Biomedical subjects

R A Brace

Publications and source records attributed to R A Brace.

At least 19 recordsLinked to original sources

PubMed1992

A unique hypertonic response to hypotonic infusion in the pregnant ewe.

OBJECTIVE: The purpose of this study was to compare the responses of the maternal ewe to intravenous volume expansion with either sufficient lactated Ringer's solution to elevate maternal venous pressure or sufficient hypotonic fluid to reduce blood osmolality. STUDY DESIGN: Chronically catheterized pregnant sheep were intravenously infused over 4 hours with either commercial lactated Ringer's solution (5.55 +/- 0.50 L/hr, 255 mOsm/kg, mildly hypotonic) or diluted Ringer's solution (2.04 +/- 0.27 L/hr, 150 mOsm/kg, markedly hypotonic). Data were statistically analyzed with two- and three-factor analyses of variance and bivariate regression analysis. RESULTS: During the mildly hypotonic infusion (n = 8) the maternal blood osmolality changes were -5.1 +/- 1.2, +2.7 +/- 1.0 and +6.8 +/- 1.1 mOsm/kg at 1 and 4 hours of infusion and 1 hour after the infusion. In four of the eight animals in this group profuse diarrhea developed. During the markedly hypotonic infusion (n = 11) the maternal blood osmolality changes were -9.9 +/- 1.1, -15.9 +/- 2.5, and -10.4 +/- 2.2 mOsm/kg at 1 and 4 hours of infusion and 1 hour after the infusion. Although urine osmolalities were significantly less than the osmolality of the infusate in both groups, only during the mildly hypotonic infusion was there a net loss of free water by the kidneys. The renal free water loss, the venous pressure increase, and the blood osmolality decrease were not significantly different whether diarrhea did or did not develop. CONCLUSION: The infusion of large volumes of mildly hypotonic Ringer's solution to the pregnant ewe produces a paradoxic increase in maternal plasma osmolality as a result of the excretion of large volumes of free water by the kidneys, and if the venous pressure is increased more than about 6 mm Hg with this infusion, diarrhea develops in the animals.

Animals↗

PubMed1992

Indomethacin-induced urinary flow rate reduction in the ovine fetus is associated with reduced free water clearance and elevated plasma arginine vasopressin levels.

OBJECTIVE: The purpose of our study was to explore the urinary responses of the ovine fetus to indomethacin levels comparable with those used therapeutically in the human fetus. STUDY DESIGN: After a 1-hour control period, chronically catheterized ovine fetuses between 125 and 139 days of gestation were given an intravenous bolus of indomethacin (0.05 mg/kg estimated fetal weight) followed by a 0.0025 mg/kg/min continuous infusion for 5 hours. The experimental group (n = 9) was compared with a vehicle-only infusion group (n = 10). RESULTS: There was a sustained 55.7% +/- 9.5% (mean +/- SEM) decrease in urinary output by 2 hours of indomethacin infusion (p < 0.00001, analysis of variance). Urinary osmolality, potassium, and chloride concentrations underwent sustained increases during the infusion period (p < 0.005). Free water clearance decreased by 67.5% +/- 12.0% (p < 0.001). Fetal arterial pressure increased only transiently (p < 0.05), and increases in venous pressure (p = 0.013) and heart rate (p < 0.0001) were sustained. Fetal plasma arginine vasopressin concentration increased during indomethacin infusion (p < 0.05) and was correlated with the fall in urinary flow rate and free water clearance (p = 0.002). During vehicle infusion no significant changes were observed in any of the variables. CONCLUSIONS: Our data indicate that the fetus undergoes antidiuresis when exposed to low levels of indomethacin and that the observed antidiuresis is mediated by a decrease in free water clearance. The reduction in free water clearance may be mediated by increases in plasma arginine vasopressin concentrations.

Animals↗

PubMed1992

Amniotic fluid composition changes during urine drainage and tracheoesophageal occlusion in fetal sheep.

