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• W189794312 abstract "Different diseases, such as acute lung injury (ALI) or its aggravated form, acute respiratory-distress syndrome (ARDS), persistent pulmonary hypertension of the newborn (PPHN), and chronic pulmonary hypertension, are characterized by an increase of pulmonary vascular resistance (PVR) and concomitant impairment of gas exchange. Aiming to dilate pulmonary vessels, systemic application of vasodilators, such as nitroprusside, prostacyclin, or nitroglycerin, was used but was found to be less beneficial or even harmful in patients with respiratory failure. Systemic infusion of vasodilators induced both pulmonary and systemic vasodilation, promoting arterial hypotension; dilation of pulmonary vessels was accompanied by deterioration of arterial oxygenation due to an increase in venous admixture by unselective perfusion of less ventilated areas (). When, in 1987, nitric oxide (NO) was identified as the biological equivalent of endothelium-derived relaxing factor (; ), investigators soon focused on NO for use as a more selective pulmonary vasodilator. Released to ventilated alveoli, lipophilic NO should, like endothelium-derived NO, rapidly diffuse into adjacent smooth-muscle cells, stimulating cyclic guanosine 3′,5′-monophosphate (cGMP) and relaxing vascular smooth muscles near ventilated areas. Unlike systemic vasodilators, NO was also presumed to be rapidly scavenged by hemoglobin (Hb), thus limiting the effects on pulmonary circulation. Since the beginning of this decade, tremendous progress has been made in introducing NO-inhalation therapy as a therapeutic option for the treatment of pulmonary hypertension and acute respiratory failure, and commercially available NO-delivery systems and monitoring devices now allow its use outside of specialized centers. In the following sections, the effects of low doses of inhaled NO on hemodynamics and pulmonary gas exchange under different conditions are described, concentrating on the most widespread use in ARDS and PPHN. Special attention is given to potential adverse effects of NO inhalation, delivery, and monitoring issues, and formation of toxic higher nitrogen oxides." @default.
• W189794312 created "2016-06-24" @default.
• W189794312 creator A5006581813 @default.
• W189794312 creator A5008633534 @default.
• W189794312 creator A5042435910 @default.
• W189794312 date "2000-01-01" @default.
• W189794312 modified "2023-09-27" @default.
• W189794312 title "Inhalation Therapy with Nitric Oxide Gas" @default.
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