Cited 14 times since 1994 (0.5 per year) source: EuropePMC Journal of vascular research, Volume 31, Issue 3, 1 1 1994, Pages 153-162 In the normal rabbit femoral artery increasing arterial wall injury does not lead to increased intimal hyperplasia. van Erven L, Post MJ, Velema E, Borst C
Angioplasty inflicts damage to the arterial wall. We studied whether augmented medial smooth muscle cell necrosis leads to augmented intimal hyperplasia and thus aggravates restenosis. Sixty-three normal femoral arteries of New Zealand White rabbits were overstretched with an angioplasty balloon during either maximal vasoconstriction with phenylephrine (32 arteries) or maximal vasodilation with nitroprusside (31 arteries). After 3 days' survival, medial necrosis was determined as percentage of cross-sectional medial area. In the 3 weeks' survival group, intimal hyperplasia was quantified as its average thickness. The dilation ratios, i.e. balloon diameter divided by arterial diameter at the time of dilation, were significantly higher in the 3 days' and 3 weeks' vasoconstriction groups (VC groups), respectively: 1.96 +/- 0.10 (mean +/- SD) and 2.14 +/- 0.08 in the VC groups versus 1.27 +/- 0.03 and 1.32 +/- 0.05, respectively, in the vasodilation groups (VD groups) (both p < 0.001). Medial necrosis was more extensive in the VC group (64 +/- 5%) than in the VD group (23 +/- 7%, p < 0.001) and proportional to the dilation ratio (r = 0.69, p < 0.01). Intimal hyperplasia, however, was equal in the VC (59 +/- 8 microns) and VD (57 +/- 6 microns, NS) groups and not dependent on dilation ratio (r = 0.10). Thus, extensive medial necrosis produced during balloon dilation in maximally vasoconstricted arteries did not lead to more intimal hyperplasia than when less medial necrosis was induced by balloon dilation during vasodilation.
