Sge. Barker et al., THE ADVENTITIA AND ATHEROGENESIS - REMOVAL INITIATES INTIMAL PROLIFERATION IN THE RABBIT WHICH REGRESSES ON GENERATION OF A NEOADVENTITIA, Atherosclerosis, 105(2), 1994, pp. 131-144
Removal of the carotid artery adventitia from rabbits induced the form
ation of an intimal hyperplastic lesion. In rabbits fed a normal diet,
the lesion (measured as the intimal:medial ratio) was maximal by day
14 (0.456 +/- 0.079, n = 5, P < 0.01) and thereafter, regressed toward
s control dimensions (0.037 +/- 0.003, n = 14) by day 28 (0.080 +/- 0.
025, n = 7, P = 0.14). In rabbits fed a high cholesterol diet, the les
ion was again maximal by day 14 (0.376 +/- 0.056, n = 8, P < 0.01). Al
though some regression was seen, the lesion persisted to day 42 (0.272
+/- 0.052, n = 8, P < 0.01). Electron microscopy and immunocytochemis
try showed two types of lesion, (a) smooth muscle cell predominant on
normal diet and, (b) macrophage predominant on high cholesterol diet.
Smooth muscle cell predominant lesions underwent almost complete regre
ssion, whereas macrophage predominant lesions persisted. We propose th
at lesion formation may be initiated following the development of arte
rial wall hypoxia, secondary to excision of the adventitial vasa vasor
um. Furthermore, we have devised a novel method to restore a highly va
scular 'neoadventitia' to an artery whose adventitia has previously be
en removed, using loosely placed PVC tubing. We suggest this 'neoadven
titia' was able to inhibit the formation of an intimal hyperplastic le
sion and to promote regression of an already established lesion by res
toring arterial wall oxygenation.