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早产儿中与不成熟相关的自由基活性

Immaturity-dependent free radical activity in premature infants.

作者信息

Varsila E, Pitkänen O, Hallman M, Andersson S

机构信息

Children's Hospital, University of Helsinki, Finland.

出版信息

Pediatr Res. 1994 Jul;36(1 Pt 1):55-9. doi: 10.1203/00006450-199407001-00009.

DOI:10.1203/00006450-199407001-00009
PMID:7936837
Abstract

To examine the role of immaturity in the free radical-mediated rate of lipid peroxidation in premature infants, we studied 27 infants [gestational age, 27.1 (SD 2.4) wk; birth weight, 970 (SD 330) g]. Ethane and pentane were quantitated in expired air during the first 18 d of life. During the first 2 postnatal d ethane [24.1 (SEM 7.8) pmol x kg-1 x min-1] and pentane [24.2 (SEM 4.1) pmol x kg-1 x min-1] were stable but increased during d 5 to maxima of 79.1 (15.8) pmol x kg-1 x min-1 and 62.1 (8.1) pmol x kg-1 x min-1, respectively. Maximum ethane and pentane correlated with gestational age (r = -0.42, p = 0.03 and r = -0.52, p = 0.005, respectively) and birth weight (r = -0.38, p = 0.05 and r = -0.59, p = 0.001, respectively). Infants with high maximum expired ethane and pentane (exceeding 40 pmol x kg-1 x min-1) had higher odds of dying or having bronchopulmonary dysplasia than those with low ethane and pentane (odds ratio, 6.5; 95% confidence interval, 1.1 to 38.5; p < 0.05 for ethane and odds ratio, 5.6; 95% confidence interval, 1.1 to 29.3; p < 0.05 for pentane). We conclude that degree of prematurity is the single most important factor explaining free radical-mediated lipid peroxidation in premature infants. A therapeutic intervention to limit the effects of free radicals should be started during the 1st postnatal d in premature infants to be effective.

摘要

为研究不成熟在自由基介导的早产儿脂质过氧化速率中的作用,我们对27例婴儿进行了研究[胎龄27.1(标准差2.4)周;出生体重970(标准差330)克]。在出生后的前18天内对呼出气体中的乙烷和戊烷进行定量分析。在出生后的头2天,乙烷[24.1(标准误7.8)皮摩尔·千克⁻¹·分钟⁻¹]和戊烷[24.2(标准误4.1)皮摩尔·千克⁻¹·分钟⁻¹]保持稳定,但在第5天增加,乙烷最大值达到79.1(15.8)皮摩尔·千克⁻¹·分钟⁻¹,戊烷最大值达到62.1(8.1)皮摩尔·千克⁻¹·分钟⁻¹。乙烷和戊烷的最大值与胎龄(分别为r = -0.42,p = 0.03和r = -0.52,p = 0.005)及出生体重(分别为r = -0.38,p = 0.05和r = -0.59,p = 0.001)相关。呼出乙烷和戊烷最大值较高(超过40皮摩尔·千克⁻¹·分钟⁻¹)的婴儿死亡或患支气管肺发育不良的几率高于乙烷和戊烷值较低的婴儿(乙烷的优势比为6.5;95%置信区间为1.1至38.5;p < 0.05;戊烷的优势比为5.6;95%置信区间为1.1至29.3;p < 0.05)。我们得出结论,早产程度是解释早产儿自由基介导的脂质过氧化的唯一最重要因素。为有效起见,应在早产儿出生后的第1天开始采取限制自由基作用的治疗干预措施。

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