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出生时酸中毒在透明膜病发生发展中的作用。

The role of acidosis at birth in the development of hyaline membrane disease.

作者信息

Kenny J D, Adams J M, Corbet A J, Rudolph A J

出版信息

Pediatrics. 1976 Aug;58(2):184-91.

PMID:951132
Abstract

To test the hypothesis that intarpartum acidosis has a role in the etiology of hyaline membrane disease (HMD), blood was collected from the umbilical artery (UA) at birth from 110 premature infants and analyzed for hydrogen ion concentration ([H+]), PCO2, standard bicarbonate, and lactic acid. The infants were followed until a definite diagnosis was made of HMD (33 infants), type II respiratory distress syndrome (16 infants) or the absence of respiratory distress (61 infants). In general, infants with HMD were more premature and had lower Apgar scores than nondistressed infants; however, there were no significant differences between the two groups in any acid-base measurement. Only in those patients of 32 to 37 weeks' gestational age was it possible to detect a significant increase in UA [H+] in infants with HMD compared to those without respiratory distress. There was evidence that the reduced Apgar score of infants with HMD may be due to immaturity and abnormal pulmonary function secondary to lung disease. It is concluded that acidosis at birth is not a factor in the development of HMD except possibly in more mature infants.

摘要

为验证产时酸中毒在透明膜病(HMD)病因学中起作用这一假说,对110例早产儿出生时脐动脉血进行采集,分析其中氢离子浓度([H⁺])、二氧化碳分压、标准碳酸氢盐及乳酸水平。对这些婴儿进行随访,直至明确诊断为HMD(33例)、II型呼吸窘迫综合征(16例)或无呼吸窘迫(61例)。总体而言,与无呼吸窘迫的婴儿相比,患HMD的婴儿早产情况更严重,阿氏评分更低;然而,两组间任何酸碱指标测量均无显著差异。仅在孕龄32至37周的患者中,与无呼吸窘迫的婴儿相比,患HMD的婴儿脐动脉[H⁺]有显著升高。有证据表明,患HMD婴儿阿氏评分降低可能是由于不成熟及肺部疾病继发的肺功能异常。得出结论:出生时酸中毒不是HMD发病的因素,可能更成熟的婴儿除外。

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