Inhaled nitric oxide in neonatal and pediatric acute respiratory distress syndrome

Demirakça, S.; Dötsch, J.; Knothe, Christoph; Magsaam, Juergen; Reiter, H L; Bauer, Juergen; Kuehl, Peter Gonne

doi:10.1097/00003246-199611000-00024

Cited by 69 publications

(23 citation statements)

References 27 publications

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“…The attenuation was twice as high as in the control group. In contrast to experiments using inhaled nitric oxide or iloprost, the reduction of pulmonary artery pressure persisted for hours after the withdrawal of ADM. To the authors9 knowledge, none of the standard inhalative therapies for pulmonary hypertension, such as iloprost or nitric oxide, shows a comparable long-term effect [22,23]. Therefore, treatment with aerosolised ADM may be an option to reduce pulmonary arterial pressure persistently.…”

Section: Discussionmentioning

confidence: 99%

Brief adrenomedullin inhalation leads to sustained reduction of pulmonary artery pressure

Hardt¹,

Kandler²,

Chada³

et al. 2004

European Respiratory Journal

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The effect of aerosolised adrenomedullin (ADM), a potent vasodilator peptide, on pulmonary artery pressure was studied for 24 h in a surfactant-depleted piglet model. Animals received either aerosolised ADM (50 ng?kg -1 ?min -1 , ADM, n=6), or aerosolised normal saline solution (control, n=6). Aerosol therapy was performed for a 2 h treatment period followed by a 22 h observation period. Ventilator settings were adapted to keep arterial oxygen tension and carbon dioxide arterial tension between 13.3-14.6 kPa and 4.9-5.7 kPa, respectively.Aerosolised ADM reduced mean pulmonary artery pressure (MPAP) compared with the control group (end-point median 24 h after therapy start: DMPAP -14.0 versus -8.0 mmHg; 23.5 h after therapy start). After therapy start, mean systemic arterial pressure (MAP) was not significantly different between the groups (end-point median: MAP ADM 70 (61/74) versus control 72 (54/81) mmHg). Endothelin-1, a potent pulmonary vasoconstrictor, is regulated by ADM via cAMP. Twenty two hours after inhalation of aerosolised ADM, endothelin-1 mRNA in lung tissue and endothelin-1 protein expression in pulmonary arteries was reduced compared with controls (median semi-quantitative immunhistochemical score: ADM 0.21, control 0.76).Aerosolised adrenomedullin significantly reduced mean pulmonary artery pressure independently of arterial oxygen tension. Pulmonary hypertension is often associated with an imbalance of vasoconstrictor and vasodilator peptides [1]. Endothelin-1 (ET-1) is the most potent constrictor and has been implicated in the pathogenesis of pulmonary hypertension [2]. Adrenomedullin (ADM), which consists of 52 amino acids, is actively produced and secreted by various cell types, particularly the vascular endothelial and smooth muscle cells [3], and has potent vasodilator properties. Transgenic mice overexpressing ADM in their vasculature have been shown to be resistant to lipopolysaccharide (LPS)-induced shock. LPS caused smaller drops in blood pressure and less severe organ damage than in the wild-type, despite lower basal blood pressure [4]. Moreover, ADM overexpression reduced reperfusion injury and superoxide production [5]. ADM -/-knock-out mice showed lethal cardiovascular pathology e.g. extreme hydrops foetalis [6], mice with ADM z/-mutation exhibited elevated blood pressures with diminished nitric oxide production and increased oxidative stress [7,8], suggesting a crucial role for ADM in the regulation of the cardiovascular system, particularly endothelial cell function. ADM plays an important role in vascular morphogenesis and the regulation of blood pressure by stimulating nitric oxide production [7].Intravenous infusion of ADM in patients with pulmonary hypertension significantly reduced pulmonary vascular resistance. However, systemic vascular resistance was simultaneously decreased [9]. Similar effects were seen with the application of ADM to the pulmonary artery [10]. To increase the pulmonary selectivity of ADM-induced vasodilation, the current authors examined the e...

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Section: Discussionmentioning

confidence: 99%

Brief adrenomedullin inhalation leads to sustained reduction of pulmonary artery pressure

Hardt¹,

Kandler²,

Chada³

et al. 2004

European Respiratory Journal

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“…PFOB aerosol at a dose of 2.5 mL · kg Ϫ1 · h Ϫ1 might dilate blood vessels in well-ventilated alveoli, whereas PFOB aerosol at a dose of 5 mL · kg Ϫ1 · h Ϫ1 might also dilate blood vessels in less ventilated alveoli. In contrast to inhaled vasodilating agents such as nitric oxide (27) or iloprost (28), reaching predominantly ventilated lung areas, PFOB aerosol might additionally recruit collapsed alveoli for ventilation. This would lead to consecutive vasodilation of corresponding pulmonary arterial vessels.…”

Section: Discussionmentioning

confidence: 99%

Dose Response to Aerosolized Perflubron in a Neonatal Swine Model of Lung Injury

et al. 2004

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“…To improve oxygenation and ventilation in preterm neonates or neonates with severe lung disease, respiratory strategies as high-frequency oscillation ventilation (3)(4)(5) and therapy with inhaled nitric oxide (6) have been developed.…”

mentioning

confidence: 99%

Aerosolized Perfluorocarbon Suppresses Early Pulmonary Inflammatory Response in a Surfactant-Depleted Piglet Model

et al. 2002

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Inhaled nitric oxide in neonatal and pediatric acute respiratory distress syndrome

Cited by 69 publications

References 27 publications

Brief adrenomedullin inhalation leads to sustained reduction of pulmonary artery pressure

Brief adrenomedullin inhalation leads to sustained reduction of pulmonary artery pressure

Dose Response to Aerosolized Perflubron in a Neonatal Swine Model of Lung Injury

Aerosolized Perfluorocarbon Suppresses Early Pulmonary Inflammatory Response in a Surfactant-Depleted Piglet Model

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