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Research Article Free access | 10.1172/JCI118824
Department of Clinical Biochemistry, Rigshospitalet, Copenhagen, Denmark.
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Department of Clinical Biochemistry, Rigshospitalet, Copenhagen, Denmark.
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Department of Clinical Biochemistry, Rigshospitalet, Copenhagen, Denmark.
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Department of Clinical Biochemistry, Rigshospitalet, Copenhagen, Denmark.
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Published July 15, 1996 - More info
The aim was to investigate the atherogenic potential of lipoprotein(a) (Lp(a)) and to further our understanding of the atherogenic process by measuring rates of transfer into the intima-inner media (i.e., intimal clearance) and rates of loss from the intima-inner media (i.e., fractional loss) of Lp(a) and LDL using cholesterol-fed rabbits with nonlesioned (n = 13) or atherosclerotic aortas (n = 12). In each rabbit, 131I-Lp(a) (or 131I-LDL) was injected intravenously 26 h before and 125I-Lp(a) (or 125I-LDL) 3 h before the aorta was removed and divided into six consecutive segments of similar size. The intimal clearance of Lp(a) and LDL was similar and markedly increased in atherosclerotic compared with nonlesioned aortas (ANOVA, effect of atherosclerosis: P < 0.0001). Fractional losses of labeled Lp(a) and labeled LDL in atherosclerotic aorta were on average 25 and 43%, respectively, of that in nonlesioned aortas (ANOVA, effect of atherosclerosis: P < 0.0001). Fractional loss of Lp(a) was 73% of that of LDL (ANOVA, effect of type of lipoprotein: P = 0.07). These data suggest that the development of atherosclerosis is associated with increased influx as well as decreased fractional loss of Lp(a) and LDL from the intima. Accordingly, Lp(a) may share with LDL the potential for causing atherosclerosis.