Endovascular dilation of rat carotid artery by ultraviolet laser light transmitted by microcatheterized optical fiber

Introduction

Mechanically-based treatments for stenosis and vasospasm of cerebral arteries are undergoing avid development, but perforation and embolus formation can still occur as complications ¹ . We describe a clinical prototype device for inducing arterial dilation, apparently via nitric oxide production in smooth muscle cells ² , by means of endovascular irradiation with ultraviolet (UV) laser light.

Methods

Male Sprague-Dawley rats (500–750 g) were anesthetized with isoflurane and mechanically ventilated. A custom microcatheter (O.D. 940 um, I.D. 760 um) with a lubricious coating and smooth bullet-shaped head (VasCon LLC) was introduced transfemorally by means of a 360 um guidewire under X-ray fluoroscopy, and positioned inside the left common carotid artery (CCA) at the C2-C3 level. A “baseline” CCA diameter was obtained by injecting contrast medium (Visipaque 320 mg/ml) at the CCA blood flow rate (15% of cardiac output assuming a cardiac index of 250 ml/min/kg) for 5 sec, followed by a 2 min “saline flush” at 1 ml/min. The beam from a Coherent 90–6 argon ion laser configured for 351 nm UV light was focused (Optics for Research) into a fused silica optical fiber (Ocean Optics). The output end of the fiber (100 um core diameter, 3 M length) featured a conical end (apex angle 35 degrees), which in aqueous media converted the input beam into an expanding ring-shaped beam. The fiber was inserted until just distal to the catheter end, and there was centered axially by a spiral fixture. The inner CCA wall was irradiated 1 min with the UV ring beam (20 watts/cm² initial intensity) during saline infusion (1 ml/min). The fiber was removed and the CCA response monitored with Visipaque at the “saline flush” and then “baseline” rate.

Results

Baseline CCA diameter was 1.15 ± 0.20 mm and the saline flush diameter (resulting from CCA compression owing to lower saline injection rate) was 0.53 ± 0.03 mm. Following UV irradiation, the saline flush diameter became 0.77 ± 0.11 mm, while the “baseline” CCA diameter expanded to 1.40 ± 0.22 mm (n = 4). The percentages of dilation with respect to the respective initial diameters thus averaged 45% at the saline infusion rate (p < 0.05) and trended toward 22% at the normal blood flow rate (n.s.) The dilations persisted for at least 15 min ³ .

Conclusions

Endovascular UV laser irradiation induces arterial dilation while avoiding the traumatic complications ¹ of mechanical methods. The UV laser method can induce dilation without damaging smooth muscle cells ³ . This is notable because UV-facilitated arterial dilation can be induced in the presence of severe endothelial damage ³ - a primary cause of vasospasm ⁴ . Finally, this UV procedure appears to lie within the range of skills known to interventionalists.