Inhaled nitric oxide in term and preterm infants

Abstract

Nitric oxide (NO) is a gas that has potent vasodilator properties. It can be administered via inhalation in situations where NO production is impaired and results in vasodilatation of the pulmonary capillaries. In term infants, the administration of inhaled NO, at a dose of 20 parts per million, may reduce the need for extracorporeal membrane oxygenation by reducing pulmonary vascular resistance and improving oxygenation. Inhaled NO is an approved therapy in term babies with severe hypoxemic respiratory failure. In premature infants, inhaled NO may increase bleeding time and decrease platelet aggregation resulting in an increased risk for intraventricular hemorrhage. Early administration of inhaled NO may also potentially decrease the risk for developing chronic lung disease in premature infants. However, since studies show conflicting results, inhaled NO should only be used in premature neonates following investigational review board approved protocols.

Chemical power for microscopic robots in capillaries

“…Other chemicals (such as NO, PGD2 and LTD4) dilate the vessels. These chemicals can produce significant activity in the endothelial cells that line (and thus form the tube geometry of) the capillary vessel, so their influence can be fairly direct and quick [78,74]. Similarly, a large robot population constantly drawing excess oxygen supply could induce elevated erythropoietin secretion (if unregulated by the robots), increasing red cell production in the erythroid marrow [26,23].…”

Aerosolized Iloprost in the Treatment of Pulmonary Hypertension in Extremely Preterm Infants: A Pilot Study

“…Iloprost may therefore be an alternative for iNO in preterm infants weighing < 1000 grams in whom Van Meurs and colleagues showed a higher mortality and increased rates of intracranial hemorrhage [16] but studies also demonstrate confl icting results [9] . Besides, early administration of inhaled NO may potentially decrease the risk for developing chronic lung disease in premature infants [1,9,14] . Further randomized clinical studies are required to establish the role of iloprost in this setting.…”

Effects of chronic hypoxia on soluble guanylate cyclase activity in fetal and adult ovine cerebral arteries

“…The results reveal that this effect is attributable to attenuation of the specific activity of soluble guanylate cyclase activity and does not involve significant changes in soluble guanylate cyclase abundance, cGMP-phosphodiesterase activity, or the vasorelaxant activity of protein kinase G. These findings emphasize that in addition to the widely reported effects in the pulmonary circulation (1,13,54), chronic hypoxia also modulates vascular reactivity in the cerebral circulation, and probably other vascular beds as well. These generalized vascular effects of chronic hypoxia are quite different from the effects of acute hypoxia and should be carefully considered when designing treatments for chronically hypoxic infants, particularly those at risk for intracranial hemorrhage (21,51). From a basic science perspective, these results also raise many additional questions.…”

“…Common therapeutic approaches to management of this pathology often involve inhalation of nitric oxide (NO) (15) and administration of phosphodiesterase inhibitors (53), even though chronic hypoxia has long been known to depress reactivity to endotheliumdependent vasodilators and NO donors in the pulmonary vascular bed (13,38). Of particular importance is the growing recognition that standard treatments for persistent pulmonary hypertension can have very different effects in pulmonary and extrapulmonary vascular beds (38,51,59) and may even increase the risk for intracranial hemorrhage in premature infants (21, 51). These findings and trends emphasize the importance of greater understanding of the effects of chronic hypoxia on the mechanisms mediating NO-dependent relaxation outside the pulmonary vasculature, and most particularly in the immature cerebral circulation (21).…”