Macdonald R L, Wallace M C, Montanera W J, Glen J A
Department of Surgery, University of Chicago, Illinois, USA.
J Neurosurg. 1995 Jul;83(1):111-7. doi: 10.3171/jns.1995.83.1.0111.
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.
为明确血管成形术对血管痉挛动脉的病理影响,36只兔子接受了血管造影,并通过在颈总动脉周围放置充满血液的(血管痉挛组)或空的(对照组)硅橡胶鞘来诱导血管痉挛。2天(第2天)或7天(第7天)后,重复血管造影,每只动物的一条颈动脉通过球囊血管成形术进行扩张。血管成形术后1天、7天或3至4周处死兔子。放置充满血液的硅橡胶鞘后出现明显的血管痉挛(第2天直径平均减少39%±6%,第7天减少48%±5%)。对照组在第2天动脉狭窄不太明显(24%±7%)。第2天进行的血管成形术显著增加了血管痉挛动脉的直径(50%±7%;p<0.05),但对对照动脉直径无显著影响(10%±6%,p>0.05)。第7天进行的血管成形术使动脉直径增加了相似程度(47%±13%,无显著性差异)。血管成形术后动脉仍保持扩张,尽管在第2天进行血管成形术时,血管成形术后7天仍有明显的血管痉挛。对动脉进行的盲法半定量组织病理学研究表明,血管成形术后3至4周,有明显的内皮细胞增殖,且中膜有变薄趋势。接受血管成形术但未发生血管痉挛的对照动脉无显著变化。通过羟脯氨酸含量测定(方差分析),血管成形术与显著的动脉纤维化无关。内皮细胞增殖增加和中膜厚度减小表明,在兔模型中,血管成形术损害了内皮细胞和平滑肌细胞。这可能是血管痉挛动脉在血管成形术后不再发生再收缩这一观察结果的基础。