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慢性胎儿高血糖对绵羊子宫及胎儿氧消耗的影响。

Effects of chronic fetal hyperglycemia upon oxygen consumption in the ovine uterus and conceptus.

作者信息

Philipps A F, Porte P J, Stabinsky S, Rosenkrantz T S, Raye J R

出版信息

J Clin Invest. 1984 Jul;74(1):279-86. doi: 10.1172/JCI111412.

DOI:10.1172/JCI111412
PMID:6429196
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC425210/
Abstract

Hyperglycemia has been shown to induce arterial hypoxemia in the chronically catheterized fetal sheep. To investigate the mechanism behind this glucose-induced hypoxemia, eight pregnant ewes and their fetuses were studied. Fetal glucose infusion (11.9 +/- 0.6 mg glucose/kg per min) was associated with a doubling of the fetal plasma glucose concentration with concomitant elevation of the umbilical vein-distal arterial O2 content difference by 24 h of infusion (P less than 0.01). Calculated fetal O2 consumption increased from 8.1 +/- 0.4 ml/kg per min in the control period to a maximum value of 10.6 +/- 0.3 ml/kg per min by third infusion day (P less than 0.01), which is an increase of approximately 30%. The degree of stimulation of fetal O2 consumption was related to the degree of fetal hyperglycemia but not to the degree of fetal hyperinsulinemia. The increase in fetal O2 consumption was accompanied by a significant increase in fetal O2 extraction with no change in either fetal O2 delivery or fetal blood O2 affinity. In addition, fetal hypercapnea with a mild fetal respiratory acidosis was induced by fetal hyperglycemia. The increase in fetal arterial PCO2 was linearly related (P less than 0.001) to the magnitude of increase in fetal O2 consumption. These studies suggest that chronic fetal hyperglycemia induces a state of accelerated fetal oxidative metabolism and may be important in explaining the etiology behind certain unusual findings in human infants of diabetic mothers.

摘要

高血糖已被证明可在慢性插管的胎羊中诱发动脉低氧血症。为了研究这种葡萄糖诱导的低氧血症背后的机制,对8只怀孕母羊及其胎儿进行了研究。胎儿葡萄糖输注(11.9±0.6毫克葡萄糖/千克每分钟)与胎儿血浆葡萄糖浓度加倍相关,输注24小时后脐静脉-远端动脉血氧含量差随之升高(P<0.01)。计算得出的胎儿耗氧量从对照期的8.1±0.4毫升/千克每分钟增加到第三天输注时的最大值10.6±0.3毫升/千克每分钟(P<0.01),增加了约30%。胎儿耗氧量的刺激程度与胎儿高血糖程度相关,但与胎儿高胰岛素血症程度无关。胎儿耗氧量的增加伴随着胎儿氧摄取的显著增加,而胎儿氧输送或胎儿血液氧亲和力均无变化。此外,胎儿高血糖诱发了胎儿高碳酸血症伴轻度胎儿呼吸性酸中毒。胎儿动脉血二氧化碳分压的升高与胎儿耗氧量增加的幅度呈线性相关(P<0.001)。这些研究表明,慢性胎儿高血糖会诱发胎儿氧化代谢加速的状态,这可能对解释糖尿病母亲所生人类婴儿某些异常发现的病因很重要。

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