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Biomedical subjects

M G Ervin

Publications and source records attributed to M G Ervin.

At least 55 records · Page 3Linked to original sources

V1- and V2-receptor contributions to ovine fetal renal and cardiovascular responses to vasopressin.

To assess the contributions of arginine vasopressin (AVP) V1- and V2-receptors to the ovine fetal responses to AVP, we studied V2-receptor stimulation in the presence of V1-receptor blockade, and selective V2-receptor stimulation in chronically catheterized fetal lambs. AVP administration (20 ng/kg) to the saline infused fetuses (n = 8; 132 +/- 2 days) significantly increased mean arterial pressure (MAP; 45 +/- 2 to 53 +/- 4 mmHg) and urine osmolality (Uosm; 134 +/- 13 to 379 +/- 42 mosmol/kgH2O) and decreased heart rate (HR; 168 +/- 3 to 147 +/- 5 beats/min) and urine flow (V; 0.48 +/- 0.10 to 0.19 +/- 0.03 ml/min). V1-receptor antagonist infusion, [d(CH2)5,Tyr(Me)]AVP (n = 7; 134 +/- 1 days) had no effect on fetal MAP, Uosm, HR, or V. V1-receptor blockade abolished the MAP response to AVP without affecting the HR and urinary responses. In a second series of animals (n = 6; 131 +/- 1 days), selective V2-receptor agonist infusion [desmopressin (DDAVP)] had no effect on fetal MAP or HR while initial changes in V and Uosm were identical to the effects of AVP alone. Our results demonstrate clear discrimination of V1- and V2-receptor-mediated events in the fetal MAP and renal responses to AVP. Moreover, the HR response to AVP is not mediated by the population of V1-receptors blocked by [d(CH2)5,Tyr(Me)]AVP or V2-receptors stimulated by DDAVP, suggesting the presence of additional AVP receptor subclass(es) during fetal life.

Animals↗

Concentration thresholds for fetal swallowing and vasopressin secretion.

In adults, plasma osmolality thresholds for hypernatremia-induced arginine vasopressin (AVP) secretion are similar or less than thresholds for stimulation of thirst. In the fetus, the thresholds for swallowing stimulation and AVP secretion have not been defined. Fetal swallowing and AVP secretory responses to hypertonic NaCl and urea were determined in six fetuses (130 +/- 1 1 days) chronically prepared with thyrohyoid, nuchal and thoracic esophagus, and diaphragm electromyograms (EMG), an esophageal flow probe, and vascular catheters. Fetuses received intracarotid injections (0.15 ml/kg) of increasing concentrations of NaCl (0.15, 0.30, 0.45, 0.60, 0.75, and 0.90 M), administered at 2-min intervals. A swallow was defined as a coordinated time-sequence of fetal thyrohyoid, nuchal esophagus, and thoracic esophagus EMG activity. The threshold saline concentration for swallowing was defined as the minimum NaCl dose eliciting swallow responses (within 20 s) after four of five injections at each dose. During a 2-h control period swallowing averaged 25.0 +/- 10.1 ml/h and 39.4 +/- 14.6 swallows/h. The mean NaCl threshold concentration for swallowing stimulation was 0.56 +/- 0.06 M. Fetal plasma AVP (2.6 +/- 0.9 pg/ml) increased significantly at the maximum subthreshold (7.6 +/- 4.0 pg/ml) and the threshold NaCl concentration (8.2 +/- 4.0 pg/ml) that stimulated swallowing. On a subsequent day, equiosmolar urea injections increased plasma AVP (from 2.2 +/- 0.7 to 7.6 +/- 2.6 pg/ml) but had no effect on swallowing activity. Fetal mean arterial blood pressure increased after injections of threshold saline and urea concentrations. Fetal arterial blood osmolality and sodium concentration did not change during any study.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Neurohypophyseal and pituitary-adrenocortical responses to the alpha 1 agonist methoxamine in humans.

