Background Reduced bioavailability of endothelium-derived nitric oxide associated with
reperfusion could potentially exacerbate the inflammatory response during reperfusion.
Evidence suggests the pharmacologic effects of inhaled nitric oxide may extend beyond the
pulmonary vasculature, and this is attributed to nitric oxide-derived complexes in blood that
ultimately orchestrate antiinflammatory effects. In this study, the authors evaluated the
potential for inhaled nitric oxide (80 ppm) to attenuate inflammation instigated by ischemia …