Arteriosclerosis, Vol 7, 367-377, Copyright © 1987 by American Heart Association
ARTICLES |
DC Schwenke and DB Zilversmit
Arterial injury exacerbates experimental atherogenesis. This report evaluates cholesteryl ester influx and loss during the first 5 days after arterial injury. Selected areas of aortas from rabbits made hypercholesterolemic by 12 to 16 days of cholesterol feeding were injured with a balloon catheter. This allowed measurements and a relatively precise comparison of cholesterol and cholesteryl ester influx into the uninjured and injured arterial wall within the same animal. The animals received oral doses of 3H- or 14C-cholesterol either just before injury or 1 day later. Most animals were given the other isotope of cholesterol 1 day before sacrifice, which took place 2 to 5 days after injury. Measurement of accumulated labelled esterified cholesterol within the same animal during two different time periods allowed the estimation of total influx and fractional loss of entered esterified cholesterol within the artery. Between 2 and 5 days after injury, total influx into areas of injured artery averaged 30 to 60 times the total influx into the adjacent uninjured areas. By the fifth day after injury, the esterified cholesterol content was about 10 times greater in injured areas than in adjacent, uninjured areas. The nonesterified cholesterol content of injured areas was about 70% greater than that of adjacent noninjured areas. Total influx and fractional loss of arterial cholesteryl ester calculated from radioactivity data could account for 117 +/- 6 (mean +/- SEM) percent of the cholesteryl ester mass that accumulated during the interval from injury to sacrifice. The total influx rates and daily increments in cholesteryl ester content of injured areas were positively related.
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