Macdonald R L, Zhang J, Han H
Department of Surgery, University of Chicago, IL, USA.
Stroke. 1995 Jun;26(6):1053-9; discussion 1059-60. doi: 10.1161/01.str.26.6.1053.
We tested the hypothesis that vasospastic arteries do not reconstrict after angioplasty because angioplasty decreases smooth muscle contractility.
Twenty-four rabbits had carotid angiography and placement of silicone elastomer sheaths around both carotid arteries in the neck. Sheaths were empty (control groups) or filled with clotted blood (vasospasm groups). Angiography was repeated 2 days later, and one carotid artery was dilated with a balloon catheter. Animals were killed 1, 5, or 28 days after angioplasty, and the carotid arteries were studied pharmacologically under isometric tension.
Before angioplasty, there was significant vasospasm in the vasospasm groups but not in the control groups (P < .05, ANOVA). Angioplasty produced significant, long-lasting dilation of arteries in the vasospasm groups. One and 5 days after angioplasty, arteries from control and vasospasm groups that had angioplasty had significantly reduced contractions to serotonin, KCl, and caffeine compared with arteries not subjected to angioplasty. Twenty-eight days after angioplasty, contractions were reduced in arteries subjected to vasospasm compared with controls, but there were no differences between arteries with or without angioplasty. At all times after angioplasty, vasospasm significantly decreased acetylcholine-induced relaxations of arteries contracted with serotonin. Relaxations were further decreased by angioplasty in the vasospasm group 1 day after angioplasty. Arterial wall compliance was significantly decreased in the vasospasm and control groups at all times after angioplasty, although there were no significant differences between arteries with and without angioplasty.
These results suggest that arteries do not reconstrict after angioplasty because angioplasty decreases smooth muscle contractility. There was no evidence that angioplasty disrupted the arterial wall matrix, as judged by the lack of increase in arterial wall compliance after angioplasty.
我们验证了以下假设,即血管成形术后血管痉挛性动脉不会再收缩,因为血管成形术会降低平滑肌收缩力。
24只兔子接受了颈动脉血管造影,并在颈部双侧颈动脉周围放置了硅橡胶弹性体鞘管。鞘管为空(对照组)或充满凝血块(血管痉挛组)。2天后重复血管造影,并用球囊导管扩张一侧颈动脉。血管成形术后1、5或28天处死动物,在等长张力下对颈动脉进行药理学研究。
血管成形术前,血管痉挛组存在明显的血管痉挛,而对照组无(方差分析,P<0.05)。血管成形术使血管痉挛组的动脉产生了显著且持久的扩张。血管成形术后1天和5天,接受血管成形术的对照组和血管痉挛组的动脉与未接受血管成形术的动脉相比,对血清素、氯化钾和咖啡因的收缩反应明显降低。血管成形术后28天,与对照组相比,血管痉挛组的动脉收缩反应降低,但接受或未接受血管成形术的动脉之间无差异。血管成形术后的所有时间点,血管痉挛均显著降低了乙酰胆碱诱导的由血清素收缩的动脉的舒张反应。血管成形术后1天,血管痉挛组的血管成形术进一步降低了舒张反应。血管成形术后,血管痉挛组和对照组的动脉壁顺应性在所有时间点均显著降低,尽管接受和未接受血管成形术的动脉之间无显著差异。
这些结果表明,血管成形术后动脉不会再收缩,因为血管成形术降低了平滑肌收缩力。没有证据表明血管成形术破坏了动脉壁基质,血管成形术后动脉壁顺应性未增加即证明了这一点。