Arterial expansive remodeling induced by high flow rates.
Driss, Ahmed Ben, Jo[diaeresis]elle Benessiano, Pierre Poitevin,
Bernard I. Levy, and Jean-Baptiste Michel.
Unit 141 INSERM, H[circumflex]opital Lariboisi[grave]ere, 41, Bd de
la Chapelle, 75010 Paris and Unit 367 INSERM, 17 rue du Fer-[grave]a
-Moulin, 75005 Paris, France
APStracts 3:0409H, 1996.
The effects of chronic increase in aortic blood flow on arterial wall
remodeling were investigated in vivo using an aorto-caval fistula
(ACF) model in rats. Phasic hemodynamics and aortic wall structure
upstream and downstream of the ACF of 30 male Wistar rats with ACF
and 30 sham-operated rats were compared immediately (D0) and 2 months
(D60) after opening the ACF in anesthetized rats. Upstream of the
ACF, opening the fistula acutely decreased aortic pressure (-30%,
p<0.001), increased blood velocity (X12, p<0.001),
blood flow (X9, p<0.001), wall shear stress (X10,
p<0.001) and cGMP wall content (+50%, p<0.01). At D60,
pressure was decreased (-22%, p<0.001), blood velocity, aortic
diameter and blood flow increased (+114%, p<0.001, +60%,
p<0.001, and +250%, p<0.001) as compared to the control
group; shear stress and cGMP dropped over time and tended to recover
control values; aortic wall tensile stress was higher than in the
control group (p<0.05). Medial cross sectional area, elastin
and collagen contents were increased (+38%, p<0.01, +50%,
p<0.01 and +30%, p<0.05) and associated with smooth
muscle cell hypertrophy (+23%, p<0.05), despite a decrease in
arterial wall thickness (-13%, p<0.01). Downstream of the ACF,
opening the fistula acutely decreased aortic pressure (-30%,
p<0.001) without any change in aortic blood velocity,
diameter, blood flow, shear stress and cGMP wall content. At D60,
pressure, blood velocity, shear stress and cGMP wall content were
decreased (-22%, p<0.001, -31%, p<0.01, -46%,
p<0.02 and -50%, p<0.05), diameter and blood flow were
unchanged; smooth muscle cell hypertrophy and hypoplasia were the
only observed changes in the aortic wall structure. These results
suggest that both shear and tensile stresses are involved in the
aortic wall remodeling. Increase in shear stress likely induces
expansive remodeling, in relation with flow dependent vasodilation
whereas increase in tensile stress is responsible for medial
hypertrophy and fibrosis.
Received 30 January 1996; accepted in final form 5 September
1996.
APS Manuscript Number H90-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 7 October 1996