To test the hypothesis that the release of neurohypophyseal peptides into plasma in humans is stimulated by a central nervous system (CNS) alpha 1 adrenergic mechanism, we measured the responses of arginine vasopressin (AVP) and oxytocin (OT) to intravenous methoxamine, an alpha 1 agonist which enters the CNS following peripheral administration. The potential confound of baroreceptor inhibition of AVP release by the pressor effect of methoxamine was addressed by measuring the plasma AVP response to infusion of norepinephrine (NE), an alpha 1 agonist which does not enter the CNS and which produced an equivalent pressor effect. We also assessed the pituitary adrenocortical system responses to methoxamine and norepinephrine infusions by measuring plasma ACTH and cortisol concentrations. In addition, plasma NE and epinephrine were measured. Methoxamine, but not NE, increased plasma AVP compared to placebo infusion. Neither methoxamine nor NE affected plasma OT. The AVP elevation was delayed until more than 60 min after the methoxamine infusion began and the peak AVP level occurred 30 min after cessation of the infusion. In contrast, ACTH and cortisol increased early during methoxamine infusion and ACTH returned to baseline promptly after the infusion ceased. Although it is possible that the AVP response to methoxamine reflected stimulation of AVP release at a CNS level, it is also possible that the AVP increase represented a rebound response to withdrawal of methoxamine.

Adrenal Cortex↗

Ovine maternal and fetal glomerular atrial natriuretic factor receptors: response to dehydration.

In pregnancy, dehydration produces marked effects on maternal and fetal body water homeostasis including an increase in fetal urinary sodium concentration and excretion. To examine the role of fetal plasma atrial natriuretic factor (ANF) and glomerular ANF receptors in dehydration-induced natriuresis, we compared plasma ANF levels and glomerular ANF binding characteristics in dehydrated and control maternal and fetal sheep. Mean (+/- SEM) maternal and fetal plasma ANF levels in control animals (n = 9) at 132-136 days gestation were 37 +/- 3 pg/ml and 138 +/- 20 pg/ml, respectively. Although mean ANF receptor maximum binding capacities (Bmax) were significantly higher in maternal than in fetal glomeruli (83 +/- 11 vs 34 +/- 12 fmol/mg protein, respectively), the dissociation constants (Kd) for ANF binding were not different (2.7 +/- 0.6 and 3.7 +/- 1.7 x 10(-10) M, respectively). In an additional 9 animals studied after 63 +/- 4 h of water deprivation, maternal plasma ANF levels were significantly lower than in the control group (14 +/- 4 vs. 37 +/- 3 pg/ml), maternal glomerular ANF receptor Bmax values were significantly higher (732 +/- 203 vs. 83 +/- 11 fmol/mg protein), and Kd values were six-fold higher (17.0 +/- 7.1 vs. 2.7 +/- 0.6 x 10(-10) M), although this difference was only marginally significant (p = 0.06). In contrast to the adult, there was a small, nonsignificant decrease in plasma ANF levels and no difference in Bmax or Kd values between the dehydrated and euhydrated fetal animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Vasopressin levels in infants during the course of aseptic and bacterial meningitis.

We measured urine vasopressin (VP) once daily on days 1 through 3 in 18 patients hospitalized with meningitis. Urine VP values were 215 +/- 100, 116 +/- 44, and 69 +/- 23 pg/mL on days 1 through 3, respectively, for children with bacterial meningitis and 34 +/- 14, 20 +/- 4, and 15 +/- 4 pg/mL for those with aseptic meningitis. Urinary VP levels of infants with bacterial meningitis were significantly greater than those of healthy ambulatory subjects (n = 18) on all three study days; VP values of infants with bacterial meningitis were also greater than those of infants with aseptic meningitis on study days 2 and 3. The VP levels for the subjects with aseptic meningitis were significantly greater than those of the controls on day 1 only. None of the infants exhibited the clinical syndrome of inappropriate antidiuretic hormone secretion.

Bacterial Infections↗

Amniotic fluid volume response to esophageal occlusion in fetal sheep.

