Abstract

Because treatments for cerebral arterial spasm-a delayed consequence of subarachnoid hemorrhage (SAH)-are clinically inconsistent, we describe here a new method for reversal of arterial spasm, possibly extensible to nitric oxide (NO)-sensitive microvasculature. We subjected dogs to the intracisternal double-hemorrhage model of SAH (autologous blood injection on days 1 and 3) and began endovascular treatment of the spasmed basilar artery (BA) on Day 4. A conical-tip fused silica optical fiber was introduced via a microcatheter (inserted femorally) into the proximal vicinity of the spasmed BA. After local saline flushing of blood, an ultraviolet (UV) pulsed laser beam (355 nm Nd:YAG) was focused into the optical fiber and converted into a concentric ring beam, which facilitated endovascular irradiation for 30s at intensities of 12-20W/cm2. BA diameters were measured angiographically using a semiautomated routine over the entire BA length as well as the proximal, medial, and distal segments. On Day 4 the BAs had constricted by 21±11%. After UV laser irradiation on Day 4, the constricted BAs dilated to 93±15% of their normal diameters within minutes, and the dilation (91±12%) persisted on Day 5. Most BA segments recovered to their respective baselines after UV irradiation, even when the UV beam was located considerably proximal to the BA origin. At days 4 and 5, the percent BA dilation normalized to Day 4 pre-treatment decreased linearly (by scatter plot, p<0.02) over a range of about 60 mm from the UV irradiation site. We conjecture that the vasodilator nitric oxide, produced at high local concentration from its vascular storage forms (chiefly nitrites) by UV laser-induced photoscission, stimulates a wave of arterial dilation, possibly by longitudinal propagation of transnitrosation reactions in the arterial wall, which reverses cerebral vasospasm semi-locally and thus avoids the deleterious effects of systemic treatment.

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