suffering from myocardial infarct]. / Plazma prosztaciklin és tromboxán koncentráció egészséges gyermekeken és fiatalkori myocardialis infarctusban megbetegedett szülök utódaiban.

6-keto-prostaglandin F1a and thromboxane B2 were determined by radioimmunoassay in 135 healthy children, as a control group, and in 125 offsprings of parents suffering from premature coronary artery disease. Plasma prostacyclin concentration had decreased in children with a positive family history of coronary artery disease. It was demonstrated a strong reduction of thromboxane level in boys from age 11 in endangered group while the thromboxane/prostacyclin ratio did not differ from the control. It was supposed that in adolescent sons of parents who have had an acute myocardial infarction before the age of 45, a compensatory mechanism exists to protect them from disturbances in regulation of the balance between prostacyclin and thromboxane.

Prostacyclin and thromboxane levels of children of parents suffering from early ischemic heart disease.

Offsprings of parents who had acute myocardial infarction before age of 45 years were investigated. The aim of this examination was to obtain information whether the variation in the balance of prostacyclin/thromboxane ratio is a common cardiovascular risk factor in children. In children whose parents have had early myocardial infarction, a significant decrease was shown in 6-keto-prostaglandin F1 alpha level while the thromboxane B2/6-keto-prostaglandin F1 alpha ratio increased in these children. Plasma tromboxane B2 levels hardly differed from those of the control in that group of children whose one parent and at least one of the grandparents or uncles or aunts suffered from coronary heart disease. Plasma thromboxane concentration was lower in another group of children whose "only" one parent had myocardial infarction. It may be supposed that this is a compensatory mechanism in the offspring of parents suffering from early coronary heart disease.