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Bench-to-bedside review: Inhaled nitric oxide therapy in adults.

Creagh-Brown BC, Griffiths MJ, Evans TW - Crit Care (2009)

Bottom Line: Nitric oxide (NO) is an endogenous mediator of vascular tone and host defence.Inhaled nitric oxide (iNO) results in preferential pulmonary vasodilatation and lowers pulmonary vascular resistance.The route of administration delivers NO selectively to ventilated lung units so that its effect augments that of hypoxic pulmonary vasoconstriction and improves oxygenation.

View Article: PubMed Central - HTML - PubMed

Affiliation: Unit of Critical Care, Faculty of Medicine, Imperial College, London, UK. drbencb@gmail.com

ABSTRACT
Nitric oxide (NO) is an endogenous mediator of vascular tone and host defence. Inhaled nitric oxide (iNO) results in preferential pulmonary vasodilatation and lowers pulmonary vascular resistance. The route of administration delivers NO selectively to ventilated lung units so that its effect augments that of hypoxic pulmonary vasoconstriction and improves oxygenation. This 'Bench-to-bedside' review focuses on the mechanisms of action of iNO and its clinical applications, with emphasis on acute lung injury and the acute respiratory distress syndrome. Developments in our understanding of the cellular and molecular actions of NO may help to explain the hitherto disappointing results of randomised controlled trials of iNO.

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Hypoxic pulmonary vasoconstriction (HPV). (a) Normal ventilation-perfusion (VQ) matching. (b) HPV results in VQ matching despite variations in ventilation and gas exchange between lung units. (c) Inhaled nitric oxide (NO) augmenting VQ matching by vasodilating vessels close to ventilated alveoli. (d) Intravenous vasodilation counteracting HPV leads to worse oxygenation. (e) In disease states that are associated with dysregulated pulmonary vascular tone, such as sepsis and acute lung injury, failure of HPV leads to worse oxygenation. (f) Accumulation of NO adducts leads to loss of HPV-augmenting effect. Reprinted with permission from the Massachusetts Medical Society [2]. Copyright© 2005 Massachusetts Medical Society. All rights reserved.
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Figure 2: Hypoxic pulmonary vasoconstriction (HPV). (a) Normal ventilation-perfusion (VQ) matching. (b) HPV results in VQ matching despite variations in ventilation and gas exchange between lung units. (c) Inhaled nitric oxide (NO) augmenting VQ matching by vasodilating vessels close to ventilated alveoli. (d) Intravenous vasodilation counteracting HPV leads to worse oxygenation. (e) In disease states that are associated with dysregulated pulmonary vascular tone, such as sepsis and acute lung injury, failure of HPV leads to worse oxygenation. (f) Accumulation of NO adducts leads to loss of HPV-augmenting effect. Reprinted with permission from the Massachusetts Medical Society [2]. Copyright© 2005 Massachusetts Medical Society. All rights reserved.

Mentions: iNO augments the normal physiological mechanism of HPV and improves ventilation-perfusion matching and systemic oxygenation (Figure 2). In the absence of hypoxaemia being caused by ventilation-perfusion mismatching and HPV, the beneficial effects of iNO on oxygenation are severely limited. Indeed, experimental data confirm that intravenously administered vasodilators worsen oxygenation by counteracting HPV [3]. Further signs of the extent of non-pulmonary effects of iNO are increased renal blood flow and improved hepatic tissue oxygenation [14].


Bench-to-bedside review: Inhaled nitric oxide therapy in adults.

Creagh-Brown BC, Griffiths MJ, Evans TW - Crit Care (2009)

Hypoxic pulmonary vasoconstriction (HPV). (a) Normal ventilation-perfusion (VQ) matching. (b) HPV results in VQ matching despite variations in ventilation and gas exchange between lung units. (c) Inhaled nitric oxide (NO) augmenting VQ matching by vasodilating vessels close to ventilated alveoli. (d) Intravenous vasodilation counteracting HPV leads to worse oxygenation. (e) In disease states that are associated with dysregulated pulmonary vascular tone, such as sepsis and acute lung injury, failure of HPV leads to worse oxygenation. (f) Accumulation of NO adducts leads to loss of HPV-augmenting effect. Reprinted with permission from the Massachusetts Medical Society [2]. Copyright© 2005 Massachusetts Medical Society. All rights reserved.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2717403&req=5

Figure 2: Hypoxic pulmonary vasoconstriction (HPV). (a) Normal ventilation-perfusion (VQ) matching. (b) HPV results in VQ matching despite variations in ventilation and gas exchange between lung units. (c) Inhaled nitric oxide (NO) augmenting VQ matching by vasodilating vessels close to ventilated alveoli. (d) Intravenous vasodilation counteracting HPV leads to worse oxygenation. (e) In disease states that are associated with dysregulated pulmonary vascular tone, such as sepsis and acute lung injury, failure of HPV leads to worse oxygenation. (f) Accumulation of NO adducts leads to loss of HPV-augmenting effect. Reprinted with permission from the Massachusetts Medical Society [2]. Copyright© 2005 Massachusetts Medical Society. All rights reserved.
Mentions: iNO augments the normal physiological mechanism of HPV and improves ventilation-perfusion matching and systemic oxygenation (Figure 2). In the absence of hypoxaemia being caused by ventilation-perfusion mismatching and HPV, the beneficial effects of iNO on oxygenation are severely limited. Indeed, experimental data confirm that intravenously administered vasodilators worsen oxygenation by counteracting HPV [3]. Further signs of the extent of non-pulmonary effects of iNO are increased renal blood flow and improved hepatic tissue oxygenation [14].

Bottom Line: Nitric oxide (NO) is an endogenous mediator of vascular tone and host defence.Inhaled nitric oxide (iNO) results in preferential pulmonary vasodilatation and lowers pulmonary vascular resistance.The route of administration delivers NO selectively to ventilated lung units so that its effect augments that of hypoxic pulmonary vasoconstriction and improves oxygenation.

View Article: PubMed Central - HTML - PubMed

Affiliation: Unit of Critical Care, Faculty of Medicine, Imperial College, London, UK. drbencb@gmail.com

ABSTRACT
Nitric oxide (NO) is an endogenous mediator of vascular tone and host defence. Inhaled nitric oxide (iNO) results in preferential pulmonary vasodilatation and lowers pulmonary vascular resistance. The route of administration delivers NO selectively to ventilated lung units so that its effect augments that of hypoxic pulmonary vasoconstriction and improves oxygenation. This 'Bench-to-bedside' review focuses on the mechanisms of action of iNO and its clinical applications, with emphasis on acute lung injury and the acute respiratory distress syndrome. Developments in our understanding of the cellular and molecular actions of NO may help to explain the hitherto disappointing results of randomised controlled trials of iNO.

Show MeSH
Related in: MedlinePlus