Τόμος 9 (1991) – Τεύχος 1 – Άρθρο 2 – Επιθεώρηση Κλινικής Φαρμακολογίας και Φαρμακοκινητικής-Ελληνική Έκδοση – Volume 9 (1991) – Issue 1 – Article 2 – Epitheorese Klinikes Farmakologias και Farmakokinetikes-Greek Edition

9: 5-14 (1991)

PHARMAKON-Press: Epitheorese Klin. Farmakol. Farmakokinet.

9: 5-14 (1991)

HDL-lipoproteins, HDL₂-lipoproteins, thrombogenesis

HDL lipoproteins are produced partially by direct secretion from liver and small intestine and partially during the metabolism of triglyceride – rich lipoproteins, derived from the same organs. Their most useful fraction regarding the protection from atherosclerosis is the HDL₂. Since several constituents of HDL₂ are necessary for the metabolism of the triglyceride-rich lipoproteins (chylomicrons and VLDL) the latter, when entering the blood circulation, detach them from the HDL_2. The resulting HDL₃ are functionally compromised. After the chylomicrons and VLDL are delipi­dized enough, so that to become intermediate density lipoproteins, these constituents return to HDL fraction and HDL₂ are reformed. The main role of HDL, subserved mainly by HDL₂, is the retrograde cholesterol-transport from the tissues to the liver for excretion. Lowering the plasma levels of ΗDL₂ not only attenuates this function, but also is the consequence of the rise in plasma levels of the atherogenetic triglyceride – rich lipoproteins; therefore the unfavourable effect of the latter lipoproteins is the result of both factors: their atherogenicity and the loss of the protection exerted by HDL₂. On the other hand, HDL₂ contribute in the attenuation of the high vascular tone and the high responsiveness of the platelets. In contrast, the atherogenic triglyceride – and cholesterol – rich lipoproteins induce blood hypercoagulabi­lity, increased thrombophilic diathesis and a rise in the vascular tone favouring vasospastic reactions.

1. Anderson, D.W.: HDL cholesterol: The variable compo­nents. Lancet 1: 819 (1978)
2. G.J. Nelson (ed.): Blood Lipids and Lipoproteins. p. 300, Krieger, New York, 1979
3. Miller, J.E., Hammett, F., Saltissi, S. et al.: Relation of angiographically defined coronary artery disease tο pla­sma lipoprotein subfractions and apolipoproteins
4. Small, D.M.: HDL System: A short review of structure and metabolism. In: Atherosclerosis Reviews (A. Cata­pano, et al., eds), Vol. 16, p. 1, Raven Press, New York, 1987
5. Παπαδόπουλος, K.: Φυσιοπαθολογία των υπερλιποπρω­τεϊναιμιών. Επιστ. Επετ. lατρ. Σχ. ΑΠΘ 13/1: 585 (1980)