Effects of antenatal glucocorticoids on pulmonary vascular reactivity in the ovine fetus

Deruelle, Philippe; Houfflin‐Debarge, V.; Magnenant, Eric; Jaillard, Sophie; Riou, Yvon; Puech, F; Storme, Laurent

doi:10.1067/mob.2003.444

Cited by 34 publications

(32 citation statements)

References 21 publications

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“…These data contrast with our findings of a marked increase in fetal PBF in response to antenatal corticosteroids, with little or no beneficial effect on the transition of the pulmonary circulation at birth. The difference between our findings and those of previous studies (25,27) is likely because of the maturity of the fetus when exposed to corticosteroids. In previous studies, fetuses were treated at 135-138 d of gestation (25,27), whereas in our study, fetuses were treated at ϳ125 d; term is ϳ147 d.…”

Section: Discussioncontrasting

confidence: 57%

“…In particular, corticosteroids can increase pulmonary vascular reactivity in response to vasodilatory stimuli, including catecholamines (24,25) prostaglandins, and NO (24,26). However, previous studies found that antenatal corticosteroids have no effect on basal PBF in fetal sheep (25,27) and were considered to enhance pulmonary vasodilation induced by alveolar ventilation at birth; this effect was independent of oxygen-mediated changes. These data contrast with our findings of a marked increase in fetal PBF in response to antenatal corticosteroids, with little or no beneficial effect on the transition of the pulmonary circulation at birth.…”

Section: Discussionmentioning

confidence: 75%

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Antenatal Corticosteroids Increase Fetal, But Not Postnatal, Pulmonary Blood Flow in Sheep

et al. 2009

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ABSTRACT:The lungs of very preterm infants have immature airways and gas exchange structures and are usually surfactant deficient. Antenatal corticosteroids are commonly used to enhance fetal lung maturation in preterm infants, but little is known of their effects on pulmonary blood flow (PBF) before and immediately after birth. Our aim was to determine the effects of antenatal betamethasone on PBF before birth and during the postnatal transition in very preterm lambs. Antenatal betamethasone treatment significantly increased mean fetal PBF from 20.2 Ϯ 5.1 to 84.3 Ϯ 18.3 mL/min at 30 h after administration; the PBF waveform was also significantly altered. Mean diastolic PBF increased from Ϫ38.5 Ϯ 4.9 pretreatment to Ϫ10.2 Ϯ 11.0 mL/min at ϳ36 h after the initial betamethasone dose (negative values indicate retrograde flow away from the lungs). Within 10 min after delivery, PBF was similar in control and betamethasone-treated lambs. These data demonstrate that antenatal betamethasone significantly increases fetal PBF and alters the PBF waveform but has little effect on postnatal PBF.

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Section: Discussioncontrasting

confidence: 57%

Section: Discussionmentioning

confidence: 75%

Antenatal Corticosteroids Increase Fetal, But Not Postnatal, Pulmonary Blood Flow in Sheep

et al. 2009

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“…Increased luminal diameter due to a reduction in medial wall thickness would be expected to lower PVR. In lambs with lung hypoplasia, prenatal GC significantly lowered the already elevated PVR (data presented as an abstract; Suzuki et al 2006 Pediatric Academic Societies, San Francisco) an effect that may be related to enhanced vasodilation to catecholamines (26).…”

Section: Tracheal Occlusion and Glucocorticoidsmentioning

confidence: 99%

Prenatal Glucocorticoids and Exogenous Surfactant Therapy Improve Respiratory Function in Lambs with Severe Diaphragmatic Hernia Following Fetal Tracheal Occlusion

et al. 2006

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Fetal tracheal occlusion (TO) accelerates lung growth and can reverse severe lung hypoplasia associated with diaphragmatic hernia (DH), however, lung compliance (CL) and respiratory gas exchange remain abnormal. We determined the individual and combined effects of prenatal glucocorticoids (GC) and exogenous surfactant therapy (S) on postnatal pulmonary function in lambs with DH that underwent prolonged TO. DH was created in 22 fetal sheep at 65 d of gestation and TO performed at 110 d. Eleven DH/TO animals received prenatal GC (betamethasone, 0.5 mg/kg) 48 h before delivery; six GC-treated and five non-GC lambs were administered surfactant (Infasurf, 3 mg/kg) at birth. Six sham-operated lambs served as controls. Lambs were delivered at 139 d gestation and ventilated for 2 h. GC or surfactant therapy alone significantly improved respiratory gas exchange, CL, and ventilatory efficiency index. Total lung capacity was normalized only in DH/TO lambs that received both GC and S. (Pediatr Res 60: 131-135, 2006)

