Pathological effects of angioplasty on vasospastic carotid arteries in a rabbit model

Abstract

To define the pathological effects of angioplasty on vasospastic arteries, 36 rabbits underwent angiography and induction of vasospasm by placement of blood-filled (vasospasm groups) or empty (control group) silastic sheaths around the cervical carotid arteries. Two (Day 2) or 7 days (Day 7) later, angiography was repeated and one carotid artery in each animal was dilated by balloon angioplasty. The rabbits were sacrificed 1 day, 7 days, or 3 to 4 weeks after angioplasty. Significant vasospasm developed after placement of silastic sheaths with blood (mean reductions in diameter 39% +/- 6% at Day 2 and 48% +/- 5% at Day 7). Arterial narrowing was less apparent in the control groups at Day 2 (24% +/- 7%). Angioplasty performed on Day 2 significantly increased arterial diameters of vasospastic arteries (50% +/- 7%; p < 0.05) but not those of control arteries (10% +/- 6%, p > 0.05). Angioplasty performed on Day 7 increased the arterial diameters by a similar degree (47% +/- 13%, not significant). Arteries remained dilated after angioplasty, although there was significant vasospasm 7 days after angioplasty when angioplasty was performed on Day 2. Blinded, semiquantitative histopathological study of the arteries showed that 3 to 4 weeks after angioplasty, there was significant endothelial proliferation and a trend for thinning of the tunica media. There were no significant changes in control arteries subjected to angioplasty. Angioplasty was not associated with significant arterial fibrosis as measured by hydroxyproline content (analysis of variance). The increase in endothelial proliferation and decrease in the thickness of the tunica media suggest that, in the rabbit model, angioplasty damages endothelial and smooth-muscle cells. This may be the basis for the observation that vasospastic arteries do not reconstrict after angioplasty.

Use of the Cascade expandable net to treat cerebral vasospasm – initial clinical experience from a single centre with in vitro benchside tests

“…Upon reaching this threshold there would be relaxation of the vessel, due to changes in the contractile properties of the smooth muscle cells, but no disruption of the extracellular matrix. Numerous in vivo studies had demonstrated that damage to the extracellular matrix was not required for successful treatment of cerebral angioplasty (Yamamoto et al, 1992 ; Macdonald et al, 1995 ; Kobayashi et al, 1993 ). The concept of a dilatation threshold built upon the earlier work of Fischell who documented ‘arterial paralysis’ occurring post balloon angioplasty in both relaxed and contracted arteries, that these vessels failed to respond to the topical application of vasoconstricting agents, and that the same degree of balloon dilatation in relaxed vessels resulted in significantly less, if any, arterial paralysis compared to contracted vessels.…”

<em>In Vivo</em> Gene Transfer to the Rabbit Common Carotid Artery Endothelium

“…For example, baseline hematological values, hemostatic regulation, and vascular longitudinal tension are similar between rabbits and humans 8 . Rabbit models of vascular diseases replicate key features of many human diseases including: aneurysms (similar geometric and flow characteristics) 9 , vasospasm (similar response to endovascular treatment) 10,11 , and atherosclerosis (intimal plaques with similar features including a core rich in lipid, macrophages, and smooth muscle cells in a fibrous cap) 12,13 . Accordingly, rabbit models have been developed for many vascular diseases such as thrombosis, vasospasm, aneurysm, diabetes, vascular graft stenosis, and atherosclerosis 8,13,14,15,16 .…”