OBJECTIVE: Recently an intramembranous pathway was reported in the ovine fetus as a route for the rapid exchange of water, ions, and molecules between the amniotic fluid and the fetal blood that perfuses the fetal surface of the placenta and the fetal membranes. Our study was designed to test the hypothesis that the amniotic fluid composition would gradually equilibrate with fetal plasma when the major flows to and from the amniotic compartment were eliminated. STUDY DESIGN: Eleven near-term fetal sheep underwent ligation of the urachus to eliminate the allantoic fluid. An inflatable cuff was placed around the esophagus and trachea, and catheters were placed in the fetal urinary bladder, fetal circulation, and maternal circulation. At > or = 5 days after surgery the animals were subjected to either a control experiment or a continuous urine drainage plus tracheoesophageal occlusion for 8 hours. RESULTS: During the urine drainage plus occlusion study, amniotic fluid osmolality (p < 0.0001), Na+ (p < 0.0001), K+ (p < 0.01) Cl- (p < 0.001), and lactate (p < 0.001) increased compared with the control experiment. These corresponded to 50% reductions in the gradients for osmolality and Na+ between fetal plasma and amniotic fluid; the K+ gradient increased, and the Cl- gradient reversed. The percentage increases in amniotic Na+, K+, Cl-, and lactate were all 10% at 8 hours. CONCLUSION: These observations suggest that water is absorbed from the amniotic fluid through the intramembranous pathway into the fetal circulation at a rate of 1.25% of the total amniotic volume per hour or approximately 240 ml/day.

Allantois↗

PubMed1992

Vascularization of the ovine amnion and chorion: a morphometric characterization of the surface area of the intramembranous pathway.

OBJECTIVE: The purpose of this study was to characterize the vascularization of the ovine amnion, allantois, and chorion. STUDY DESIGN: A white silicone vascular casting material was infused into both umbilical arteries of nine fetal sheep ranging in age from 58 to 142 days' gestation. A morphometric analysis of photomicrographs of the membranes was then performed with computerized image analysis techniques. RESULTS: After removal of the uterus, the fetus was surrounded by a layer of white silicone-filled microvessels in the chorion. The amniotic membrane after separation from the chorion was covered by a fine mesh of microvessels, whereas the allantois was avascular. The amniotic membrane readily separated into an outer vascularized layer and an inner, avascular layer containing the amnion. Approximately 50% of the surface of the chorionic membrane was covered by microvessels; this appeared independent of gestational age. At midgestation 30% of the surface of the amnion was covered by microvessels, and this decreased to 17% at 142 days. Relative to fetal weight, the amniotic and chorionic vascular surface areas decreased from 6 to 0.3 and from 15 to 1.5 cm2/gm fetal weight, respectively, over the last half of gestation. CONCLUSIONS: There is an extensive network of microscopic fetal blood vessels within the ovine chorion and covering the outer surface of the amnion. These vessels appear to be ideally situated to facilitate a direct exchange of water and solutes between amniotic or allantoic fluids and fetal blood through the intramembranous pathway.

Allantois↗

PubMed1992

Urinary and cardiovascular responses to indomethacin infusion in the ovine fetus.

OBJECTIVE: Our objective was to explore the urinary and cardiovascular responses of the near-term ovine fetus to plasma indomethacin levels similar to those in the human neonate undergoing indomethacin therapy. STUDY DESIGN: Chronically catheterized ovine fetuses between 125 and 139 days of gestation were studied. After a 1-hour control period we gave a bolus of 0.35 mg/kg estimated fetal weight of indomethacin into a fetal vein, followed by a 0.017 mg/kg/min continuous infusion for 5 hours (n = 9). Results were compared with a vehicle-infusion-only group (n = 10). RESULTS: During the first 3 hours of indomethacin infusion, fetal urinary output was increased by an average of 84.9% +/- 55.6% (analysis of variance, p less than 0.01). Urinary osmolality and sodium and chloride concentrations underwent sustained increases throughout the infusion period (p less than 0.001). Sodium excretion increased by 212% +/- 111% (p less than 0.05). Fetal arterial and venous pressures increased (p less than 0.001), and the change in urinary flow correlated positively with the change in arterial pressure (R = 0.55, p = 0.014). Fetal heart rate increased by 10% +/- 4% 1 hour after the bolus and remained elevated throughout the remainder of the infusion relative to vehicle-infused animals (p less than 0.001). Vehicle infusion had no effect on any fetal variable. CONCLUSIONS: This study does not support the hypothesis that indomethacin acutely reduces urinary flow rate in the late-gestation ovine fetus. Further, the observed urinary flow increases may be mediated in part by a pressure diuresis.

