Jl. Unthank et al., WALL REMODELING DURING LUMINAL EXPANSION OF MESENTERIC ARTERIAL COLLATERALS IN THE RAT, Circulation research, 79(5), 1996, pp. 1015-1023
Wall remodeling associated with rapid luminal enlargement of collatera
l mesenteric arteries in rats was investigated 1 and 4 weeks after cre
ation of a collateral pathway by ligating three to four sequential art
eries. Paired observations were made of inner diameters of collateral
and normal arteries in the same animals, Arterial blood flow was measu
red at the final observation. Sections of arteries were processed for
morphological measurements. After 4 weeks, inner arterial diameter was
increased more at the beginning (63 +/- 6%) than the end (25 +/- 9%)
of the collateral pathway. At 1 and 4 weeks, respectively, cross-secti
onal areas of collateral relative to normal arteries were increased by
46 +/- 5% and 59 +/- 13% (lumen), 55 +/- 8% and 65 +/- 4% (media), an
d 89 +/- 18% and 60 +/- 31% (intima). The wall expansion during lumina
l enlargement resulted in a normal medial thickness:luminal radius rel
ationship. At 1 week postligation, wall shear rate remained elevated a
nd endothelial but not smooth muscle hyperplasia had occurred (intimal
nuclei: 40 +/- 1.7 collateral versus 24 +/- 3.0 normal; medial nuclei
: 42 +/- 6.8 collateral versus 37 +/- 2.1 normal). At 4 weeks, wall sh
ear rate in collaterals was similar to normal arteries, and smooth mus
cle hyperplasia had taken place (medial nuclei: 84 +/- 9.4 collateral
versus 44 +/- 4.7 normal). The data demonstrate that wall expansion as
sociated with rapid luminal enlargement of these collaterals involves
hyperplasia of both endothelial and smooth muscle cells; however, smoo
th muscle proliferation does not occur until after wall shear rate is
reduced. The specific cellular adaptations that occur during collatera
l development may depend on the level of wall shear and shear-dependen
t modulation of endothelial growth factors.