Inhaled nitric oxide dilates retinal arterioles in minipigs

Abstract

AbstractPurpose To investigate the effect of inhaled nitric oxide (NO) on the retinal arteriolar diameter in minipigs.Methods Seven minipigs were anesthetized, intubated and mechanically ventilated. A Swan‐Ganz catheter was inserted for measuring cardiac output by the thermodilution technique. Fundus image (one eye per animal) was recorded in a digital videotape under stable hemodynamic and ventilatory conditions. After baseline recordings, NO was added to the breathing circuit first at 20 ppm for 30 minutes and then at 40 ppm for another 30 minutes. NO was then weaned off. Retinal arteriolar diameter was measured in arbitrary units (AU) at baseline and 30 minutes after each manipulation, using Retinal Vessel Analyzer. Systemic and pulmonary hemodynamic parameters were also measured.Results Mean baseline retinal arteriolar diameter was 231.0±38.1 AU. Thirty minutes after initiation of 20‐ppm NO inhalation, this diameter had increased only by 3.2±3.5% compared to baseline (p>0.05), to 237.9±36.5 AU. Thirty minutes after initiation of 40‐ppm NO inhalation, this diameter had increased by 7.6±4.7% compared to baseline (p<0.05), to 248.3±39.8 AU. Thirty minutes after weaning off the inhaled NO, this diameter had decreased to 232.9±39.1 AU, having returned practically to baseline (p>0.1 compared to baseline). Hemodynamic parameters (mainly cardiac output, blood pressure, and systemic vascular resistance) did not change significantly.Conclusion In minipigs, NO inhalation at a concentration increased stepwise from 20 to 40 ppm induces a retinal arteriolar vasodilation which is reversed 30 minutes after weaning off the inhaled NO. A potential clinical application of this treatment modality in vascular diseases of the retina needs to be evaluated.