Exogenous infusion of adenosine depresses whole body O2 use in fetal/neonatal sheep.
Exogenous infusion of adenosine depresses whole body O2 use in fetal/neonatal sheep.
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外源性输注腺苷可抑制胎儿/新生羊全身氧气的使用。
DOI：
10.1152/jappl.1996.81.2.541
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Power,GG
中科院分区：
文献类型：
--
作者：
Karimi,A;Ball,KT;Power,GG
为了研究腺苷可能的代谢调节作用，在子宫内模拟出生期间，向11只近足月胎羊输注腺苷和腺苷脱氨酶。测量胎儿动脉血气、多种代谢产物的浓度、胰岛素和全身耗氧量（VO 2）。在宫内通气和脐带阻断后，通过闭路呼吸测定法测量的胎儿/新生儿VO 2平均值为11.0 +/- 1.1（SE）ml（STPD）·min-1.kg胎儿wt-1，血浆腺苷浓度（[Ado]）为1.29 +/- 0.21 μ M。在接下来的30分钟间隔内输注腺苷（1.5 μ mol.min-1.kg-1）使[Ado]增加至1.57 +/- 0.28 microM（无显著性），使VO 2降低至7.7 +/- 0.5 ml.min-1.kg-1（P < 0.05）。收缩压降低19%（P < 0.01），舒张压降低25%（P < 0.01），心率增加19%（P < 0.01）。在研究的最高腺苷输注速率（6 μ mol.min-1. kg-1）下，[Ado]增加到4.27 +/- 0.46 microM（P < 0.001），VO 2没有进一步下降，尽管血压进一步下降，心率增加。在给予腺苷脱氨酶后，[Ado]降至0.58 +/- 0.13 microM（P < 0.05），而VO 2增至11.2 +/- 0.8 ml.min-1. kg-1（P < 0.05）;血压和心率恢复到基础水平。VO 2与[Ado]的关系为VO 2 = 6.14 + 4.89exp（-0.45[Ado]）（n = 144; r = 0.34; P < 0.001）。在整个实验过程中，动脉O2含量和血浆葡萄糖、乳酸盐、甘油和脂肪酸浓度均正常或升高，因此，O2缺乏和底物缺乏不太可能导致VO 2减少。我们的结论是，血浆腺苷可以作为信使的能量状态的羊胎儿/新生儿，并可能有助于维持O2供应和O2需求之间的平衡。
To examine a possible metabolic regulatory role for adenosine, infusions of adenosine and adenosine deaminase were given to 11 near-term fetal sheep during the simulation of birth in utero. Fetal arterial blood gases, the concentration of a number of metabolites, insulin, and whole body O2 consumption (VO2) were measured. After intrauterine ventilation and cord occlusion, fetal/neonatal VO2, measured by closed-circuit respirometry, averaged 11.0 +/- 1.1 (SE) ml (STPD).min-1.kg fetal wt-1 and plasma adenosine concentration ([Ado]) was 1.29 +/- 0.21 microM. Infusion of adenosine (1.5 mumol.min-1.kg-1) during the next 30-min interval increased [Ado] to 1.57 +/- 0.28 microM (not significant) and decreased VO2 to 7.7 +/- 0.5 ml.min-1.kg-1 (P < 0.05). The infusion reduced systolic blood pressure by 19% (P < 0.01) and diastolic blood pressure by 25% (P < 0.01) and increased heart rate by 19% (P < 0.01). At the highest rate of adenosine infusion studied (6 mumol.min-1.kg-1), [Ado] increased to 4.27 +/- 0.46 microM (P < 0.001) and VO2 did not measurably decline further, although there were further decreases in blood pressure and increases in heart rate. After administration of adenosine deaminase, [Ado] decreased to 0.58 +/- 0.13 microM (P < 0.05), whereas VO2 increased to 11.2 +/- 0.8 ml.min-1.kg-1 (P < 0.05); blood pressure and heart rate returned to basal levels. The dependence of VO2 on [Ado] is described by the relationship VO2 = 6.14 + 4.89 exp(-0.45[Ado]) (n = 144; r = 0.34; P < 0.001). Throughout the experiment, arterial O2 content and plasma glucose, lactate, glycerol, and fatty acid concentrations were normal or elevated, and, therefore, O2 lack and substrate deficiency were unlikely to have caused the reduction in VO2. We conclude that plasma adenosine may act as a messenger of energy status for the ovine fetus/neonate and may contribute thereby to a maintenance of a balance between O2 supply and O2 demand.