Animals↗

PubMed1991

Elevated fetal plasma lactate produces polyhydramnios in the sheep.

In human fetuses with hemolytic diseases such as erythroblastosis fetalis, hydrops fetalis or polyhydramnios often develops. The mechanism(s) that produces these fluid imbalances is unknown, although lactate concentrations have been reported to be elevated in hydropic human fetuses with erythroblastosis. In this study we explored the role of lactate in producing fetal fluid imbalances. In seven near-term fetal sheep, we infused 5 mol/L sodium lactate at a rate of 10 mmol/hr for 3 days. Fetal plasma lactate rose by 6.0 +/- 1.0 (mean +/- SE) mmol/L above control. Fetal plasma osmolality and Na+ increased slightly, Cl- decreased, and bicarbonate rose in proportion to the Cl- decrease. Fetal renal lactate excretion was 1.1 +/- 0.3 mmol/hr while Na+ excretion was 10.6 +/- 1.9 mEq/hr. Fetal urine flow increased by 1.9 +/- 0.4 L/day and the urine remained hypotonic relative to fetal plasma throughout the infusion. Amniotic fluid lactate and Na+ rose during the infusion period and remained elevated during a 24-hour recovery period. Amniotic plus allantoic fluid volume at autopsy was 5.3 +/- 0.8 L compared with a normal of 0.5 to 1.0 L. There was little evidence of fetal edema. In summary, a moderate sustained elevation in fetal plasma lactate concentration appears to be a powerful osmotic agent for fetal accumulation of fluid from the maternal compartment over a period of days. This may be the primary mechanism whereby hydrops fetalis or polyhydramnios develops in severely anemic human fetuses.

Animals↗

PubMed1991

Left thoracic duct lymph flow responses to angiotensin II or atrial natriuretic factor infusion in the ovine fetus.

In the ovine fetus it is known that left thoracic duct lymph flow rate relative to body weight is four to five times adult levels, but it is not known whether the circulating hormones modulate fetal lymph flow. To explore this, we intravenously infused either angiotensin II (10 to 400 ng/min, n = 8) or atrial natriuretic factor (500 to 1000 ng/min, n = 8) into chronically catheterized fetal sheep for 30 minutes. Significant increases occurred in fetal arterial (p less than 0.0001) and venous (p = 0.018) pressures during the angiotensin II infusion, and thoracic duct lymph flow rate underwent a dose-dependent increase (r = 0.888, p = 0.0033). With termination of the angiotensin II infusion, fetal vascular pressures rapidly returned to control levels, and lymph flow fell from 18.8% +/- 10.1% (mean +/- SE) above control to 13.7% +/- 7.7% below preinfusion levels (p less than 0.01). During the atrial natriuretic factor infusion, fetal arterial pressure and circulating blood volume decreased significantly (p less than 0.01), whereas thoracic duct lymph flow was unchanged. After termination of the atrial natriuretic factor infusion, fetal arterial pressure returned toward control, blood volume remained reduced, and lymph flow rate underwent a transient rise to 35.6% +/- 15.7% (p less than 0.05) above control levels. These data suggest that angiotensin II and atrial natriuretic factor have significant but opposite effects on fetal thoracic duct lymph flow rate, with angiotensin II stimulating and atrial natriuretic factor suppressing lymph flow.

Angiotensin II↗

PubMed1991

Oral-nasal membranes are not the major route for fetal absorption of amniotic fluid arginine vasopressin.

