Bases physiologiques de l'utilisation des antagonistes muscariniques dans les dysplasies bronchopulmonaires

Fisher, John T.; Froese, A. B.; Brundage, K. L.

doi:10.1016/0929-693x(96)89886-1

Cited by 14 publications

(5 citation statements)

References 69 publications

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“… 18 Studies evaluating the use of ipratropium bromide in the treatment of infants with BPD are limited to case reports following short-term use. 19 , 20 …”

Section: Discussionmentioning

confidence: 99%

Inhaled bronchodilator use for infants with bronchopulmonary dysplasia

et al. 2014

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ObjectiveTo identify factors associated with bronchodilator administration to infants with bronchopulmonary dysplasia (BPD) and evaluate inter-institutional prescribing patterns.Study DesignA retrospective cohort study of <29-week-gestation infants with evolving BPD defined at age 28 days within the Pediatric Health Information System database. Controlling for observed confounding with random-effects logistic regression, we determined demographic and clinical variables associated with bronchodilator use and evaluated between-hospital variation.ResultDuring the study period, 33% (N=469) of 1429 infants with BPD received bronchodilators. Lengthening mechanical ventilation duration increased the odds of receiving a bronchodilator [OR 19.6(11–34.8) at ≥54 days]. There was profound between-hospital variation in use, ranging from 0–81%.ConclusionBronchodilators are frequently administered to infants with BPD at U.S. children’s hospitals with increasing use during the first hospital month. Increasing positive pressure exposure best predicts bronchodilator use. Frequency and treatment duration vary markedly by institution even after adjustment for confounding variables.

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“… 18 Studies evaluating the use of ipratropium bromide in the treatment of infants with BPD are limited to case reports following short-term use. 19 , 20 …”

Section: Discussionmentioning

confidence: 99%

Inhaled bronchodilator use for infants with bronchopulmonary dysplasia

et al. 2014

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“…Interestingly, our study suggests that the physiological action of M 2 receptors in the newborn is minimal. Nevertheless, specific M 3 muscarinic receptor blockade would eliminate tachycardia due to nonspecific blockade of cardiac M 2 receptors by current antagonists (Kao et al 1989;Stokes et al 1983;Brundage et al 1990;Fisher et al 1995), which we have shown to exert a physiologic action in the newborn (see Figs. 2 and 4).…”

Section: Af-dx 116 P-f-hhsid Pirenzepine Atropinementioning

confidence: 90%

“…The rank order of potencies for cardiac versus airway responses for the antagonists that we employed is consistent with current knowledge of muscarinic receptor biology in the adult, and the actions and locations of cardiopulmonary muscarinic receptor subtypes. Our in vivo data provide physiologic evidence that cardiopulmonary muscarinic receptor differentiation has occurred at birth in the newborn dog, an important prerequisite in the rationale for the use and development of muscarinic receptor antagonists in the neonate (reviewed in Fisher et al 1995). The level of specificity of the antagonists we studied is illustrated by the HR/RL ED 50 ratios and ranged from modest to highly specific for selected antagonists and values are consistent with those reported in vitro (Buckley et al 1989;Dorje et al 1991;Waelbroeck et al 1991;Eltze and Galvan 1994).…”

Section: Muscarinic Receptor Subtypes At Birthmentioning

confidence: 92%

“…Although highly selective antagonists of the M 3 muscarinic receptor subtype are not yet available (Dorje et al 1991;Waelbroeck et al 1991;Buckley et al 1989;Eltze and Galvan 1994), current consensus suggests that M 3 antagonists would eliminate the untoward effects of nonspecific antagonists such as ipratropium bromide (Barnes 1993a;Loenders et al 1992). The advantage of specific M 3 receptor antagonists is twofold: firstly, they would eliminate cardiovascular side effects due to M 2 receptor blockade (i.e., tachycardia) and, secondly, they would allow prejunctional M 2 receptors to continue to exert autoinhibitory actions limiting neurally mediated bronchoconstriction (Barnes 1993a;Loenders et al 1992;Fisher et al 1995). Indeed, low-dose blockade of airway prejunctional M 2 receptors has been suggested to potentially exacerbate vagally induced bronchoconstriction (Barnes 1993b).…”

Section: Af-dx 116 P-f-hhsid Pirenzepine Atropinementioning

confidence: 99%

“…In both the adult (Richardson 1979) and newborn (for review see Waldron and Fisher 1991;Fisher et al 1995) muscarinic receptor mediated contraction reflects the dominant excitatory vagal innervation to airway smooth muscle (ASM) among mammalian species. Indeed, contractile responses are present early in fetal development (McCray 1993;Booth et al 1992).…”

Section: Introductionmentioning

confidence: 99%

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Cardiopulmonary actions of muscarinic receptor subtypes in the newborn dog

Fisher

Brundage²,

Anderson³

1996

Can. J. Physiol. Pharmacol.

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We addressed the role of muscarinic receptor subtypes in neurally mediated bronchoconstriction in vivo and airway smooth muscle contraction in vitro in the newborn dog. The in vivo dose-response effects of "selective" muscarinic antagonists on changes in lung resistance (RL) and heart rate (HR) in response to electrical stimulation of the vagus nerves were obtained in four groups of newborns. Each group was exposed to a different muscarinic antagonist: M1-selective pirenzepine (pir), M2-selective AF-DX 116 (11-[2-[(diethylamino)methyl]-1-piperidinyl]acetyl-5,11-dihydro-6H-pyrid o- [2,3-b]-[1,4]-benzodiazepine-6-one), M3-selective p-F-HHSiD (p-fluoro-hexahydro-sila-difenidol), and nonselective atropine (atr). In vitro concentration-response effects of pir and AF-DX 116 were obtained for neurally induced contractions of tracheal smooth muscle, elicited by electrical field stimulation. In a separate series of experiments we measured the bronchoconstrictor response to the muscarinic agonist acetylcholine delivered by right heart injection. Muscarinic antagonists reduced RL and HR responses to vagal stimulation in a dose-dependant fashion; however, ED50 values and selectivity for airway and cardiac responses (HR/RL ED50 ratio) were significantly different between antagonists. The rank order of potencies for inhibition of the increase in RL was atr > pir, M1 > p-F-HHSiD, M3 > AF-DX 116, M2, while that for HR was atr > AF-DX 116 > pir > p-F-HHSiD. AF-DX 116 preferentially inhibited the HR response, as reflected by the lowest HR/RL ED50 ratio (p < 0.001). The remaining antagonists preferentially inhibited RL, with the highest HR/RL ED50 ratio seen for p-F-HHSiD. These data suggest that muscarinic receptor subtypes are differentiated at birth and mediate cardiac and airway responses to vagal stimulation. We did not find autoinhibitory actions of airway M2 receptors on either the in vivo bronchoconstrictor response or the in vitro contractile response to electrical field stimulation. This suggests that neonatal airway M2 receptors, but not myocardial M2 receptors, are reduced in number or weakly coupled to muscarinic signal transduction mechanisms. Direct activation of airway smooth muscle by acetylcholine caused dose-dependent increases in RL that reached a plateau at approximately 200% at 100 micrograms, similar to values reported for vagal stimulation.

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