Fitzgerald D, Van Asperen P, O'Leary P, Feddema P, Leslie G, Arnold J, Sullivan C
Royal Alexandra Hospital for Children, Sydney, Australia.
Pediatr Pulmonol. 1998 Oct;26(4):241-9. doi: 10.1002/(sici)1099-0496(199810)26:4<241::aid-ppul2>3.0.co;2-1.
This study assessed whether respiratory rates (RRs) correlate with urinary growth hormone (U-GH) excretion and sleep architecture in infants with chronic neonatal lung disease (CNLD) in early (1 month), middle (6 months), and late (10 months) infancy. Twenty-three preterm infants (CNLD=16, controls=7) were studied on 51 occasions. CNLD infants were stratified according to mean non-REM sleep respiratory rate (NREM RR) in early infancy into "High RR CNLD" infants (mean NREM RR >2 SD higher than controls) and "Normal RR CNLD" infants (mean NREM RR within 2 SD of controls' mean). "High RR CNLD" infants (RR >45) had a lower mean birthweight (P=0.015), current weight (P=0.042), current length (P=0.02), and growth velocity in early infancy (grams/week gained: P=0.042) than "Normal RR CNLD" and control infants. Mean (95% CI) U-GH excretion (ng U-GH/g urinary creatinine) was higher in "High RR CNLD" infants in air or their usual O2 (1,932 [459, 3,406]) than "Normal RR CNLD" (394 [147, 642]) and controls (320 [147, 492]) (P=0.024). With resolution of tachypnea by mid-infancy, hemoglobin oxygen saturation (SaO2) >93%, mean growth parameters and U-GH excretion for the "High RR CNLD" group were not significantly different from "Normal RR CNLD" and control groups. CNLD infants demonstrated increased sleep efficiency (P=0.016), whereas controls had similar sleep efficiency between early and middle infancy (P=0.452). Mean percent time in REM sleep (REM%) and slow wave sleep (SWS%) were not significantly different between early and middle infancy and did not vary in relation to respiratory rate. We conclude that tachypneic infants with CNLD have slower growth and elevated U-GH excretion in early infancy. With resolution of tachypnea, growth improved, U-GH excretion decreased, and sleep consolidation occurred. An elevated U-GH in tachypneic CNLD infants may reflect stress, compromised nutrition (GH resistance), or a feedback loop involving a direct effect of GH on lung growth and repair.
本研究评估了慢性新生儿肺病(CNLD)婴儿在婴儿早期(1个月)、中期(6个月)和晚期(10个月)时呼吸频率(RRs)是否与尿生长激素(U-GH)排泄及睡眠结构相关。对23例早产儿(16例CNLD患儿,7例对照)进行了51次研究。CNLD患儿在婴儿早期根据平均非快速眼动睡眠呼吸频率(NREM RR)分为“高RR CNLD”婴儿(平均NREM RR比对照组高>2个标准差)和“正常RR CNLD”婴儿(平均NREM RR在对照组均值的2个标准差范围内)。“高RR CNLD”婴儿(RR>45)的平均出生体重(P=0.015)、当前体重(P=0.042)、当前身长(P=0.02)以及婴儿早期的生长速度(每周增加的克数:P=0.042)均低于“正常RR CNLD”婴儿和对照婴儿。“高RR CNLD”婴儿在空气中或其常用氧气条件下的平均(95%可信区间)U-GH排泄(ng U-GH/g尿肌酐)(1,932 [459, 3,406])高于“正常RR CNLD”婴儿(394 [147, 642])和对照婴儿(320 [147, 492])(P=0.024)。到婴儿中期呼吸急促缓解、血红蛋白氧饱和度(SaO2)>93%时,“高RR CNLD”组的平均生长参数和U-GH排泄与“正常RR CNLD”组和对照组无显著差异。CNLD患儿的睡眠效率增加(P=0.016),而对照组在婴儿早期和中期的睡眠效率相似(P=0.452)。快速眼动睡眠(REM%)和慢波睡眠(SWS%)的平均时间百分比在婴儿早期和中期无显著差异,且与呼吸频率无关。我们得出结论,患有CNLD的呼吸急促婴儿在婴儿早期生长较慢且U-GH排泄升高。随着呼吸急促的缓解,生长改善,U-GH排泄减少,睡眠巩固发生。呼吸急促的CNLD婴儿中U-GH升高可能反映应激、营养受损(生长激素抵抗)或涉及生长激素对肺生长和修复直接作用的反馈回路。