Intraamniotically injected substances such as arginine vasopressin and digoxin have been found to rapidly appear in the ovine fetal circulation, irrespective of whether the fetal esophagus has been ligated or occluded. To determine if the ovine fetal oral-nasal membrane plays a significant role in this fetal absorption of amniotic substances, we used two groups of chronically catheterized fetal sheep with a surgical glove sewed over the fetal head to prevent access of the head to amniotic fluid. In the first group 22.5 micrograms of arginine vasopressin was injected into the amniotic cavity; in the second group 22.5 micrograms was injected into the glove over the fetal head. We found that, after injection into the amniotic cavity, there were rapid and highly significant increases in amniotic fluid arginine vasopressin concentrations, from 6.1 +/- 1.3 to 51,249 +/- 18,182 pg/ml (mean +/- SE) (p less than 0.00001). Concurrently there was a rapid increase in fetal plasma arginine vasopressin concentrations from 4.5 +/- 1.3 to 93.8 +/- 18.9 pg/ml (p less than 0.00001). The increase was significant within 15 minutes and reached a maximum at 60 minutes after the injection. Fetal arterial pressure increased by 10 +/- 2 mm Hg, whereas heart rate decreased by 30 +/- 5 beats/min (p less than 0.00001). In contrast, after the injection into the glove covering the fetal head, there were no significant changes in any of the measured parameters. This suggests that the ovine fetal oral-nasal membrane is not a significant route of absorption of amniotic fluid arginine vasopressin and that the most likely route of absorption is the vascularized fetal surface of the placenta and vascularized fetal membranes, i.e., the intramembranous pathway.

Absorption↗

PubMed1991

Hemorrhage-induced reductions in plasma atrial natriuretic factor in the ovine fetus.

To investigate the effects of blood volume reduction on fetal plasma atrial natriuretic factor concentrations, chronically catheterized ovine fetuses at 109 to 138 days' gestation were subjected either to withdrawal of two consecutive blood samples or to a moderate hemorrhage. In fetuses from which two blood samples of 3.5 ml each (approximately 1% of fetal blood volume) were withdrawn under basal conditions at 15- to 30-minute intervals, plasma atrial natriuretic factor concentrations in the second sample decreased by 17 +/- 7 pg/ml from 178 +/- 8 pg/ml in the first sample (p less than 0.02). If the fetal blood removed during the first sample was replaced with an equal volume of maternal blood, plasma atrial natriuretic factor concentrations did not change significantly. In these same samples, plasma arginine vasopressin and angiotensin II concentrations were unchanged between the two samples regardless of whether volume was replaced. In fetuses subjected to hemorrhages of 21% +/- 2% over 10 minutes without blood replacement, plasma atrial natriuretic factor concentration at 1.5 hours after hemorrhage was suppressed by 42 +/- 10 pg/ml from basal level of 139 +/- 9 pg/ml (p less than 0.05). Plasma atrial natriuretic factor returned to control levels by 5.5 hours after hemorrhage as blood volume returned to normal. Thus in the ovine fetus a reduction in blood volume results in a decrease in plasma atrial natriuretic factor concentrations. Also, atrial natriuretic factor appears to be more sensitive to changes in blood volume than other vasoactive hormones studied.

Angiotensin II↗

PubMed1991

Fetal cardiovascular and fluid responses to maternal volume loading with lactated Ringer's or hypotonic solution.

To determine whether elevations in maternal vascular pressures or reductions in maternal osmolality would promote fluid transfer to the fetus, we intravenously infused either lactated Ringer's solution or diluted (hypotonic) lactated Ringer's solution continuously over 4 hours into late-gestation pregnant sheep. During the Ringer's solution infusion, the increases in maternal arterial (20.7 +/- 1.7 mm Hg, mean +/- SE) and venous (6.6 +/- 0.9 mm Hg) pressures were significantly greater (p less than 0.00001) than those during the hypotonic infusion (6.6 +/- 1.5 and 1.7 +/- 0.6 mm Hg, respectively). The maternal osmolality changes during the Ringer's infusion (-5.7 +/- 1.2 mOsm/kg at 1 hour and +6.8 +/- 1.1 mOsm/kg at 1 hour and -15.9 +/- 2.5 mOsm/kg at 5 hours). Fetal vascular pressures and blood volume were unchanged during either infusion. Fetal heart rate decreased by 15 to 20 beats/min by 1.5 hours of infusion in both groups but remained decreased only in the hypotonic group. Fetal urine flow decreased at the end of the Ringer's infusion and increased during the hypotonic infusion. These urine flow changes correlated with opposite changes in fetal plasma osmolality. The four-quadrant amniotic fluid index tended to increase in both groups, with an overall nonsignificant increase of 32% +/- 16% 1 hour after the infusions. In summary, our findings suggest that (1) acute increases in maternal vascular pressures do not appear to promote fluid transfer to the ovine fetus and (2) acute decreases in maternal osmolality result in a small shift of fluid into the fetus as evidenced by an increase in fetal urine flow.

Amniotic Fluid↗

PubMed1991

Dose-dependent effects of angiotensin II on the ovine fetal cardiovascular system.

The purpose of this experiment was to establish dose-response relationships for the effects of angiotensin II on arterial pressure, venous pressure, heart rate, and blood volume in the ovine fetus. Chronically catheterized fetal sheep at 132 +/- 1 (SE) days' gestational age were infused with angiotensin II at 4.8 +/- 1.1 (n = 7), 27.7 +/- 4.6 (n = 7), 102.2 +/- 16.7 (n = 6), or 239.0 +/- 30.9 (n = 4) ng/min/kg fetal body weight for 30 minutes. Fetal arterial pressure increased at the three highest doses. Fetal venous pressure, heart rate, and blood volume responded only at 102.2 and 239.0 ng/min/kg. At 239.0 ng/min/kg, arterial pressure increased by 17.7 +/- 1.6 mm Hg (p less than 0.00001), venous pressure increased by 1.5 +/- 0.3 mm Hg (p less than 0.0005), blood volume decreased by 7.8 +/- 2.2% (p less than 0.0001), and heart rate initially decreased by 14 +/- 4 beats/min, followed by an increase of 52 +/- 17 beats/min from control (p less than 0.0005) at the end of angiotensin II infusion. Thus this study shows that angiotensin II affected multiple fetal cardiovascular variables in a dose-dependent manner, suggesting that it is an important regulatory hormone for the entire fetal cardiovascular system.

Angiotensin II↗

PubMed1991

Transplacental, amniotic, urinary, and fetal fluid dynamics during very-large-volume fetal intravenous infusions.

With rapid intravenous infusion of very large volumes of isotonic saline solutions into the fetus, the fluid could stay within the fetal body, thereby creating hydrops fetalis, be transferred into the amniotic fluid through the fetal kidneys, thereby creating polyhydramnios, or be transferred across the placenta into the maternal circulation. This study was designed to explore these possibilities. After a 1-hour control period, 10 near-term chronically catheterized ovine fetuses were infused intravenously with 4 L (greater than 100% of fetal weight) of either isotonic saline solution or lactated Ringer's solution over 4 hours. Fetal arterial pressure was significantly elevated by 7 mm Hg throughout the infusion (p less than 0.00001). Venous pressure underwent a transient rise (4.8 mm Hg) at 20 minutes of infusion and remained elevated (2.7 mm Hg) during the rest of the infusion (p less than 0.00001). Fetal urine flow increased by an average of 5.7 +/- 0.4 ml/min throughout the infusion (p less than 0.00001) and accounted for 34.1% +/- 2.6% of the infused volume. Estimated fetal extracellular fluid volume increased by 17.7% +/- 1.8% of the infused volume. Because fetal fluid retention, urine flow, and amniotic fluid volume changes accounted for only half of the infused fluid, the remainder of the infused volume must have crossed the placenta and entered the maternal circulation. Given the above changes in vascular pressures, this requires a filtration coefficient of the placenta 50 to 100 times the previously reported values. Thus we conclude that relatively small changes in fetal vascular pressures dramatically alter the filtration capacity of the ovine placenta and transplacental volume flow.

Amniotic Fluid↗

PubMed1991

Rapid intramembranous absorption into the fetal circulation of arginine vasopressin injected intraamniotically.

Recently an intramembranous pathway was reported in the ovine fetus as a route for the movement of a significant volume of water from the amniotic cavity directly into the fetal blood, which perfuses the fetal membranes and fetal surface of the placenta. To test whether this pathway could be an avenue for the movement of arginine vasopressin from the amniotic cavity into the fetal circulation, we injected 1 to 25 micrograms of arginine vasopressin into the amniotic cavity of two groups of chronically catheterized fetal sheep: a control group of seven animals and a group of seven animals with surgical ligation of the fetal esophagus. We found similar and highly significant increases of arginine vasopressin concentrations in both control and surgically ligated fetuses in amniotic fluid (p less than 0.00001), fetal plasma (p less than 0.0001), and fetal urine (p less than 0.0001). Both groups had similar increases in arterial (p less than 0.0001) and venous (p less than 0.003) pressures with simultaneous decreases in urine flow (p less than 0.001) and heart rate (p less than 0.0001) after the intraamniotic injection of arginine vasopressin. We conclude that amniotic arginine vasopressin can be rapidly absorbed in its biologically active form directly into the fetal circulation through the intramembranous pathway. Furthermore, the observation that esophageal ligation did not alter this absorption suggests that the intramembranous pathway may be important in the regulation of amniotic fluid volume and composition.

Absorption↗

PubMed1991

Fetal fluid responses to long-term 5 M NaCl infusion: where does all the salt go?

The fetus must obtain Na and Cl ions in order to grow. However, the regulation of electrolyte acquisition by the fetus is not well understood. To explore fetal electrolyte balance, we intravenously infused 5 M NaCl at a rate equal to 80% of the total fetal body Na+ and Cl- content per day (240 mM/day) for 3 days into late-gestation fetal sheep. We hypothesized that the increase in fetal osmolality resulting from the infusion would cause a transplacental water movement into the fetal compartment, leading to hydrops fetalis and/or polyhydramnios. The fetal-to-maternal osmotic gradient was initially -2.8 +/- 0.9 (SE) mosmol/kgH2O and rose by 4.8 +/- 1.8 mosmol/kgH2O during the infusion. Fetal plasma [Na+] and [Cl-] increased (3.0 +/- 0.4 and 5.5 +/- 0.5 meq/l, respectively), but the normal maternal-to-fetal transplacental concentration gradients for these ions were not reversed. Most of the infused Na+ (92 +/- 14%) and Cl- (82 +/- 12%) was excreted by the fetus in large volumes of hypotonic urine. Amniotic fluid osmolality and [Na+] were unchanged, but amniotic [Cl-] increased 5.7 +/- 2.4 meq/l. The amniotic plus allantoic fluid volume, as estimated by ultrasonography, was increased (43.5 +/- 14.5%) at day 2 and returned to control by day 3 of infusion. There was no fetal edema during the study or at autopsy. In light of these results, we propose a novel and somewhat complex mechanism for transplacental fluid and electrolyte movement in which placental capillary permeability increases along the length of the capillary.(ABSTRACT TRUNCATED AT 250 WORDS)

Amniotic Fluid↗

PubMed1991

Diurnal rhythms in fetal urine flow, vascular pressures, and heart rate in sheep.

Conflicting indirect data exist as to whether diurnal variations occur in fetal urine flow rate. In addition, the extent of diurnal rhythms in fetal venous pressure or arterial pressure is unknown, although 24-h rhythms do exist in fetal heart rate. In the present study, we used on-line computer techniques to continuously monitor these variables in chronically catheterized ovine fetuses. Fetal urine flow rate and vascular pressures were successfully recorded in 6 of 11 animals over a 24-h period on 21 days out of a total of 45 days of monitoring. We found highly significant diurnal variations in fetal urine flow rate (P less than 10(-6). Hourly means displayed a maximum at 2130 h and a minimum at 1330 h with a maximum amplitude of 28 +/- 5% of the 24-h mean. A secondary maximum (at 0630 h) and minimum (at 0330 h) of smaller amplitude also occurred. There were simultaneous and highly significant (P less than 0.0001) diurnal rhythms in fetal arterial pressure (+/- 2%), venous pressure (+/- 7%), and heart rate (+/- 5%). The maxima in arterial pressure and heart rate occurred within 1 h of the maximum in urine flow, while venous pressure changes were opposite those in arterial pressure. Hourly mean urine flow correlated significantly with arterial pressure but not venous pressure or heart rate, suggesting that the observed 24-h variations in fetal urine flow rate may be partially mediated by a pressure diuresis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

The development of hydrops fetalis in the ovine fetus after lymphatic ligation or lymphatic excision.

Sixteen ovine fetuses underwent either ligation or excision of the left thoracic, left cervical, and left brachiocephalic lymphatic ducts. Our purpose was to test the hypothesis that interruption of lymphatic flow would lead to hydropic changes in the ovine fetus. Of the 11 animals in the group that underwent ligation, hydrops developed in 1. All five of the fetuses that underwent excision of these major lymphatic ducts were hydropic at the time of autopsy (3 to 7 days), with 62 to 502 ml of free fluid collected from the thoracic and abdominal cavities. The mean edema fluid total protein concentration in the hydropic fetuses was 2.6 gm/dl. This value was 71% to 94% of that found in the plasma, suggesting that the fetus is capable of producing new plasma proteins at a high rate. The observation that lymphatic excision led to hydropic changes in the ovine fetus, whereas ligation did not consistently produce hydrops, suggests that fetal lymph vessels may be capable of very rapid regrowth over short distances. Thus lymphatic excision, but not ligation, produces an animal model for the study of hydrops fetalis.

Analysis of Variance↗

PubMed1990

Role of vasopressin in mediation of fetal cardiovascular responses to acute hypoxia.

The present study was designed to test the hypothesis that arginine vasopressin mediates the fetal cardiovascular response to acute hypoxia. Chronically catheterized sheep fetuses at 126 to 138 days' gestation were infused with either an arginine vasopressin pressor antagonist (n = 8) or saline solution as control (n = 8). A 30-minute hypoxia was induced by infusion of nitrogen containing 5% carbon dioxide into the maternal trachea. Fetal arterial PO2 decreased 13.1 +/- 1.3 (SE) mm Hg from a basal value of 23.8 +/- 1.5 mm Hg and there was no significant difference in the degree of hypoxia between the two groups. Fetal arterial and venous pressures increased significantly, whereas the blood volume decreased, but these changes were similar between the control and arginine vasopressin-blocked fetuses. Heart rate fell similarly in both groups during hypoxia by an average of 35 beats/min. At the termination of hypoxia, heart rate in the blocked group rebounded to levels significantly above baseline and remained elevated for 30 minutes, whereas heart rate in the control group returned slowly to basal values. Recovery of arterial pressure, venous pressure, and blood volume were similar in the two groups. Thus it appears that arginine vasopressin may mediate in part the fetal heart rate response to acute hypoxia. However, the blood volume, arterial pressure, and venous pressure responses to hypoxia appear to be induced by factors other than arginine vasopressin.

Animals↗

PubMed1990

Fetal blood volume restoration following rapid fetal hemorrhage.

In a previous study, we found that ovine fetal blood volume returned to normal in 3 h after a slow hemorrhage of 31% over 2 h; volume was slightly elevated at 24-25 h. In the present study, we explored the time required for blood volume restoration in late gestation fetal sheep following a rapid hemorrhage over 10 min. The rate of hemorrhage was constant within each fetus but varied among fetuses from 13.5 to 32.2%. Two fetuses that were hemorrhaged 32% of their initial blood volume over 10 min underwent cardiovascular collapse during the hemorrhage. In 10 fetuses that were hemorrhaged 21.0 +/- 1.7% (SE) over 10 min, 6.5 h were required for blood volume to return to control. Fetal arterial pressure, venous pressure, and heart rate decreased during and immediately after the hemorrhage and returned to normal within 1 h. Plasma arginine vasopressin (AVP) concentration and plasma renin activity (PRA) underwent large increases following the rapid hemorrhage. Volume restoration at 5-7 h posthemorrhage correlated negatively with PRA and norepinephrine (NE) concentration immediately after the hemorrhage. Three of the 10 fetuses died overnight, and in the remaining seven fetuses blood volume was 8.8 +/- 3.3% below control (P less than 0.01) at 24-25 h posthemorrhage. The fetuses were also hypoxic, acidotic, and had greatly elevated plasma AVP and NE concentrations at this time. We conclude that ovine fetuses are less able to survive a rapid hemorrhage compared with a slow hemorrhage of the same extent. In addition, fetal blood volume restoration is delayed after rapid hemorrhage, and the impaired restoration is to the detriment of the fetus.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