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“…Stress hormones have also been shown to modulate the pulmonary vascular tone and reactivity during the perinatal life (12,26,29). These data suggest that perinatal stress may alter the pulmonary circulation.…”

mentioning

confidence: 71%

“…Heart rate was determined from the phasic Q p signal. Pulmonary vascular resistance (PVR) in the left lung was calculated as the difference between mean pulmonary artery pressure (PAP) and left atrial pressure divided by mean left Q p. From earlier observations (12,26) in which left atrial pressure was found constantly close to 2 cmH 2 O, a value of 2 cmH 2 O was used as an estimate of left atrial pressure.…”

Section: Physiological Measurementsmentioning

confidence: 99%

Effects of nociceptive stimuli on the pulmonary circulation in the ovine fetus

Houfflin‐Debarge¹,

Delelis²,

Jaillard³

et al. 2005

American Journal of Physiology-Regulatory, Integrative and Comp

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The fetus is able to exhibit a stress response to painful events, and stress hormones have been shown to modulate pulmonary vascular tone. At birth, the increased level of stress hormones plays a significant role in the adaptation to postnatal life. We therefore hypothesized that pain may alter pulmonary circulation in the perinatal period. The hemodynamic response to subcutaneous injection of formalin, which is used in experimental studies as nociceptive stimulus, was evaluated in chronically prepared, fetal lambs. Fetal lambs were operated on at 128 days gestation. Catheters were placed into the ascending aorta, superior vena cava, and main pulmonary artery. An ultrasonic flow transducer was placed around the left pulmonary artery. Three subcutaneous catheters were placed in the lambs' limb. The hemodynamic responses to subcutaneous injection of formalin, to formalin after fetal analgesia by sufentanil, and to sufentanil alone were recorded. Cortisol and catecholamine concentrations were also measured. Pulmonary vascular resistances (PVR) increased by 42% (P Ͻ 0.0001) after formalin injection. Cortisol increased by 54% (P ϭ 0.05). During sufentanil infusion, PVR did not change significantly after formalin. Cortisol increased by 56% (P Ͻ 0.05). PVR did not change during sufentanil infusion. Norepinephrine levels did not change during any of the protocols. Our results indicate that nociceptive stimuli may increase the pulmonary vascular tone. This response is not mediated by an increase in circulating catecholamine levels. Analgesia prevents this effect. We speculate that this pulmonary vascular response to nociceptive stimulation may explain some hypoxemic events observed in newborn infants during painful intensive care procedures. experimental pain animal model; fetal pain; fetal analgesia; pulmonary vascular reactivity; stress hormones THE DEVELOPMENT OF FETAL INVASIVE procedures and a better knowledge about pain in preterm and full-term newborn infants have led to increased interest in the subject of fetal pain. Nociception during early development is poorly understood. However, numerous indirect evidence such as behavioral or neurohormonal responses to invasive procedures suggests that the fetus can feel pain very early in gestation (17,18,20). Fetal brain-sparing response has been observed after procedures involving transgression of fetal trunk from as early as 16 wk (54). Furthermore, transfusion through the intrahepatic veins is associated with substantial rises in stress hormones (norepinephrine, cortisol, ␤-endorphin) from as early as 18 wk of gestation (17,18).At birth, the increase in stress hormones plays a significant role in the adaptation to postnatal life, including increased left ventricular contractility, lung fluid reabsorption, and surfactant release (11,25,35,47,49,60). Stress hormones have also been shown to modulate the pulmonary vascular tone and reactivity during the perinatal life (12,26,29). These data suggest that perinatal stress may alter the pulmonary circulation. Furthermore, hyp...

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Effects of antenatal glucocorticoids on pulmonary vascular reactivity in the ovine fetus

Cited by 34 publications

References 21 publications

Antenatal Corticosteroids Increase Fetal, But Not Postnatal, Pulmonary Blood Flow in Sheep

Antenatal Corticosteroids Increase Fetal, But Not Postnatal, Pulmonary Blood Flow in Sheep

Prenatal Glucocorticoids and Exogenous Surfactant Therapy Improve Respiratory Function in Lambs with Severe Diaphragmatic Hernia Following Fetal Tracheal Occlusion

Effects of nociceptive stimuli on the pulmonary circulation in the ovine fetus

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