Although ovine and human fetuses swallow considerable volumes of fluid, the impact of absence of fetal swallowing on amniotic fluid volume regulation is unclear. To study the role of fetal swallowing on urine production and amniotic fluid, seven ovine fetuses (126 +/- 1 days) were chronically prepared with fetal bladder and vascular catheters, an esophageal flow probe, an inflatable esophageal cuff, and amniotic fluid catheters. In the five fetuses that underwent esophageal ligation after the control period, fetal swallowing averaged 0.27 ml/min before occlusion. In response to esophageal occlusion, significant increases were noted in fetal plasma arginine vasopressin (6.9 +/- 2.6 to 16.6 +/- 4.4 pg/ml) and urine osmolality (159 +/- 1 to 324 +/- 30 mOsm/kg), whereas urine volume (0.25 ml/min) did not change. Amniotic fluid volume increased nearly threefold after 3 days of esophageal occlusion (582 +/- 180 to 1530 +/- 271 ml). Amniotic fluid volume remained normal (334 to 419 ml) in the one fetus in which the occluder did not inflate. In the one fetus in which the esophagus was occluded at surgery, amniotic fluid volume was increased after the surgical recovery period (1489 ml). These data indicate an important role of fetal swallowing in amniotic fluid homeostasis and the potential interaction of swallowing with fetal urine production.

Amniotic Fluid↗

Fetal and maternal plasma atrial natriuretic factor responses to angiotensin II infusion.

Plasma atrial natriuretic factor and angiotensin II have opposing actions in the regulation of body fluid homeostasis and systemic blood pressure. Angiotensin II infusions stimulate atrial natriuretic factor release in some, but not all, studies in adult mammals. To examine the response during the perinatal period, graded intravenous angiotensin II infusions were administered to four chronically instrumented pregnant ewes and fetuses (132 +/- 1 days of gestation). Fetuses received successive 20-minute intravenous angiotensin II infusions at 25, 50, and 100 ng/kg/min. After a 90-minute recovery, maternal ewes received successive 20-minute angiotensin II infusions (5, 10, and 25 ng/kg/min). During the fetal infusions, mean (+/- SEM) fetal arterial blood pressure (47 +/- 2 to 61 +/- 2 mm Hg, p less than 0.05) and heart rate (155 +/- 16 to 196 +/- 36 beats/min, p less than 0.05) increased, although there was no change in maternal measured parameters. In response to the maternal infusion, maternal mean arterial blood pressure increased (92 +/- 7 to 110 +/- 8 mm Hg, p less than 0.05) and maternal heart rate decreased (136 +/- 4 to 125 +/- 2 beats/min, p less than 0.05) without change in fetal parameters. Fetal plasma atrial natriuretic factor levels (210 +/- 27 to 664 +/- 250 pg/ml, p less than 0.05) significantly increased during the fetal angiotensin II infusions in spite of no change in maternal plasma atrial natriuretic factor (85 +/- 21 to 124 +/- 22 pg/ml) during the maternal angiotensin II infusions. These findings indicate that similar increases in systemic blood pressure in response to angiotensin II infusions stimulate increased fetal, but not maternal, plasma atrial natriuretic factor.

Angiotensin II↗

Ovine fetal renal and hormonal responses to changes in plasma epinephrine.

Circulating epinephrine alters atrial natriuretic factor (ANF) and arginine vasopressin (AVP) secretion, and all three hormones influence renal function. To quantify the relationships among fetal plasma epinephrine levels, fetal ANF and AVP secretion, and fetal renal function, six chronically catheterized fetal lambs (132 +/- 1 days gestation) received successive 40-min epinephrine infusions (0.1, 0.4, and 1.8 micrograms.min-1.kg-1). The second epinephrine infusion dose evoked significant increases in urine flow (V; 0.7 +/- 0.2 to 1.2 +/- 0.2 ml/min), free water clearance (CH2O; 0.3 +/- 0.1 to 0.7 +/- 0.1 ml/min), glomerular filtration rate (GFR; 3.9 +/- 0.7 to 5.4 +/- 0.8 ml/min), fractional water excretion (V/CH2O; 19 +/- 3 to 25 +/- 2%), mean arterial pressure (MAP; 45 +/- 3 to 51 +/- 4 mmHg), and a 94% increase in plasma ANF levels. A fourfold increase in the infusion dose significantly increased osmolar clearance (0.3 +/- 0.1 to 0.6 +/- 0.1 ml/min), sodium excretion (28 +/- 8 to 53 +/- 13 mueq/min), and plasma AVP levels (2.4 +/- 0.5 to 6.4 +/- 2.4 pg/ml) with no additional effect on V, CH2O, GFR, V/GFR, MAP, or plasma ANF levels. Urine osmolality and fractional sodium excretion did not change in response to epinephrine infusion. Our results demonstrate that epinephrine infusion stimulates fetal ANF secretion and to a lesser extent AVP secretion and significantly influences fetal renal function.

