IMMATURITY-DEPENDENT FREE-RADICAL ACTIVITY IN PREMATURE-INFANTS

被引:74
作者
VARSILA, E
PITKANEN, O
HALLMAN, M
ANDERSSON, S
机构
[1] HOSP SICK CHILDREN,DIV NEONATOL RES,TORONTO M5G 1X8,ON,CANADA
[2] UNIV CALIF IRVINE,IRVINE,CA 92717
[3] UNIV HELSINKI,DEPT OBSTET & GYNECOL 1,HELSINKI,FINLAND
[4] UNIV HELSINKI,DEPT OBSTET & GYNECOL 2,HELSINKI,FINLAND
关键词
D O I
10.1203/00006450-199407001-00009
中图分类号
R72 [儿科学];
学科分类号
100202 ;
摘要
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 Ist postnatal d in premature infants to be effective.
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页码:55 / 59
页数:5
相关论文
共 30 条
[1]  
BANCALARI E, 1986, PEDIATR CLIN N AM, V33, P1
[2]   OXYGEN-TOXICITY IN THE PREMATURE BABOON WITH HYALINE-MEMBRANE DISEASE [J].
DELEMOS, RA ;
COALSON, JJ ;
GERSTMANN, DR ;
KUEHL, TJ ;
NULL, DM .
AMERICAN REVIEW OF RESPIRATORY DISEASE, 1987, 136 (03) :677-682
[3]  
DORMANDY TL, 1988, LANCET, V2, P1126
[4]   HYDROCARBON GASES PRODUCED DURING INVITRO PEROXIDATION OF POLYUNSATURATED FATTY-ACIDS AND DECOMPOSITION OF PREFORMED HYDROPEROXIDES [J].
DUMELIN, EE ;
TAPPEL, AL .
LIPIDS, 1977, 12 (11) :894-900
[5]   FAILURE OF PREMATURE RABBITS TO INCREASE ANTIOXIDANT ENZYMES DURING HYPEROXIC EXPOSURE - INCREASED SUSCEPTIBILITY TO PULMONARY OXYGEN-TOXICITY COMPARED WITH TERM RABBITS [J].
FRANK, L ;
SOSENKO, IRS .
PEDIATRIC RESEARCH, 1991, 29 (03) :292-296
[6]   THE BACTERIAL ORIGIN OF RAT BREATH PENTANE [J].
GELMONT, D ;
STEIN, RA ;
MEAD, JF .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1981, 102 (03) :932-936
[7]   AN EVALUATION OF VITAMIN-E STATUS IN PREMATURE-INFANTS [J].
GUTCHER, GR ;
RAYNOR, WJ ;
FARRELL, PM .
AMERICAN JOURNAL OF CLINICAL NUTRITION, 1984, 40 (05) :1078-1089
[8]  
HOCHSTEIN P, 1981, FED PROC, V40, P183
[9]   PERSISTENT LOW PLASMA VITAMIN-E LEVELS IN PREMATURE-INFANTS SURVIVING RESPIRATORY-DISTRESS SYNDROME [J].
HUIJBERS, WAR ;
SCHRIJVER, J ;
SPEEK, AJ ;
DEELSTRA, BA ;
OKKEN, A .
EUROPEAN JOURNAL OF PEDIATRICS, 1986, 145 (03) :170-171
[10]   PREMATURE-INFANT, VITAMIN-E-DEFICIENCY AND RETROLENTAL FIBROPLASIA [J].
JOHNSON, L ;
SCHAFFER, D ;
BOGGS, TR .
AMERICAN JOURNAL OF CLINICAL NUTRITION, 1974, 27 (10) :1158-1173