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Biomedical subjects

C Y Cheung

Publications and source records attributed to C Y Cheung.

At least 19 recordsLinked to original sources
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

Autonomic and arginine vasopressin modulation of the hypoxia-induced atrial natriuretic factor release in immature and mature ovine fetuses.

OBJECTIVE: This study investigated the maturational change in the atrial natriuretic factor response to hypoxia in ovine fetuses and the role of the autonomic nervous system and arginine vasopressin in modulating this response. STUDY DESIGN: Chronically catheterized ovine fetuses from 110 to 135 days' gestation were subjected to 30 minutes of hypoxia. The fetuses were either intact, treated with hexamethonium to block the autonomic nervous system, or treated with a pressor antagonist of arginine vasopressin. RESULTS: Hypoxia elevated plasma atrial natriuretic factor levels by 1635 +/- 265 pg/ml in immature fetuses; this response was greater than the increase of 748 +/- 189 pg/ml in mature fetuses (p < 0.0001). Blockade of the autonomic nervous system reduced the atrial natriuretic factor response and suppressed the vascular pressure changes to hypoxia in immature but not in mature fetuses. A vasopressin pressor antagonist suppressed the atrial natriuretic factor but not vascular pressure responses to hypoxia in mature fetuses. CONCLUSIONS: This study demonstrates that the immature fetus manifested a greater atrial natriuretic factor response to hypoxia than did the mature fetus. This enhanced response appeared to be dependent on the modulatory effects of the autonomic nervous system on vascular pressures during hypoxia. In addition, arginine vasopressin appeared to augment the atrial natriuretic factor response to hypoxia in the mature fetus independent of vascular pressure changes.

Animals↗
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

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

Role of endogenous atrial natriuretic factor in the regulation of fetal cardiovascular and renal function.

The purpose of the present study was to determine whether endogenous atrial natriuretic factor participates in the maintenance of normal vascular pressure and renal function in ovine fetuses at 128 to 130 days' gestation. Circulating atrial natriuretic factor in the fetus was immunoneutralized by an intravenous bolus injection of an atrial natriuretic factor antiserum at a dilution of 1:2000 (low dose, n = 7) or 1:400 (high dose, n = 6). In the high-dose group, plasma atrial natriuretic factor concentration was significantly reduced by 65 +/- 14 pg/ml from basal levels of 165 +/- 12 pg/ml within 10 minutes and remained reduced for the 90-minute period after the injection. Fetal arterial pressure acutely and transiently decreased, but at 50 minutes arterial pressure increased and was elevated for the remainder of the experiment. Urine flow and urinary excretion rates of sodium, potassium, and chloride were reduced within 10 minutes after the injection. Urine flow rate was suppressed for as long as plasma atrial natriuretic factor concentrations were reduced. Fetuses in the low-dose and control groups showed no significant change in cardiovascular or renal function. In response to atrial natriuretic factor antiserum injection, plasma angiotensin II concentrations were increased, whereas plasma arginine vasopressin concentrations were unchanged. These results suggest that endogenous atrial natriuretic factor is involved in the maintenance of arterial pressure and urinary excretion in the ovine fetus.

Angiotensin II↗
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↗
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↗
PubMed1990

Temporal relationships among fetal urine flow, ANF, and AVP responses to hypertonic infusions.

The fetal urine flow response to acute increases in osmolality may be mediated by changes in the plasma concentrations of atrial natriuretic factor (ANF), arginine vasopressin (AVP), and/or angiotensin II (ANG II). To explore this, hypertonic NaCl or mannitol was infused intravascularly over 10 min into chronically catheterized fetal sheep and their mothers simultaneously, followed by a 2-h maternal infusion at 1-2 ml/min to maintain the elevated osmolality. Fetal osmolality rose by 16 mosmol/kgH2O during 13% mannitol and 2.5% NaCl infusions and by 57 mosmol/kgH2O during 7% NaCl infusions. Large increases in fetal urine flow occurred in the three groups with peak flows (average of 304%, P less than 10(-6)) at 0-4 min after the end of the infusion. Flow declined to preinfusion values in all groups at 30-40 min. These changes in urine flow occurred in parallel with a rise (to 223%, P less than 10(-6)) and fall in plasma ANF concentrations. One hour after the infusions, urine flow declined to 50% of control concomitant with elevations in plasma AVP (to 414%, P less than 10(-6)), whereas plasma ANG II concentration did not change. Thus the initial increase in fetal urine flow in response to acute hypertonic infusions is temporally related to a rise in fetal plasma ANF, whereas the subsequent fall in urine flow is temporally related to a fall in plasma ANF and a simultaneous rise in AVP concentration. This suggests that ANF may contribute to the acute urine flow increase after hypertonic infusion, whereas AVP appears to be more important for the long-term regulation of fetal urine flow.

