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Objective: We hypothesized that the proinflammatory response to intra-amniotic endotoxin would induce lung maturation in preterm lambs.Study Design: Ewes were randomly assigned to receive 20 mg Escherichia coli endotoxin by intra-amniotic injection, maternal betamethasone (0.5 mg/kg), or sodium chloride solution. Preterm lambs were delivered at 125 days' gestation and underwent ventilation to assess lung function. Lung gas volume, surfactant concentrations, and inflammation were subsequently evaluated, with data analyzed by analysis of variance.Results: Fetal endotoxin exposure 6 days before delivery increased compliance by 59%, increased lung gas volume 2.3-fold, increased concentrations of surfactant lipids, increased surfactant A and B protein levels, and increased messenger ribonucleic acid expressions for surfactant proteins (all P <.01, vs control group). Betamethasone exposure resulted in less consistent effects. White blood cell counts were increased in fetal membranes and lungs after endotoxin exposure, but there was no severe inflammation.Conclusion: A single fetal exposure to endotoxin resulted in large improvements in postnatal lung function and increases in surfactant concentrations after preterm delivery. These effects were qualitatively larger than those achieved with betamethasone. [ABSTRACT FROM AUTHOR]

Objective: Fetal arginine vasopressin contributes to fetal and amniotic fluid homeostasis by increasing water resorption in the kidney and, at higher plasma levels, circulatory homeostasis by vasopressor effects. In utero and neonatal exposure of rat pups to prolonged alterations in plasma osmolality may permanently alter (imprint) pituitary arginine vasopressin content and adult responses to osmotic challenges. Our objective was to investigate fetal developmental changes and the impact of maternal dehydration and maternal hyponatremia on fetal pituitary arginine vasopressin content and hypothalamic arginine vasopressin messenger ribonucleic acid expression.Study Design: Ten pregnant ewes with singleton fetuses (135 +/- 1 day) were chronically prepared with maternal vascular catheters. Ewes were assigned to receive water deprivation (n = 4) [desamino, D-Arg8]-arginine vasopressin-induced plasma hyponatremia (n = 3), or 4 days of observation (n = 3). Three additional pregnant ewes with preterm (110 +/- 1 day) singleton fetuses were also included for a study of maturational effects. Daily maternal blood samples were analyzed for determination of plasma arginine vasopressin, electrolytes, and osmolality. After the study protocol, fetuses were operatively delivered, umbilical blood samples obtained, and fetuses put to death for pituitary and hypothalamic tissues. Pituitary arginine vasopressin content was determined by radioimmunoassay, and hypothalamus arginine vasopressin messenger ribonucleic acid expression was detected by Northern blotting.Results: Dehydration significantly (P < .05) increased, and hyponatremia significantly decreased maternal plasma sodium concentration compared with controls. Fetal plasma sodium concentration significantly changed in parallel with maternal values (dehydration: 139 +/- 1 to 150 +/- 1 mEq/L; hyponatremia: 138 +/- 1 to 128 +/- 5 mEq/L). Fetal hypothalamic arginine vasopressin messenger ribonucleic acid expression and pituitary content did not change in relation to these relatively acute alterations in plasma tonicity. However, among all animals, arginine vasopressin messenger ribonucleic acid expression was significantly negatively correlated with pituitary arginine vasopressin content (r2 = 0.563; P = .02). Arginine vasopressin messenger ribonucleic acid expression was significantly lower in both preterm and near-term fetuses (P < .05) than that in the maternal ewe, although pituitary arginine vasopressin content (in micrograms per milligram of protein) was significantly greater in preterm fetuses (P < .01, vs maternal; P < .05, vs near term).Conclusions: The significant inverse relation between arginine vasopressin content and arginine vasopressin messenger ribonucleic acid suggests a dynamic arginine vasopressin synthesis-content feedback relationship is functional in the near-term fetus. Although relatively acute periods of maternal hypertonicity or hypotonicity do not alter fetal pituitary arginine vasopressin content or hypothalamic arginine vasopressin messenger ribonucleic acid expression, longer-term plasma tonicity alterations may potentially have an impact on the fetal arginine vasopressin hypothalamic-pituitary axis. [ABSTRACT FROM AUTHOR]

