Acetylated low-density lipoproteins promote the release and metabolism of arachidonic acid by murine macrophages.

We studied the effect of acetyl-LDL on the synthesis of eicosanoids by primary cultures of mouse-resident peritoneal macrophages. A dosis of 150 micrograms of acetyl-LDL proteins promotes a maximal release of arachidonic acid metabolites into extracellular medium. This process is very rapid and reaches the maximal value about ten minutes after stimulation. The pattern of arachidonic acid metabolites released is different from that obtained when the cells are stimulated with a phagocytosable particle like zymosan or calcium ionophore A23187. The data show that the metabolism of arachidonic acid by cycloxigenase is diminished. In an unusual way the amounts of prostaglandin PGE2, 6-keto-prostaglandin PGF1 alpha and thromboxane TXB2 synthesized are similar.

[Lipoprotein Lp(a): a risk factor for atherosclerosis]. / Lipoproteína Lp(a): factor de riesgo para la aterosclerosis.

To evaluate whether lipoprotein Lp(a) favors the development of coronary atherosclerosis and may be considered as a risk factor for acute myocardial infarction, we studied 185 patients with this conditions who where compared with a control group. Total cholesterol and cholesterol bound to the several lipoprotein fractions were simultaneously evaluated. Comparisons were carried out, the subjects being subdivided into age groups of 40-49, 50-59 and more than 60 years; they were also subdivided depending on the level of Lp(a) cholesterol (lower than 25 mg/dl, between 25 and 50 mg/dl and higher than 50 mg/dl). Lp(a) appeared as indicative of a vascular risk in the younger groups. The incidence of myocardial infarction was higher when Lp(a) level was greater than 50 mg/dl.