Animals↗

Fetal renal response to atrial natriuretic factor decreases with maturation.

The presence of atrial natriuretic factor (ANF) in fetal tissues and plasma early in gestation suggests that ANF may have a physiological role in cardiocirculatory homeostasis in utero. However, reported responsiveness of the fetal kidney to ANF varies markedly. To characterize the ontogeny of fetal renal responsiveness to ANF, chronically catheterized ovine fetuses at 114 +/- 1 days (n = 6) and 131 +/- 1 days (n = 6) received successive (30 min each) intravenous infusions of ANF at rates of 5, 25, and 100 ng.min-1.kg-1. Mean (+/- SE) fetal plasma ANF levels increased from 328 +/- 54 to 1,866 +/- 482 and 521 +/- 135 to 1,579 +/- 295 pg/ml in the younger and more mature fetuses, respectively. Mean urine volume (0.17 +/- 0.03 to 0.37 +/- 0.09 ml.min-1.kg-1) and GFR (0.9 +/- 0.2 to 1.8 +/- 0.4 ml.min-1.kg-1) increased in the early gestation fetuses but did not change in the older fetuses. Mean urine sodium excretion and osmolar clearance increased by 352 and 155% in the early gestation fetal lambs and 118 and 50% in the older animals. The fetal plasma ANF clearance rates (PCANF) were lower in the early vs. the late gestation fetuses (68 +/- 15 vs. 116 +/- 28 ml.min-1.kg-1, respectively). These results demonstrate a decrease in fetal renal responsiveness to ANF with advancing fetal age. Multiple factors appear to contribute, including changes in PCANF and maturational changes in glomerular filtration rate, renal tubular function and ANF receptor metabolism.

Animals↗

Intraruminal rehydration of ovine fetuses.

During oral rehydration of adult mammals, oropharyngeal stimulation, the act of swallowing, and/or gastric factors contribute to a rapid decrease in plasma arginine vasopressin (AVP) that precedes plasma osmolality changes. To determine whether similar mechanisms are present in the developing fetus, six chronically prepared ovine fetuses were rehydrated with intraruminal (IR) distilled water infusions (1 ml.kg-1.min-1 for 60 min) after 43 +/- 3 h of maternal water deprivation. In response to maternal dehydration, significant increases were noted in maternal and fetal mean plasma osmolalities, sodium and AVP concentrations, and fetal urine osmolality. As estimated by hematocrit, fetal intravascular volume decreased by 11%. Fetal rehydration via IR distilled water infusion evoked a significant decrease in fetal plasma osmolality but no change in urine osmolality. Unexpectedly, fetal arterial blood pressure increased and arterial PO2 decreased while fetal hematocrit indicated a further 7% decrease in intravascular volume after the IR infusion. There was a nonsignificant trend toward increased fetal glomerular filtration rate, urine volume, and plasma AVP concentrations. Identical IR water infusions to five euhydrated fetuses resulted in significant decreases in fetal plasma osmolality and increases in glomerular filtration rate, urine flow, and osmolar excretion. The euhydrated fetuses also exhibited significant increases in mean arterial blood pressure and hematocrit and decreased fetal arterial PO2. These results indicate that IR water does not suppress AVP secretion in the dehydrated ovine fetus. Rather, both euhydrated and dehydrated fetuses exhibit an idiosyncratic vasoconstrictive response to IR water.

