Table 3.
NO-releasing materials for the inhibition of neointimal hyperplasia.
| Authors | Ref. | Animal model | Application | NO source | Delivery system | NO detection method | NO release or flux | Time point in vivo | I/M ratio decrease |
|---|---|---|---|---|---|---|---|---|---|
| Kaul et al. | [122] | Rat | Periadventitially in balloon-injured ileofemoral arteries | SPER/NO | Atrigel | Chemiluminescence | Peak at 4.5 μmol (40 min) 95% released (150 min) | 14 d | ~75% |
| Pearce et al. | [123] | Rat | Perivascularly in balloon-injured carotid arteries | PAN/NO PROLI/NO | Poloxamer | N/A | N/A | 14 d | 86% (PROLI/NO powder) |
| Kapadia et al. | [126] | Rat | Perivascularly in balloon-injured carotid arteries | PROLI/NO DPTA/NO | Peptide amphiphile and heparin (nanofiber gels) | Griess | Peak at 0.6 μmol day−1 and 1.2 μmol day−1, respectively (2 d) | 14 d | 77% and 45%, respectively |
| Lipke et al. | [37] | Rat | Periadventitially in balloon-injured carotid arteries | Cys/NO | PEG | Griess (HEPES buffer) | 35% released (4 h)[127] | 14 d | 77% compared to control hydrogel |
| Serrano et al. | [39] | Rat | Perivascularly balloon-injured carotid arteries | diamine diol/N2O2 | POC, PDDC | Griess | Peak flux 35.4 · 10−9 mol cm−2 min−1 (4 h) and 6.6 · 10−9 mol cm−2 min−1 (24 h), respectively | 14 d | 38% |
| Do et al. | [129] | Rabbit | Microsphere-loaded stent deployed in infrarenal abdominal aorta | NOC-12/N2O2 | PLGA and PEG (microspheres) | Griess | ~18 mM (1 week) | 7 d & 28 d | 46% and 32%, respectively, compared to control microspheres |
| ~8 mm (4 weeks) | |||||||||
| Yoon et al. | [130] | Porcine | Coated stent deployed in coronary arteries | SNP | PU | Famotidine assay to measure SNP (no specified temp) | 85% of total SNP mass eluted from stents (30 d) | 28 d | No improvement |
| Buergler et al. | [131] | Porcine | Coated stent deployed in left anterior descending and right coronary arteries | DETA/NO | Polycaprolactone | Chemiluminescence (flushed with He, no specified temp and buffer) | 9.0 · 10−5 μmol min−1 mg−1 (0 h) and 0.5 · 10−5 μmol min−1 mg−1 (72 h) | 28 d | No improvement |
| Abbasi et al. | [132] | Rabbit | Perivascularly in aortic intimal injured hyper-cholesterolemic rabbits | DETA/NO | Silastic elastomer | N/A | N/A | 6 wks | No improvement |
Note: Time points for NO release or flux are the same as the in vivo time points unless otherwise specified. NO detection was conducted at 37 °C in PBS. I/M ratio decrease is compared to injury alone unless otherwise specified.
Cys/NO: S-nitrosocysteine, DETA/NO: diazeniumdiolated diethylenetriamine, DPTA/NO: 1-[N-(3-aminopropyl)-N-(3-ammoniopropyl] diazen-1-ium-1,2-diolate, I/M: Intima/media, NOC-12/N2O2: diazeniumdiolated N-ethyl-2-(1-ethyl-2-hydroxy-2-nitrosohydrazino)ethanamine, PAN/NO: diazeniumdiolated poly(acrylonitrile), PDDC: poly(1,12-dodecanediol-co-citrate), PEG: poly(ethylene glycol), PLGA: poly(lactic-co-glycolic acid), POC: poly(1,8-octanediol-co-citrate), PROLI/NO: 1-[2-(carboxylato)pyrrolidin-1-yl]diazen-1-ium-1,2-diolate, PU: polyurethane, SNP: sodium nitroprusside, SPER/NO: diazeniumdiolated spermine.