Sleep, respiratory rate, and growth hormone in chronic neonatal lung disease

Fitzgerald, Dominic A.; Asperen, Peter Van; O’Leary, Peter; Feddema, Peter; Leslie, Garth I.; Arnold, John D.; Sullivan, Colin E.

doi:10.1002/(sici)1099-0496(199810)26:4<241::aid-ppul2>3.0.co;2-1

Cited by 23 publications

(15 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These authors further speculated that an increased percentage of slow-wave sleep may contribute to improved growth in CNLD infants who maintained higher oxygenation; the latter coincides with normalization of growth hormone urinary excretion. 25 The association between improved oxygenation and resultant changes in QS density and accelerated growth would be predicted from the wellknown interactions between decreased work of breathing induced by enhanced respiratory stability during SupOx breathing, as well as by the beneficial effect that SupOx would impose on growth hormone end-organ downstream signaling pathway. 26,27 Furthermore, QS will enhance growth hormone pulsatile release, 28 and increased growth hormone levels will further induce increased QS density.…”

Section: Discussionmentioning

confidence: 99%

Effect of Supplemental Oxygen on Sleep Architecture and Cardiorespiratory Events in Preterm Infants

et al. 2002

View full text Add to dashboard Cite

Asymptomatic preterm infants exhibit frequent and potentially clinically adverse cardiorespiratory events when assessed in the sleep laboratory. Administration of SupOx to these infants is associated with an increase in the overall duration and percentage TST spent in quiet sleep with reciprocal changes in active sleep. In addition, improvement in respiratory stability is observed with the use of low-flow SupOx, as evidenced by a decrease in apnea, periodic breathing, and bradycardia, without adverse effects on alveolar ventilation.

show abstract

Section: Discussionmentioning

confidence: 99%

Effect of Supplemental Oxygen on Sleep Architecture and Cardiorespiratory Events in Preterm Infants

et al. 2002

View full text Add to dashboard Cite

show abstract

“…The results of polysomnography in these infants in middle and late infancy are reported in a companion article in this journal. 13 CNLD was defined as continuing oxygen dependency at a postconceptional age (PCA) of 36 weeks or 28 days for infants born after 30 weeks gestation. 14 The term CNLD incorporates patients with bronchopulmonary dysplasia (BPD) and was preferred, as it is a clinical term and avoids the limitations of the histological term BPD.…”

Section: Methodsmentioning

confidence: 99%

Higher SaO2 in chronic neonatal lung disease: Does it improve sleep?

et al. 1998

Self Cite

View full text Add to dashboard Cite

Sleep fragmentation, decreased rapid eye movement (REM) sleep time, and REM sleep hypoxemia have been reported in infants with chronic neonatal lung disease (CNLD) in early infancy despite an awake hemoglobin oxygen saturation (SaO2) >93%. Interestingly, higher inspired O2 concentrations have been demonstrated to reduce REM sleep fragmentation in CNLD patients in middle infancy. However, the effect of increased SaO2 on sleep architecture in infants with CNLD near the time of discharge from neonatal intensive care has not been reported. We performed paired overnight polysomnography in a sleep laboratory on 16 infants with CNLD (4 weeks median corrected age) in air or their usual inspired oxygen (SaO2 >93%) and again when receiving 0.25 L/min higher than baseline inspired oxygen via nasal catheters (SaO2 >97%). A control group of seven healthy preterm infants was similarly studied. For CNLD infants on supplemented O2, sleep duration decreased by 15% (422 ± 66 min vs. 359 ± 89 min; P < 0.005), and sleep efficiency decreased by 7% (73.2 ± 10.6% vs. 66.4 ± 14.0%; P < 0.005) but percentage of time in REM sleep (REM%) (31.5 ± 8.9% vs. 29.8 ± 8.6%; P = 0.560), REM epoch duration (12.4 ± 2.8 min vs. 13.4 ± 4.3 min; P = 0.420), and REM arousal index (18.6 ± 6.5 vs. 18.8 ± 7.2; P = 0.990) were not significantly affected. Conversely, higher O2 did not alter sleep architecture in the control group. The mean non‐REM (NREM) respiratory rate decreased (CNLD: P = 0.003; controls: P = 0.02), NREM SaO2 increased (P < 0.05), although the mean transcutaneous CO2 was unaltered in both CNLD and control groups. This study confirmed low REM% in CNLD infants in early infancy and demonstrated that a higher SaO2 adversely affected sleep time but did not influence REM sleep duration or arousal frequency. A target SaO2 >93% is, therefore, as efficacious as an SaO2 >97% in optimizing sleep architecture in CNLD infants. Pediatr Pulmonol. 1998; 26:235–240. © 1998 Wiley‐Liss, Inc.

show abstract

“…Also eliminating sleep-associated hypoxia improves growth in infants with CNLD 39 60. See also section 2.5.4.…”

Section: Indications For Ltotmentioning

confidence: 98%