Immediate and long-term effects of angioplasty-balloon dilation on normal rabbit iliac artery.

Abstract

The present study was performed to determine the immediate (hours) and long-term (28-day) effects of angioplasty-balloon dilatation on arterial wall diameter, histology, response to vasoconstrictors, and passive mechanics. Dilated left iliac arteries of New Zealand rabbits were compared to control, right iliac arteries. In the immediate studies, dilation increased arteriographic diameter by 32%, denuded the endothelium, stretched and may have lysed smooth muscle cells, decreased arterial wall thickness, and increased passive stress and incremental elastic modulus. The dilated arteries failed to contract to norepinephrine or potassium chloride. In contrast, 28 days after dilation, arteriographic diameter had returned to normal, an intimal thickening had formed, passive stress and the incremental elastic modulus had decreased to below normal, and the arteries contracted, but to only 53% to 67% of control. Angioplasty had no long-term effect on arterial sensitivity (EC50) to potassium chloride or serotonin but did produce a decreased sensitivity (6X) to norepinephrine. These studies demonstrate that the effects of dilatation of the normal artery are partially reversible, suggest that restenosis after angioplasty is more likely to be due to intimal proliferation than increased arterial stiffness, and suggest that vasospasm of arteries after long-term recovery from the dilation is more likely to be mediated by serotonin than by norepinephrine.

Balloon catheter injury to rabbit carotid artery. II. Selective increase in reactivity to some vasoconstrictor drugs.

“…In fact, the injured arteries showed a small increase in sensitivity to both serotonin and U46619, particularly at 6 weeks after endothelial denudation. These results are consistent with the study of Consigny et al, 21 who examined vascular reactivity of the rabbit iliac artery after injury with a balloon catheter. Immediately after injury, these researchers found that the arteries were unable to contract in response to either noradrenaline or KCI.…”

“…These changes in phenotype may be important in the observed changes in reactivity, since the maximum tension ( E^) developed to methoxamine increased significantly between 2 and 6 weeks and also the sensitivity of the experimental arteries to both serotonin and U46619 was highest at 6 weeks when the smooth muscle cells had a greater V v myo. In further support of this, Consigny et al 21 observed a sixfold decrease in arterial sensitivity to noradrenaline after balloon catheter injury and suggested that this may be the result of an altered phenotype of the smooth muscle cells.…”

Coronary artery vasoconstriction routinely occurs after percutaneous transluminal coronary angioplasty. A quantitative arteriographic analysis.

“…In an in vitro model of balloon angioplasty in rabbit aorta and pig carotid arteries, only severe degrees of arterial stretching (e.g., >60-70% beyond physiological relaxed diameter) produced significant impairment of arterial vasoconstrictor responsiveness. 13 In contrast to the findings of angioplasty-induced arterial paralysis cited above, there is evidence in both animal models" [1][2][3][4][5][6][7][8][9][10][11][12][13] that intravascular thrombus formation may occur despite full heparinization, it is unlikely that the loss of coronary artery diameter after PTCA was primarily the result of thrombus formation because no intraluminal filling defects were identified even in those cases in which orthogonal projections were analyzed. More importantly, nitroglycerin was very effective in both reversing and preventing the loss of diameter after PTCA, a finding that would not be expected if the luminal compromise were due primarily to thrombus.…”

Restenosis after coronary angioplasty. Potential biologic determinants and role of intimal hyperplasia.

“…A significant degree of intimal hyperplasia has been consistently observed to occur in normal arteries after balloon injury, but this intimal thickening is usually not associated with any significant decrease in luminal diameter. 60 Other factors must play a role in luminal reduction in atherosclerotic arteries after PTCA in addition to the initial severity of intimal proliferation.…”