Objective: We evaluated the effects of single or three repeated doses of maternal betamethasone on fetal growth at preterm and term delivery in sheep.Study Design: Pregnant ewes were randomly assigned to receive one dose of 0.5 mg/kg betamethasone at 104 days' gestational age; three doses of betamethasone at 104, 111, and 118 days' gestational age; or saline for controls. Lambs were delivered at 125 days' (preterm) or at 145 days' (term) gestational age for assessments of fetal growth.Results: The single betamethasone exposure at 104 days' gestational age caused symmetric growth retardation of 11% at 125 days' gestational age and 14% at term. The three-dose exposures decreased body weights by 25% in preterm lambs and by 19% at term. Organ protein and deoxyribonucleic acid per kilogram of body weight were selectively decreased in preterm lambs. At term the decreases in organ weight, protein, and deoxyribonucleic acid were proportionate to the decreased birth weight.Conclusion: One or three doses of maternal glucocorticoids begun at an early gestational age caused symmetric growth retardation in lambs delivered prematurely, and the decreased fetal size persisted to term. [ABSTRACT FROM AUTHOR]

Objective: Previously we have shown that neonatal lung function in sheep after preterm birth is profoundly enhanced by intra-amniotic injection of endotoxin, with a magnitude at least equal to that induced by maternal betamethasone administration. This study investigated the effects of betamethasone on lung maturation and growth in the presence of inflammation by treating sheep with both maternal intramuscular betamethasone and intra-amniotic endotoxin injections., Study Design: Time-mated pregnant ewes at 118 days' gestation were allocated at random to receive maternal intramuscular or intra-amniotic saline solution injection (n = 10), maternal intramuscular betamethasone injection (0.5 mg/kg; n = 7), intra-amniotic endotoxin injection (20 mg Escherichia coli B055;B5; n = 11) by ultrasonographic guidance, or both betamethasone and endotoxin injections (n = 7). The lambs were delivered abdominally at 125 days' gestation (term is 150 days' gestation), and the neonates were ventilated for 40 minutes before postmortem examination., Results: Combined treatment with betamethasone and endotoxin resulted in significantly greater improvements in neonatal lung function than occurred after treatment with either agent alone, and this effect was not accompanied by a further increase in surfactant levels. The reduction in birth weight that is seen after maternal betamethasone treatment was not seen when this treatment was combined with endotoxin. Endotoxin treatment resulted in inflammatory responses in cord blood and alveolar wash, and these responses were not inhibited by betamethasone treatment. There were no pregnancy losses., Conclusion: Both intra-amniotic endotoxin injection and maternal intramuscular betamethasone injection promoted fetal lung maturation. When these treatments were combined, there were additive effects on short-term postnatal lung function but not on surfactant levels. Endotoxin negated the growth restriction in sheep caused by maternal betamethasone treatment. These findings provide evidence that the lung maturation induced by glucocorticoids and that induced by endotoxin are mediated by different mechanisms.

Glucocorticoids are administered for preterm labor to improve postnatal adaptation. We assessed the effect of antenatal betamethasone (Beta) treatment on preterm newborn lamb neuroendocrine [catecholamine, arginine vasopressin (AVP)] and endocrine [triiodothyronine (T(3)), ANG II, and atrial natriuretic factor (ANF)] adaptive responses following delivery and a hypoxic challenge. Beta treatment included direct fetal injection at 0.2 (F(0.2); n = 8) or 0.5 (F(0.5); n = 7) mg/kg estimated fetal body weight or maternal injection with 0.2 (n = 8) or 0.5 mg/kg (M(0.5); n = 8). Control animals received fetal and maternal intramuscular injections of saline (n = 8). After 24 h, lambs were delivered by cesarean section, surfactant treated, and ventilated for 4 h. Relative to the control lambs, 3 h after delivery, there was a marked suppression of plasma cortisol, epinephrine, norepinephrine, and ANG II levels and elevated plasma T(3) and ANF levels, systolic blood pressure, and left ventricular contractility (dP/dt; F(0.5) and M(0.5)) values in F(0.5) and both maternal Beta-treated groups. However, Beta treatment augmented the cardiac output, cortisol, norepinephrine, AVP, and ANF responses to 20 min of hypoxia (PO(2) = 25-30 mmHg). We concluded that short-term (24 h) antenatal glucocorticoid exposure 1) alters preterm newborn postnatal blood pressure regulation in the face of marked depression of plasma cortisol, catecholamine, and ANG II levels and 2) augments the postnatal neuroendocrine and endocrine responses to a hypoxic challenge.

We assessed renal and cardiovascular function in preterm newborn lambs after antenatal glucocorticoid exposure. Pregnant ewes were randomly assigned to receive betamethasone or saline via either direct fetal or maternal injection at 122 d gestation. Lambs were delivered 15 h later, and cardiovascular and renal function was assessed. Two hours after delivery, baseline urine flow, urinary sodium excretion, and urinary osmolar clearance were similar in all groups. Volume expansion (saline, 2.5% of body weight, for 10 min) increased values for urine flow (0.23 +/- 0.04 to 0.58 +/- 0.09 mL x min(-1) x kg(-1)), urinary sodium excretion (29.7 +/- 5.8 to 76.2 +/- 12.3 microEq x min(-1) x kg(-1)), and osmolar clearance (12.2 +/- 1.2 to 24.3 +/- 1.6 mL/100 mL GFR) in the fetal group. Increases in urine values were also observed in the maternal group, but control values did not change significantly. Mean arterial pressure was increased in both betamethasone-treated groups relative to controls. Short-term antenatal betamethasone exposure 1) augments preterm newborn kidney adaptive responses to acute volume expansion, and 2) increases postnatal blood pressure in preterm newborn lambs.

Unlabelled: Renal and cardiovascular immaturity has been linked with poor outcomes in the premature human newborn. Despite extensive study in the fetus, the contribution of the renin-angiotensin system to renal and cardiovascular function in the premature newborn has not been well characterized. To evaluate the angiotensin II contribution to preterm newborn renal and cardiovascular functions, preterm (120-day) and near-term (136-day) lambs were Caesarean delivered and ventilated. One hour following delivery, animals were randomized to receive angiotensin II receptor-blockade (saralasin; 20 microg kg(-1) min(-1)) or saline (CON). Prior to blockade, mean +/- SEM values for urine flow (U(Flow)), urinary sodium excretion (U(NaV)), and fractional excretion of sodium (FENa) were similar in all groups. Angiotensin II receptor-blockade decreased U(Flow), U(NaV) and FENa in the 120-day group with no changes in the 136-day animals. No changes in mean arterial pressure, or plasma angiotensin II, aldosterone, and renin activity levels were noted at either gestational age., Conclusions: (1) angiotensin II contributes to the regulation of renal function in 120-day preterm lambs without changing blood pressure and (2) angiotensin II-mediated feedback inhibition of renin release is uncoupled in preterm newborns.

Renal adaptive responses during the 24 h after delivery in term newborn lambs include marked increases in both glomerular filtration rate (GFR) and sodium reabsorption. This study investigated the effects of ventilation style on cardiovascular, renal, and endocrine adaptations in preterm newborn lambs. Lambs (n = 62) were delivered by cesarean section at 131 days gestation (term = 150 days), treated with surfactant, and randomized to one of three ventilation strategies: high-frequency oscillation (12 Hz), high rate (50 breaths/min; tidal volume = 8 ml/kg), or low rate (15 breaths/min; tidal volume = 15 ml/kg). Lambs (5 or 6/group) were ventilated for 2, 5, 10, and 24 h to maintain arterial PCO2 between 45 and 50 mmHg. Plasma vasopressin levels decreased to <25 pg/ml by 10 h, and fractional sodium excretion decreased to <1% by 16 h in all groups. However, cardiac output, renal plasma flow, and GFR values did not change over time for any of the groups. The style of ventilation employed had no measurable effects on overall cardiovascular, renal, or endocrine function. We conclude in ventilated preterm lambs that 1) the ventilation style does not affect the time course for postnatal adaptation, 2) adaptive changes in renal tubular sodium reabsorption are evident by 16 h after birth, and 3) changes in preterm newborn renal sodium reabsorption occur in the absence of postnatal changes in renal plasma flow or GFR.

Previous studies have shown that female rats consume significantly more water than males on a weight basis. Because exposure to alcohol during the last week of gestation is associated with incomplete behavioral defeminization in male rats, we examined daily water intake in fetal alcohol-exposed (FAE) males and females. Time-pregnant multiparous Sprague-Dawley dams were administered an ethanol liquid diet containing 35% ethanol-derived calories from day 14 through parturition. At 80 days of age, daily water consumption of FAE males and female litter representatives was measured for 7 days. FAE males, but not females, consumed significantly more water than their pair-fed counterparts. Subsequent experiments determined that the increased water consumption in FAE males is present prepubertally, persists into mature adulthood, and is not influenced by prenatal or postnatal castration. Chronic estrogen treatment induced large increases in water consumption, but consumption of FAE males remained elevated over elevated pair-fed male consumption, indicating that pituitary sensitivity to estrogen was not increased in FAE males. Morphometric studies of hypothalamic nuclei containing vasopressin cells revealed no long-term effects of prenatal ethanol exposure on the volume of the supraoptic nucleus or paraventricular nucleus in males, nor was an effect observed in the ventromedial nucleus measured as a control. In FAE females, the volume of the paraventricular nucleus was significantly smaller than chow-fed controls. Whereas baseline plasma and pituitary arginine vasopressin (AVP) levels of FAE animals and pair-fed controls were not significantly different, AVP content was significantly reduced in the septal/bed nucleus region in brains of FAE animals of both sexes. Overall, these data indicate that prenatal ethanol exposure increases male water consumption in the absence of alterations in basal plasma AVP.

Abnormalities of premature newborn adaptation after preterm birth result in significant perinatal mortality and morbidity. We assessed the effects of short-term (24 h) fetal betamethasone exposure on preterm newborn baboon pulmonary and cardiovascular regulation and renal sodium handling during the first 24 h after birth. Male fetal baboons (Papio) (124-day gestation, term 185 days) received ultrasound-guided intramuscular injections of saline (n = 5) or betamethasone (0.5 mg/kg; n = 5). Fetuses were cesarean delivered 24 h later, treated with 100 mg/kg surfactant, and ventilated by adjusting peak inspiratory pressures to maintain PCO2 values of 35-50 mmHg for 24 h. Betamethasone- vs. saline-treated mean +/- SE newborn body weights (0.45 +/- 0.02 vs. 0.41 +/- 0.01 kg) were similar. Although prenatal betamethasone did not affect postnatal lung function (PCO2, arterial/alveolar O2 gradient, or dynamic compliance), plasma hormone (cortisol or thyroxine), or catecholamine levels, mean arterial pressure (25 +/- 1 vs. 32 +/- 1 mmHg), plasma sodium concentration (132 +/- 2 vs. 138 +/- 1 meq/l), glomerular filtration rate (0.07 +/- 0.02 vs. 0.16 +/- 0.02 ml.min-1.kg-1), and renal total sodium reabsorption (1.5 +/- 0.5 vs. 16.0 +/- 3.0 mu eq.min-1.kg-1) values were significantly lower in saline-treated than in betamethasone-treated newborns at 24 h. We conclude that despite the fact that there are no pulmonary and endocrine effects, antenatal glucocorticoid exposure alters premature newborn baboon vascular and renal glomerular function and improves sodium reabsorption after preterm delivery.

Background: The mechanism(s) of hyponatremia of cirrhosis is not completely clarified. Although increased vasopressin activity has been proposed in some studies, there have been reports disputing its role in the pathogenesis of profound hyponatremia in patients with decompensated liver disease. Methodologic flaws and lack of correlation with indices of circulatory dysfunction may have contributed to these discrepancies. The aims of the present study were to measure levels of vasopressin both in plasma and in urine and to correlate them with the volume-dependent hormonal systems of plasma renin activity (PRA) and atrial natriuretic factor (ANF)., Methods: Plasma vasopressin, ANF, and PRA were measured by radioimmunoassay in 19 patients with cirrhosis, ascites, and severe hyponatremia (mean serum sodium, 121.8 mmol/l) and 11 patients with cirrhosis and normal serum sodium (mean, 137.6 mmol/l). Vasopressin levels were also assessed by radioimmunoassay in urine., Results: Patients with hyponatremia had higher plasma and urine vasopressin levels than patients with normal serum sodium concentrations (plasma, 2.9 versus 1.0 pg/ml, P = 0.0009; urine, 38.3 versus 12.3 ng/g creatinine, P = 0.0008). PRA was higher (4.8 versus 1.0 ng/ml/h, P = 0.0004) and plasma ANF lower (111.1 versus 148.7 pg/ml, P = 0.01) in patients with hyponatremia., Conclusions: These results indicate that plasma and urine vasopressin levels are inappropriately increased in patients with cirrhosis and severe hyponatremia. The concomitant increase of PRA and decrease of plasma ANF suggest that decreased 'effective' plasma volume generates nonosmotic stimuli for vasopressin hypersecretion in these patients.

We evaluated postnatal lung function and intravascular albumin loss to tissues of 123-days-gestation preterm surfactant-treated and ventilated lambs 15 h after direct fetal (n = 8) or maternal (n = 9) betamethasone treatment or saline placebo (n = 9). The betamethasone-treated groups had similar increases in dynamic compliances, ventilatory efficiency indexes, and lung volumes relative to controls (P < 0.05). The losses of 125I-labeled albumin from blood, a marker of intravascular integrity, and the recoveries of 125I-albumin in muscle and brain were similar for control and betamethasone-exposed lambs. Betamethasone-treated lambs had lower recoveries of 125I-albumin in lung tissues and in alveolar washes than did controls (P < 0.01). Although blood pressures were higher for the treated groups (P < 0.05), all groups had similar blood volumes, cardiac outputs, and organ blood flows. Maternal or fetal treatment with betamethasone 15 h before preterm delivery equivalently improved postnatal lung function, reduced albumin recoveries in lungs, and increased blood pressures. However, prenatal betamethasone had no effects on the systemic intravascular losses of albumin or did not change blood volumes.

We measured the physiological and biochemical responses of preterm lambs to intra-amniotic injection of interleukin-1 alpha (IL-1 alpha). Singleton lamb fetuses at 126 days of gestation were randomized to receive 125 micrograms IL-1 alpha or vehicle control via ultrasound-guided intra-amniotic injection. Each lamb was delivered 48 h later by caesarian section and ventilated for 120 min. Relative to controls, IL-1 alpha-treated lambs had higher dynamic compliance, ventilatory efficiency indices, and saturated phosphatidylcholine levels (all p < 0.05). Umbilical cord plasma cortisol and catecholamine levels, white blood cells and differentials, cardiac output, regional blood flow, and kidney function did not differ between the groups. However, at 120 min after delivery, the cortisol levels for IL-1 alpha-treated animal were higher than for controls. Single intra-amniotic IL-1 alpha treatment increases surfactant pool size and improves dynamic compliance in the absence of an inflammatory response or differences in other indicators of fetal or newborn organ function.

Unlabelled: These studies determined the effects of fetal treatment with betamethasone alone, or in combination with thyroid hormone (thyroxine; T4), on postnatal renal and endocrine adaptations in preterm newborn lambs. Ovine fetuses (126 d of gestation; term = 150 d) received single, ultrasound-guided intramuscular injections of saline, 0.5 mg/kg betamethasone (Celestone Soluspan, or 0.5 mg/kg betamethasone plus 60 micrograms/kg T4. After 48 h, lambs were delivered, treated with surfactant (Survanta, 100 mg/kg), and ventilated for 3 h. Due to maintained urine flow in the betamethasone-treated animals and a significant decrease in the saline group, betamethasone versus saline urine flow values (0.11 +/- 0.03 versus 0.03 +/- 0.004 mL.min-1.kg-1) were significantly elevated by the end of studies. GFR (1.5 +/- 0.3 versus 0.8 +/- 0.2 mL.min-1.kg-1) and mean blood pressure (61 +/- 4 versus 42 +/- 3 mm Hg) values also were higher in the betamethasone-treated animals. Although renal blood flow, renal plasma flow, and fractional sodium excretion rates did not differ, betamethasone versus saline values for the filtration fraction (11.9 +/- 1.5 versus 7.4 +/- 1.5%) and total sodium reabsorption (196 +/- 38 versus 81 +/- 16 microEq.min-1.kg-1) were increased. Betamethasone versus saline treatment also was associated with significant reductions in plasma angiotensin II (125 +/- 23 versus 550 +/- 140 pg/mL) and AVP (116 +/- 19 versus 230 +/- 77 pg/mL) levels. Overall, the effects of combined betamethasone + T4 treatment were similar to the effects of betamethasone alone., Conclusions: 1) fetal betamethasone injection 48 h before delivery stabilizes GFR and significantly alters endocrine function in preterm newborn lambs, and 2) the addition of T4 does not augment betamethasone-induced renal and endocrine responses.

Objectives: Although antenatal corticosteroids improve outcomes for preterm newborns, negative effects could result if preterm delivery does not occur. We investigated whether betamethasone treatment of preterm fetal sheep would alter cardiovascular, renal, and lung function after delivery at term., Methods: Preterm fetal lambs were randomized at 126-128 days' gestation to receive single doses of saline (n = 6) or 0.5 mg/kg betamethasone (n = 7) by ultrasound-guided fetal intramuscular injection. The lambs were delivered by cesarean at term, 20 days after fetal treatment, then ventilated for 4 hours to evaluate lung, cardiovascular, renal, and endocrine newborn adaptive responses, as well as responses to mild hypoxia., Results: Body and organ weights (brain, lung, heart, kidney, adrenal) were similar in the two groups. Values for blood gases and pH, mean arterial pressures, heart rates, glomerular filtration rates, renal osmolar clearance, and plasma cortisol, angiotensin II, epinephrine, and norepinephrine levels were similar between groups for 3 hours after delivery and before hypoxia. A 20-minute period of mild hypoxia resulted in increases in catecholamines, arginine vasopressin, and atrial natruretic factor in both betamethasone-treated and control lambs. However, hypoxia did not alter cardiovascular or lung function in either group. After reversal of hypoxia, measured physiologic parameters did not differ between groups. Kidney Na, K-adenosine triphosphatase activity was significantly higher for the betamethasone-treated lambs., Conclusion: Preterm fetal betamethasone administration does not alter neonatal pulmonary, cardiovascular, renal, or endocrine physiology after term delivery or in response to mild hypoxia.

In the late-gestation human or ovine fetus, daily swallowed volumes (100-300 ml/kg body weight) are markedly greater than adult values (40-60 ml/kg). This volume of amniotic fluid water, electrolytes and cellular debris is almost completely resorbed within the fetal gastrointestinal (GI) tract, resulting in the formation of meconium within the distal fetal colon. Despite this capacity for fetal GI water resorption, little is known regarding the sites or processes by which absorption occurs. We examined the composition of GI contents of 13 ovine fetuses (121-148 days). Fetuses were operatively delivered and killed and the Gi tract (rumen to sigmoid colon) was ligated in sections. Luminal samples were obtained and analysed for water and organic content and osmolality and electrolyte composition. The water content significantly decreased (98.7% to 70.1%) while the organic content significantly increased (55.0% to 95.3% of dry weight) from the rumen to colon. Osmolality significantly increased from the rumen to the distal small intestine (303 +/- 3 to 596 +/- 50 mOsm/kg) and returned to near isotonic values in the sigmoid colon. These results indicate significant water absorption within the fetal GI tract, with a pattern similar to that of the adult. However, fetal colonic sodium absorption is either suppresses or immature near term.

Objective: Fetal urine is the main source of amniotic fluid, and alterations in urine production have an impact on amniotic fluid dynamics. Intraamniotic arginine vasopressin is absorbed into fetal plasma, but fetal antidiuretic responses may be obscured by vasoconstrictor (V1 receptor) actions of arginine vasopressin. We determined the effects of intraamniotic administration of a specific V2 receptor agonist, deamino(D-Arg8)-vasopressin, on fetal plasma arginine vasopressin immunoreactivity, fetal urine output, and swallowing., Study Design: Six chronically prepared pregnant ewes (129 +/- 1 days' gestation) received a single deamino(D-Arg8) (50 micrograms injection into the amniotic fluid with subsequent measurement of fetal plasma arginine vasopressin immunoreactivity, fetal urine flow and osmolality, and fetal swallowing., Results: Within 30 minutes of deamino(D-Arg8)-vasopressin administration, fetal plasma arginine vasopressin immunoreactivity (4.5 +/- 0.5 to 76.4 +/- 21.9 pg/ml) and urine osmolality (135 +/- 13 to 285 +/- 43 mOsm/kg H2O) significantly increased and urine flow decreased (0.18 +/- 0.01 to 0.05 +/- 0.01 ml/kg per minute). After 48 hours urine flow remained reduced (0.08 +/- 0.03 mg/kg per minute) and osmolality remained elevated (399 +/- 18 mOsm/kg H2O). There were no changes in fetal swallowing, systolic (64 +/- 3 mm Hg) or diastolic (42 +/- 3 mm Hg) blood pressure, or heart rate (169 +/- 6 beats/min)., Conclusions: Intraamniotic deamino(D-Arg8)-vasopressin administration evokes persistent fetal antidiuresis in the absence of arginine vasopressin-induced fetal cardiovascular effects or changes in fetal swallowed volume, indicating its suitability as a potential therapeutic agent in amniotic fluid volume disorders such as polyhydramnios.