Animals↗

Fetal swallowing: response to graded maternal hypoxemia.

A computer-based system, incorporating electromyography (EMG) and esophageal fluid flow measurement, was used to determine fetal breathing and swallowing responses to graded maternal hypoxemia. Five chronically prepared ewes with singleton fetuses at a gestational age of 130 +/- 2 (SE) days were subjected to successive 30-min periods of mild and moderate hypoxemia (inspired O2 fraction = 0.16 and 0.13, respectively). Mild and moderate maternal hypoxemia evoked significant reductions in fetal arterial PO2 (21 +/- 1 to 17 +/- 1 and 13 +/- 1 Torr, respectively), while fetal arterial pH, hematocrit, plasma osmolality, heart rate, and mean blood pressure did not change. Moderate hypoxemia was associated with significant increases in fetal plasma arginine vasopressin and renin activity and significant reductions from basal values in percent time breathing (53 +/- 4 to 25 +/- 12%), percent time swallowing (11.5 +/- 3.1 to 1.3 +/- 0.7%), and volume swallowed (21.3 +/- 2.1 to 4.8 +/- 2.7 ml/30 min). Fetal swallowing activity was better correlated with arterial PO2 (r = 0.8) than breathing activity (r = 0.45). We conclude that fetal swallowing is suppressed during mild and moderate hypoxemia. It is suggested that several sites and/or mechanisms may account for the hypoxemic inhibition of fetal activities.

Animals↗

Ovine fetal breathing and swallowing activity in response to plasma glucose changes.

Fetal swallowing activity generally occurs simultaneously with fetal breathing movements (FBM) in sheep. The present study investigated the FBM and swallowing responses to altered fetal plasma glucose. Fetal lambs were chronically prepared with laryngeal, esophageal and diaphragm electromyogram (EMG) wires, an esophageal flow probe and vascular catheters. Beginning at 138 +/- 1 day, FBM and swallowing were monitored during control periods and in response to intravenous glucose infusions (14 mg/kg/min for 120 min) to fetuses of fed and fasted ewes. Glucose infusions to fetuses of fed ewes resulted in significant increases in fetal plasma glucose (21.2 +/- 0.7 to 40.5 +/- 1.9 mg/dl) and time breathing (46.2 +/- 6.3 to 60.0 +/- 9.5 min/2 h). In response to maternal fasting, fetal glucose levels (13.4 +/- 1.0 mg/dl) and time breathing (23.0 +/- 7.2 min/2 h) decreased significantly. Glucose infusion to fetuses of fasted ewes resulted in significant increases in time breathing (50.3 +/- 13.4 min/2 h) and diaphragmatic EMG activity (1,295 +/- 654 to 3,012 +/- 1,182 spikes/2 h). There was no change from basal levels of fetal EMG swallows (83.2 +/- 4.3 swallows/2 h) or esophageal flow (40.8 +/- 7.9 ml/2 h) in response to maternal fasting or fetal glucose infusions.

Animals↗

Ontogeny of atrial natriuretic factor receptors and cyclic GMP response in rabbit renal glomeruli.

Atrial natriuretic factor (ANF) has been identified in fetal and newborn mammals, and considerable data regarding fetal ANF metabolism are available. However, there is limited information concerning ANF receptors or receptor ontogenesis in developing mammals. We measured ANF receptor binding capacity, affinity, and ANF-induced cyclic GMP (cGMP) generation in isolated renal glomeruli from fetal (29 d gestation, term = 31 d), newborn (3 d), juvenile (28 d), and adult rabbits. The (mean +/- SEM) glomerular receptor binding capacity values for ANF in fetal and newborn animals (10 +/- 1 and 12 +/- 3 fmol/mg protein) were similar and significantly lower than the values for juvenile and adult animals (30 +/- 8 and 74 +/- 15 fmol/mg protein, respectively). In contrast, there were no significant differences in ANF receptor affinity values or dose-dependent increases in ANF-stimulated cGMP generation among the age groups studied. In competition studies, we observed effective displacement of 125I-ANF by C-ANF4-23, a ring-deleted ANF analogue, in adult, juvenile, and newborn glomeruli; however, C-ANF displaced only about 50% of the 125I-ANF in fetal tissue. The addition of C-ANF did not elicit cGMP generation, nor did C-ANF affect ANF-induced cGMP generation in fetal, newborn, or adult glomeruli. These results indicate that 1) the ANF receptor-guanylate cyclase system is intact in 29-d fetal rabbit glomeruli, and 2) the ANF-induced cGMP formation is similar in fetal and adult animals, whereas receptor binding capacity is relatively higher in adult glomeruli. These results suggest a higher proportion of nonguanylate cyclase-coupled ANF receptors in the mature rabbit.

