The mechanisms following intimal injury predisposing towards atherosclerotic changes have not been fully elucidated. We speculated that a local increase in the enzyme lipoprotein lipase (LPL) might explain a higher susceptibility of the damaged intima to lipid accretion, and so we investigated the effect of balloon endothelial denudation on LPL activity and cholesterol content (LPL(a) and Chol(c), respectively), in aortas from normolipidemic male New Zealand white rabbits. Arteries were 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 increased 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 normolipidemic rabbit model. We conclude that physical damage to the intima markedly and soon increases LPL(a). This finding might account for the higher lipid accumulation by injured vessels, providing additional support to the hypothesis of LPL as an atherogenic mediator.
- Animal model
- Intimal proliferation
- Lipoprotein lipase
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine