The roles of arginine vasopressin in fetal sodium balance and as a mediator of the effects of fetal "stress".

Journal of developmental physiology Pub Date : 1993-03-01
K J Gibson, E R Lumbers
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Abstract

To see if arginine vasopressin (AVP) influenced fetal sodium balance, we infused AVP i.v. (45 mU h-1 kg-1) into two groups of chronically catheterized fetal sheep. One group had urinary osmolalities of 147 +/- 23 mosm kg-1 (SEM, n = 6) and the other group had higher urinary osmolalities (339 +/- 3 mosm kg-1, n = 4, P < 0.001). The group with high urinary osmolalities had higher systolic pressures (P < 0.05), higher glomerular filtration rates (GFR; P < 0.05), and higher urinary electrolyte excretion rates (P < 0.05), but lower membrane blood flows (P < 0.05) and lower fractional reabsorption of sodium by the proximal tubule (P < 0.01). In the group with low urinary osmolalities, AVP caused a rise in arterial blood pressure (P < 0.001), a fall in heart rate (P < 0.001), a fall in membrane blood flow (P < 0.02), but no change in placental or renal blood flow. Renal sodium excretion increased (P < 0.001) because GFR rose (P < 0.001) and proximal fractional sodium reabsorption fell (P < 0.001). Distal fractional sodium reabsorption increased (P < 0.001), but not enough to compensate for the fall in proximal fractional reabsorption. Lung liquid flow decreased (P = 0.006), as did lung liquid sodium excretion (P = 0.002). There were no changes in fetal plasma sodium, blood volume or haematocrit. The effects of AVP infusion were similar in the group with high urinary osmolalities. This study shows that high levels of AVP, such as occur in fetal "stress", have widespread effects on fetal cardiovascular, renal and lung functions. The characteristic profile of the fetuses with high urinary osmolalities prior to AVP infusion could be entirely explained by high endogenous AVP levels and AVP could possibly be a sole mediator of these widespread effects of fetal "stress". Furthermore, although during infusion of AVP sodium excretion increased, blood volumes did not change. Therefore, the fetuses must have accessed additional sodium from either their extracellular fluids, the amniotic and/or allantoic cavities or across the placenta.

精氨酸加压素在胎儿钠平衡中的作用及作为胎儿“应激”效应的中介。
为观察精氨酸抗利尿素(AVP)是否影响胎儿钠平衡,我们将45 μ h-1 kg-1的AVP静脉滴注于两组长期插管的胎羊。其中一组尿渗透压为147 +/- 23 mosm kg-1 (SEM, n = 6),另一组尿渗透压较高(339 +/- 3 mosm kg-1, n = 4, P < 0.001)。尿渗透压增高组收缩压增高(P < 0.05),肾小球滤过率(GFR)增高;P < 0.05),尿电解质排泄率升高(P < 0.05),但膜血流量降低(P < 0.05),近端小管钠重吸收分数降低(P < 0.01)。在低尿渗透压组,AVP引起动脉血压升高(P < 0.001),心率下降(P < 0.001),膜血流量下降(P < 0.02),但胎盘和肾血流量没有变化。肾钠排泄增加(P < 0.001),因为GFR升高(P < 0.001),近端钠重吸收下降(P < 0.001)。远端部分钠重吸收增加(P < 0.001),但不足以弥补近端部分钠重吸收的下降。肺液流量减少(P = 0.006),肺液钠排泄量减少(P = 0.002)。胎儿血浆钠、血容量或红细胞压积均无变化。AVP输注在高尿渗透压组的效果相似。本研究表明,高水平的AVP,如胎儿“应激”时出现的AVP,对胎儿心血管、肾脏和肺功能有广泛的影响。AVP输注前高尿渗透压胎儿的特征可以完全由高内源性AVP水平解释,AVP可能是胎儿“应激”这些广泛影响的唯一中介。此外,虽然在输注AVP期间钠排泄量增加,但血容量没有变化。因此,胎儿必须通过细胞外液、羊膜腔和/或尿囊腔或胎盘获得额外的钠。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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