Age Factors↗

Effect of a ring-deleted atrial natriuretic factor analogue on ovine fetal renal and cardiovascular function.

The proposed actions of atrial natriuretic factor (ANF) are mediated through specific plasma membrane (R1) receptors coupled to guanylate cyclase. A second receptor, R2, has been characterized by its ability to bind to an acyclic, truncated ANF analog (C-ANF4-23). The ANF-R2 receptor has not been identified in the fetus. Our study was conducted to determine the effects of C-ANF on fetal renal and cardiovascular function and plasma ANF clearance rates. Chronically catheterized ovine fetuses (n = 6) at 111 to 117 d gestation (term 145 d) received a C-ANF infusion (1 microgram/min/kg) for 30 min followed by a combined infusion of C-ANF and ANF (C-ANF, 1 microgram/min/kg; ANF, 100 ng/min/kg) for an additional 30 min. C-ANF infusion significantly increased (mean +/- SEM) plasma ANF concentration (437 +/- 45 to 1067 +/- 297 pg/mL), urinary flow rate (0.26 +/- 0.04 to 0.38 +/- 0.07 mL/min/kg), sodium excretion (12.9 +/- 3.5 to 21.7 +/- 6.1 mumol/min/kg), and osmolar clearance (0.14 +/- 0.02 to 0.21 +/- 0.04 mL/min/kg) (p less than 0.05). The combined C-ANF/ANF infusion further increased plasma ANF concentration to 2394 +/- 532 pg/mL and resulted in significant increases in urinary flow rate, sodium excretion, osmolar clearance, GFR, and free water clearance compared with C-ANF infusion alone (p less than 0.05). These renal responses, however, were not significantly different from the responses to ANF infusion alone (100 ng/min/kg).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Fetal and maternal response to intravenous infusion of a thromboxane synthetase inhibitor.

Pharmacologic inhibition of thromboxane synthetase activity has reversed the clinical manifestations of toxemia in the ovine model. To investigate placental transfer and fetal effects of a selective thromboxane synthetase inhibitor, CGS13080 (Ciba-Geigy, Summit, N.J.) was intravenously infused into eight singleton- or twin-bearing ewes near term. During CGS 13080 infusion (0.1 mg/kg/hr), maternal steady-state CGS 13080 levels of 102 +/- 18 ng/ml were achieved within 30 minutes and maternal serum thromboxane generation decreased significantly (13 +/- 3 to 4 +/- 1 ng/ml). However, fetal serum levels of CGS 13080 were only 4% of peak maternal concentrations and fetal serum thromboxane generation did not change. There was no evidence of change in uterine blood flow, maternal or fetal blood pressure, heart rate, blood gas values, or fetal or maternal metabolites of prostacyclin or prostaglandin E2 during the study. We speculate that CGS 13080 may be efficacious in the treatment of human pregnancy-induced hypertension.

Animals↗

Fetal swallowing: response to systemic hypotension.

