Effects of stenting on adjacent vascular distensibility and neointima formation: Role of nitric oxide

Intravascular stents increase long-term patency but their effects on the vascular mechanics of adjacent segments have not been studied. In this study, stents were deployed in the rabbit abdominal aorta after 1 week of normal diet, 1% cholesterol diet or 1% cholesterol diet with L-nitro arginine (L-NA 60 mg/l water). Intravascular ultrasound showed a small distal decrease in vessel distensibility (area/pressure * 100) before stenting. Distensibility was almost abolished by stenting (0.12 ± 0.01, p < 0.001), but was increased proximal to the stent and decreased distal to the stent both acutely (proximal: 1.18 ± 0.10 vs distal: 0.65 ± 0.06, p < 0.001), and at 4 weeks (proximal: 1.05 ± 0.08 vs distal: 0.37 ± 0.07, p < 0.001). Nitric oxide (NO) activity was enhanced proximal to and within the stent, and remained constant distal to the stent, (versus control, proximal: 57 ± 23%, stent: 136 ± 35%, distal: 2 ± 12%, p < 0.01). The I/M ratio was significantly higher proximal to and within the stent than in the distal segment (proximal: 0.40 ± 0.10, stent: 0.37 ± 0.12, distal: 0.12 ± 0.11, p < 0.01). NO blockade with L-NA prevented hyperdistensibility proximally, and significantly increased the I/M ratio within the stent and distally (stent: 0.81 ± 0.19, distal: 0.30 ± 0.10, p < 0.05) but not proximally (0.38 ± 0.09). In conclusion, aortic stenting increases proximal vascular distensibility and intimal lesion formation. Nitric oxide blockade augments intimal growth within but not proximal to the stent.