Use of a Beta-Agonist in Ventilated, Very-Low-Birth-Weight
Babies: A Longitudinal Evaluation

Kovacs, Stephen J.; Fisher, Joie; Brodsky, Nancy L.; Hurt, Hallam

doi:10.1159/000457623

Cited by 4 publications

(4 citation statements)

References 7 publications

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“…A Cochrane Database Systemic Review found that this was the only study adequate to assess bronchodilator effect on the prevention of BPD, and there were no eligible studies to determine the effect of bronchodilation on the treatment of BPD [56]. Because of the potential side effects, variability of administration, and paucity of long-term benefits, one must reserve bronchodilator therapy for infants with evidence of bronchospasm (ie, prolonged expiratory phase, increased work of breathing) and clinical improvement after therapy [57][58][59].…”

Section: Bronchodilatorsmentioning

confidence: 99%

Lung Injury and Bronchopulmonary Dysplasia in Newborn Infants

Christou

Brodsky

2005

J Intensive Care Med

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Bronchopulmonary dysplasia is the most common morbidity among surviving premature infants. Injury to the developing lung is the result of the interaction between a susceptible host and a number of contributing factors such as mechanical ventilation and infection. The resulting persistent impairment of pulmonary function and need for ongoing therapy are the underlying characteristics of bronchopulmonary dysplasia. Important insights into the pathogenesis of bronchopulmonary dysplasia have led to numerous therapies and preventive approaches. Although significant progress has been made, in order to further affect the incidence and severity of the disease, we need to further study (a) the genetically determined predisposing factors, (b) the relative contribution of the various pathogenetic pathways, and, most important, (c) how to best translate the knowledge gained from these studies into effective clinical approaches.

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Section: Bronchodilatorsmentioning

confidence: 99%

Lung Injury and Bronchopulmonary Dysplasia in Newborn Infants

Christou

Brodsky

2005

J Intensive Care Med

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“…Airway smooth muscle is present in the preterm airways and contains neural elements responsive to cholinergic and other constrictive stimuli [ 3 ], which may precipitate airway narrowing, worsen respiratory mechanics, and lead to hypoxemia. The preterm airways also contain β2-adrenergic receptors (β2-AR) capable of agonist-stimulated bronchodilation [ 4 ]. Preterm infants at high risk for chronic lung disease show evidence of hypertrophy of airway muscle as early as 10 days of age [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

“…Therefore, it is not uncommon for NICU clinicians and respiratory therapists to use inhaled β2-AR agonists, such as albuterol, to potentially relieve bronchoconstriction and wheezing, decrease airway resistance, and improve oxygenation in preterm infants with evolving and established chronic lung disease [ 6 – 10 ]. While systematic reviews have not shown convincing data of their efficacy in the prevention of chronic lung disease or other long-term morbidities associated with prematurity [ 11 , 12 ], many preterm infants do show improvements in pulmonary function testing following inhaled β2-AR agonist therapy [ 4 , 13 – 16 ]. Of note, some infants may never be responders in the NICU [ 4 , 16 ] or have the potential to develop tolerance and become non-responders over time [ 13 , 17 ].…”

Section: Introductionmentioning

confidence: 99%

Response to first dose of inhaled albuterol in mechanically ventilated preterm infants

et al. 2021

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Background Bronchodilator responses among preterm infants are heterogeneous. Bedside measurements may identify responders. Study design Respiratory measurements (Resistance, Compliance, FiO 2 ) and pulse oximetry (SpO 2 ) patterns were downloaded from infants <30 weeks gestational age during the first 2 months of life. Mechanically ventilated infants who received albuterol were included ( n = 33). Measurements were compared before and after first albuterol. Secondary analyses assessed subsequent doses. Results Median gestation and birthweight were 25 3/7 weeks and 730 g, respectively. Mean Resistance decreased post-albuterol ( p = 0.007). Sixty-eight percent of infants were responders based on decreased Resistance. Compliance and FiO 2 did not significantly differ. Percent time in hypoxemia (SpO 2 < 85%) decreased post albuterol ( p < 0.02). In responders, Resistance changes diminished with subsequent administration (all p = 0.01). Conclusions Ventilator resistance decreased in two-thirds of preterm infants, consistent with studies that utilized formal pulmonary function testing. Albuterol had a variable effect on delivered FiO 2 ; however, hypoxemia may be useful in evaluating albuterol response.

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“…In the perinatal period, infants with evolving BPD are frequently treated for airway hyperreactivity ( Mhanna et al, 2009 ; Slaughter et al, 2015 ), but first-line therapies such as β 2-adrenergic agonists lack consistent bronchodilator efficacy ( Motoyama et al, 1987 ; Kovacs et al, 1990 ; Denjean et al, 1992 ) and have not been shown to prevent BPD nor facilitate weaning of respiratory support ( Denjean et al, 1998 ). Of note, older children with BPD also have airway hyperreactivity that is distinct from allergic T-helper-2-high asthma ( Halvorsen et al, 2005 ; Siltanen et al, 2011 ; Filippone et al, 2013 ) and may have minimal or even a paradoxical response to traditional asthma medications ( Yuksel and Greenough, 1993 ; De Boeck et al, 1998 ; Baraldi et al, 2005 ).…”

Section: Introductionmentioning

confidence: 99%

S-Nitrosoglutathione Attenuates Airway Hyperresponsiveness in Murine Bronchopulmonary Dysplasia

et al. 2016

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Bronchopulmonary dysplasia (BPD) is characterized by lifelong obstructive lung disease and profound, refractory bronchospasm. It is observed among survivors of premature birth who have been treated with prolonged supplemental oxygen. Therapeutic options are limited. Using a neonatal mouse model of BPD, we show that hyperoxia increases activity and expression of a mediator of endogenous bronchoconstriction, S-nitrosoglutathione (GSNO) reductase. MicroRNA-342-3p, predicted in silico and shown in this study in vitro to suppress expression of GSNO reductase, was decreased in hyperoxia-exposed pups. Both pretreatment with aerosolized GSNO and inhibition of GSNO reductase attenuated airway hyperresponsiveness in vivo among juvenile and adult mice exposed to neonatal hyperoxia. Our data suggest that neonatal hyperoxia exposure causes detrimental effects on airway hyperreactivity through microRNA-342-3p–mediated upregulation of GSNO reductase expression. Furthermore, our data demonstrate that this adverse effect can be overcome by supplementing its substrate, GSNO, or by inhibiting the enzyme itself. Rates of BPD have not improved over the past two decades; nor have new therapies been developed. GSNO-based therapies are a novel treatment of the respiratory problems that patients with BPD experience.

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Use of a Beta-Agonist in Ventilated, Very-Low-Birth-Weight Babies: A Longitudinal Evaluation

Cited by 4 publications

References 7 publications

Lung Injury and Bronchopulmonary Dysplasia in Newborn Infants

Lung Injury and Bronchopulmonary Dysplasia in Newborn Infants

Response to first dose of inhaled albuterol in mechanically ventilated preterm infants

S-Nitrosoglutathione Attenuates Airway Hyperresponsiveness in Murine Bronchopulmonary Dysplasia

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