The fetal swallowing and endocrine responses to systemic hypotension were studied in five chronically instrumented ovine fetuses (125 +/- 2 days). Fetuses were prepared with bipolar electrodes inserted in the thyrohyoid muscle, nuchal esophagus, and thoracic esophagus, a flow probe surrounding the thoracic esophagus, and arterial and venous catheters. In response to an intravenous infusion of sodium nitroprusside, fetal mean arterial blood pressure decreased from 50.8 +/- 3.6 to 41.7 +/- 3.8 mmHg. Fetal plasma renin activity (5.0 +/- 1.4-25.1 +/- 10.3 ng.ml-1.h-1) and arginine vasopressin (5.6 +/- 4.5-26.3 +/- 21.0 pg/ml) increased, while fetal swallowing electromyogram activity (7.3 +/- 1.1-1.9 +/- 0.3 swallows/10 min) and esophageal flow (5.5 +/- 3.1-1.2 +/- 0.9 ml/10 min) significantly decreased during the nitroprusside infusion. These results indicate a suppression of fetal swallowing in response to systemic hypotension despite stimulation of the renin-angiotensin system.

Animals↗

Fetal swallowing: correlation of electromyography and esophageal fluid flow.

Patterns of fetal drinking behavior were quantified in five singleton fetuses (128 +/- 1 days gestation) by computer analysis of laryngeal-esophageal electromyography (EMG) and thoracic esophageal fluid flow. Esophageal flow was noted to be bidirectional with an average antegrade flow-to-retrograde flow ratio of 4.4 +/- 1.5. Retrograde esophageal flow coincided with diaphragmatic contractions, suggesting that inspiratory gastroesophageal pressure gradients may be operative. The regurgitated fluid was returned to the fetal rumen by thoracic esophageal contractions. Significant net fluid intake was noted during periods of primarily unidirectional antegrade esophageal flow. Fetuses swallowed an average of 35 +/- 9 ml/h during the 12-h study, extrapolating to an average daily volume of 840 +/- 224 ml. An EMG "propagated swallow" representing coordinated contractions of the thyrohyoid, nuchal esophagus, and thoracic esophagus averaged 43 +/- 3 swallows/h and was highly correlated with net esophageal flow. Nearly 60% of the total fluid intake occurred during "bouts" of propagated swallows, which represented only 8% of the study period. Bouts averaged 11.7 +/- 0.4 propagated swallows, lasted 2.1 +/- 0.2 min, and occurred every 27.6 +/- 1.7 min. Although EMG swallowing activity was similar, there were significant differences among fetuses in net esophageal fluid flow and volume per propagated swallow. We speculate that fetal fluid intake is dependent on the availability and physical properties of the swallowed fluid, whereas swallowing activity is primarily related to cortical maturation and thirst stimulation.

Animals↗

Maternal dehydration: impact on ovine amniotic fluid volume and composition.

Maternal dehydration consistent with mild water deprivation or moderate exercise results in maternal and fetal plasma hyperosmolality and increased plasma arginine vasopressin (AVP). Previous studies have demonstrated a reduction in fetal urine and lung fluid production in response to maternal dehydration or exogenous fetal AVP. As fetal urine and perhaps lung liquid combine to produce amniotic fluid, maternal dehydration may affect the amniotic fluid volume and/or composition. In the present study, six chronically-prepared pregnant ewes with singleton fetuses (128 +/- 1 day) were water deprived for 54 h to determine the effect on amniotic fluid. Maternal plasma osmolality (306.5 +/- 0.9 to 315.6 +/- 1.9 mOsm/kg) and AVP (1.9 +/- 0.2 to 22.2 +/- 3.2 pg/ml) significantly increased during dehydration. Similarly, fetal plasma osmolality (300.0 +/- 0.9 to 312.7 +/- 1.7 mOsm/kg) and AVP (1.4 +/- 0.1 to 10.4 +/- 2.4 pg/ml) increased in parallel to maternal values. Amniotic fluid osmolality (276.8 +/- 5.7 to 311.6 +/- 6.5 mOsm/kg) and sodium (139.8 +/- 4.8 to 154.0 +/- 5.4 mEq/l) and potassium (9.1 +/- 1.3 to 13.9 +/- 2.4 mEq/l) concentrations increased while a significant (35%) reduction in amniotic fluid volume occurred (871 +/- 106 to 520 +/- 107 ml). These results indicate that maternal dehydration may have marked effects on maternal-fetal-amniotic fluid dynamics, possibly contributing to the development of oligohydramnios.

Amniotic Fluid↗