Angioplasty reduces pharmacologically mediated vasoconstriction in rabbit carotid arteries with and without vasospasm.
OBJECTIVE
We tested the hypothesis that vasospastic arteries do not reconstrict after angioplasty because angioplasty decreases smooth muscle contractility.


METHODS
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.


RESULTS
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.


CONCLUSIONS
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.
Macdonald
R L
RL
Department of Surgery, University of Chicago, IL, USA.
Zhang
J
J
Han
H
H
D000109:Acetylcholine / Q000494:pharmacology; D000704:Analysis of Variance; D017130:Angioplasty; D000818:Animals; D002339:Carotid Arteries / Q000187:drug effects / Q000502:physiology* / Q000503:physiopathology*; D066298:In Vitro Techniques; D002546:Ischemic Attack, Transient / Q000503:physiopathology*; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology / Q000503:physiopathology; D009529:Nicardipine / Q000494:pharmacology; D010208:Papaverine / Q000494:pharmacology; D011188:Potassium / Q000494:pharmacology; D011817:Rabbits; D012701:Serotonin / Q000494:pharmacology; D013997:Time Factors; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology*
D012701:Serotonin; D009529:Nicardipine; D010208:Papaverine; D000109:Acetylcholine; D011188:Potassium