© 1998 American Heart Association, Inc.
Original Contributions |
Direct Assessment of Lipoprotein Outflow From In Vivo–Labeled Arterial Tissue as Determined in an In Vitro Perfusion System
From the Wallenberg Laboratory for Cardiovascular Research, University of Göteborg, Göteborg, Sweden.
Correspondence to Dr Tom Björnheden, The Wallenberg Laboratory for Cardiovascular Research, Sahlgrenska University Hospital, S 413 45 Gothenburg, Sweden. E-mail tom.bjornheden{at}wlab.wall.gu.se
Abstract—The rate of
cholesterol deposition during the atherosclerotic process
is determined by the balance between the inflow and outflow of plasma
lipoproteins in the arterial wall. Whereas the rate of
inflow may be measured directly, the rate of outflow has most often
been calculated indirectly from lipoprotein uptake by using the
2-compartment model. One objection against such calculations is that
lipoprotein binding is not being considered. In the present
study 2 different protocols were used to obtain a direct measure of the
outflow of lipoproteins from atherosclerotic rabbit aortas. Thus, 3
rabbits with experimental atherosclerosis were
given 125I-LDL intravenously and 3 were given
[14C]cholesterol perorally. Twenty-four hours
later the aortas were removed and the outflow of label was monitored
during in vitro perfusion. Despite the different protocols, our results
were consistent and indicated that fractional loss relative to
whole tissue was 
0.01 pool/h, which is 1 order of magnitude lower
than current estimates based on the 2-compartment model (0.04 to 0.4
pool/h). Furthermore, whereas as much as 2/3 to 3/4 of
the tracer that had entered the arterial wall was
effectively trapped, the remainder equilibrated at a faster rate (0.06
pool/h). In conclusion, it seems that tissue binding constitutes a
prominent and possibly underrated mechanism of lipoprotein deposition,
at least in the atherosclerotic rabbit aorta. Furthermore, this means
that current estimates of lipoprotein exchange parameters
based on the 2-compartment model (eg, fractional loss) may rest on
invalid assumptions and should be regarded with caution.
Key Words: arterial wall • atherosclerosis • lipoprotein outflow
This article has been cited by other articles:
 |
|
 |
|
  S. D. Proctor and J. C.L. Mamo Intimal Retention of Cholesterol Derived From Apolipoprotein B100- and Apolipoprotein B48-Containing Lipoproteins in Carotid Arteries of Watanabe Heritable Hyperlipidemic Rabbits Arterioscler. Thromb. Vasc. Biol., September 1, 2003; 23(9): 1595 - 1600. [Abstract] [Full Text] [PDF]
|
|