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精氨酸加压素在胎儿钠平衡中的作用以及作为胎儿“应激”效应的介质。

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

作者信息

Gibson K J, Lumbers E R

机构信息

School of Physiology and Pharmacology, University of New South Wales, Kensington, Australia.

出版信息

J Dev Physiol. 1993 Mar;19(3):125-36.

PMID:8089438
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.

摘要

为研究精氨酸加压素(AVP)是否影响胎儿钠平衡,我们对两组长期留置导管的胎羊静脉输注AVP(45 mU h⁻¹ kg⁻¹)。一组尿渗透压为147±23 mosm kg⁻¹(标准误,n = 6),另一组尿渗透压较高(339±3 mosm kg⁻¹,n = 4,P < 0.001)。尿渗透压高的组收缩压较高(P < 0.05),肾小球滤过率(GFR)较高(P < 0.05),尿电解质排泄率较高(P < 0.05),但膜血流较低(P < 0.05),近端小管钠的分数重吸收较低(P < 0.01)。在尿渗透压低的组中,AVP使动脉血压升高(P < 0.001),心率下降(P < 0.001),膜血流下降(P < 0.02),但胎盘或肾血流无变化。肾钠排泄增加(P < 0.001),因为GFR升高(P < 0.001)且近端钠分数重吸收下降(P < 0.001)。远端钠分数重吸收增加(P < 0.001),但不足以补偿近端分数重吸收的下降。肺液流量下降(P = 0.006),肺液钠排泄也下降(P = 0.002)。胎儿血浆钠、血容量或血细胞比容无变化。在尿渗透压高的组中,AVP输注的效果相似。本研究表明,胎儿“应激”时出现的高水平AVP对胎儿心血管、肾脏和肺功能有广泛影响。AVP输注前尿渗透压高的胎儿的特征性表现完全可以用内源性AVP水平高来解释,AVP可能是胎儿“应激”这些广泛影响的唯一介质。此外,虽然输注AVP期间钠排泄增加,但血容量没有变化。因此,胎儿必定从细胞外液、羊膜腔和/或尿囊腔或通过胎盘获取了额外的钠。

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