Kipshidze N, Keelan M H, Petersen J R, Bachutashvili I, Vossoughi J, Karanian J, Ghosh C, Iversen P, Roubin G S, Leon M B, Moses J W
Lenox Hill Heart and Vascular Institute, New York, NY, USA.
Photochem Photobiol. 2000 Oct;72(4):579-82. doi: 10.1562/0031-8655(2000)072<0579:poviae>2.0.co;2.
Recently, intravascular low-power red laser light (LPRLL) therapy has been proposed for the prevention of postangioplasty restenosis due to the observed inhibition of experimental neointimal formation. The objective of this study was to determine the impact of endoluminal LPRLL on vascular levels of inducible nitric oxide synthase (iNOS) and cyclic guanosine monophosphate (cGMP) to help define the mechanism of this effect. Eight atherosclerotic male adult New Zealand White rabbits weighing 4-6 kg were used in these studies. The iliac arteries were treated in separate zones with: (1) balloon inflation only; (2) laser illumination only; and (3) balloon inflation + laser illumination. An uninjured zone of the iliac artery served as a control. Laser irradiation (630 nm) was delivered to the vessel wall via a Cold laser Illuminator (Cook, Inc., Bloomington, IN), with a 3 mm-diameter balloon. Experiments demonstrated that vascular cGMP levels obtained immediately following treatment in the balloon only group was the lowest (0.29 +/- 0.05 pmol/mg protein) and significantly lower compared with the uninjured controls (1.01 +/- 0.07 pmol/ mg protein) (P < 0.001). In the laser only treated group cGMP levels were significantly increased (2.87 +/- 0.12 pmol/mg protein) compared with the uninjured control (P < 0.001) and the balloon only group (P < 0.001). Vascular cGMP levels in the balloon + laser group (2.09 +/0.07 pmol/mg protein) was also increased compared to the balloon only (P < 0.001) and control (P < 0.001) groups. Qualitative analysis of Western blot demonstrated that laser illumination induces iNOS. In contrast balloon dilatation did not induce iNOS. Balloon + laser treatment, however, tended to restore the expression of iNOS. Our study demonstrated that intravascular low dose laser irradiation induces iNOS and elevates vascular cGMP in an in vivo atherosclerotic rabbit model.
最近，由于观察到血管内低功率红色激光（LPRLL）疗法对实验性新生内膜形成有抑制作用，故有人提出将其用于预防血管成形术后再狭窄。本研究的目的是确定腔内LPRLL对诱导型一氧化氮合酶（iNOS）和环磷酸鸟苷（cGMP）血管水平的影响，以帮助明确这种作用的机制。这些研究使用了8只体重4 - 6千克的雄性成年新西兰白兔，它们患有动脉粥样硬化。对髂动脉的不同区域进行如下处理：（1）仅球囊扩张；（2）仅激光照射；（3）球囊扩张 + 激光照射。髂动脉未损伤区域作为对照。通过冷激光照明器（Cook公司，印第安纳州布鲁明顿）将激光（630纳米）通过直径3毫米的球囊照射到血管壁。实验表明，仅球囊扩张组治疗后立即测得的血管cGMP水平最低（0.29±0.05皮摩尔/毫克蛋白），与未损伤对照组（1.01±0.07皮摩尔/毫克蛋白）相比显著降低（P < 0.001）。与未损伤对照组（P < 0.001）和仅球囊扩张组（P < 0.001）相比，仅激光治疗组的cGMP水平显著升高（2.87±0.12皮摩尔/毫克蛋白）。与仅球囊扩张组（P < 0.001）和对照组（P < 0.001）相比，球囊 + 激光组的血管cGMP水平（2.09±0.07皮摩尔/毫克蛋白）也有所升高。蛋白质印迹法的定性分析表明，激光照射可诱导iNOS。相比之下，球囊扩张并未诱导iNOS。然而，球囊 + 激光治疗倾向于恢复iNOS的表达。我们的研究表明，在体内动脉粥样硬化兔模型中，血管内低剂量激光照射可诱导iNOS并提高血管cGMP水平。
