The mechanisms following intimal injury predisposing towards atheroscl
erotic changes have not been fully elucidated. We speculated that a lo
cal increase in the enzyme lipoprotein lipase (LPL) might explain a hi
gher susceptibility of the damaged intima to lipid accretion, and so w
e investigated the effect of balloon endothelial denudation on LPL act
ivity and cholesterol content (LPL(a) and Chol(c), respectively), in a
ortas from normolipidemic male New Zealand white rabbits. Arteries wer
e obtained from injured and control animals after 2, 6, 8 and 10 weeks
to evaluate the shortest period after de-endothelialization necessary
to detect LPL(a) changes. Injury resulted in a 4-fold LPL(a) rise (P
< 0.01), as early as 2 weeks, and the enzymatic activity remained incr
eased throughout the study period. A mild but significant 22% Chol(c)
increase (P < 0.03) was found after 2 weeks of injury, even in this no
rmolipidemic rabbit model. We conclude that physical damage to the int
ima markedly and soon increases LPL(a). This finding might account for
the higher lipid accumulation by injured vessels, providing additiona
l support to the hypothesis of LPL as an atherogenic mediator.