Animals↗
PubMed1990

Fetal adrenal medulla catecholamine response to hypoxia-direct and neural components.

In the fetus, the adrenal medullary catecholamine responses to hypoxia are mediated by direct and neural mechanisms. The present study determined the maturation of these responses in unanesthetized ovine fetuses from 109 to 136 days gestation. In intact fetuses at 109-119 days gestation, hypoxia lowered arterial PO2 from 23.4 +/- 0.9 to 9.5 +/- 0.4 mmHg and induced acute increases in plasma norepinephrine (P less than 10(-5)) and epinephrine (P less than 10(-5)) concentrations. Fetuses at 130-136 days gestation showed similar changes in PO2 and plasma catecholamines as in younger fetuses. Blockade of neural input to the adrenal by hexamethonium (25 mg/kg) reduced but did not eliminate the increases in plasma norepinephrine and epinephrine concentrations in fetuses at 109-119 days gestation, while it completely abolished these responses in fetuses at 130-136 days gestation. These results suggest that in unanesthetized ovine fetuses a direct response of the adrenal medulla to hypoxia is present at 110 days gestation. In contrast, at 130 days gestation the response to hypoxia is entirely neurally mediated. Thus neural innervation to the ovine fetal adrenal medulla matures before 110 days gestation, much earlier than previously reported.

Adrenal Medulla↗
PubMed1989

Direct adrenal medullary catecholamine response to hypoxia in fetal sheep.

The present study was designed to investigate the direct response of fetal adrenomedullary cells to hypoxia, and the possible change in this responsiveness with maturation. Ovine fetal adrenomedullary cells, when exposed to 30 min of hypoxia induced by perfusing with Krebs-Henseleit solution equilibrated with 1% O2, released significantly greater amounts of total catecholamine into the perfusate, compared to basal conditions. After a 1-h control period, a second 30-min hypoxic episode stimulated a catecholamine response which was significantly smaller in magnitude than the first. Following the two hypoxic episodes, the cells were capable of responding to 50 mM KCl with a large increase in total catecholamine release. During the first hypoxic episode, the release of both norepinephrine and epinephrine was stimulated by equal magnitude. Fetal adrenomedullary cells obtained from fetuses at 100, 120, and 130 days gestation showed similar responsiveness to the same hypoxic stimulus, and these responses were not different from that observed in maternal adrenomedullary cells. On the contrary, responsiveness to KCl-induced depolarization was greatest in cells obtained from fetuses at 130 days gestation when compared to that in the younger fetuses. This increased responsiveness to KCl was accompanied by a greater catecholamine store in the adrenal medulla of the fetuses at this gestational age. These results suggest that ovine fetal adrenomedullary cells can respond directly to hypoxia by releasing catecholamines. This direct responsiveness became desensitized after repeated exposure. Finally, a decrease in direct responsiveness to hypoxia associated with maturation could be demonstrated.

Adrenal Medulla↗
PubMed1989

Hyperosmolality elevates plasma atrial natriuretic factor in the ovine fetus.

This study was designed to explore the effect of hyperosmolality on fetal plasma atrial natriuretic factor (ANF) concentrations in chronically catheterized sheep fetuses averaging 133 days gestation. An isotonic solution of 0.9% NaCl or hypertonic solution of 2.5% NaCl, 13% mannitol, or 7% NaCl was infused intravascularly into the fetuses at 20 ml/kg over 10 min and simultaneously into their mothers. Fetal plasma osmolality changed by -2 +/- 1 (SE) mosmol/kg in the isotonic group and by 16 +/- 2, 20 +/- 4, and 56 +/- 3 mosmol/kg in the 2.5% NaCl, 13% mannitol, and 7% NaCl groups, respectively (P less than 0.00001). Preinfusion fetal ANF levels were similar in all four groups and averaged 145 +/- 7 (SE) pg/ml. With infusion, fetal plasma ANF increased significantly in the isotonic group by 28 +/- 6%. In the 2.5% NaCl and 13% mannitol groups, the increment in plasma ANF was four times, whereas in the 7% NaCl group it was eight times that in the isotonic group (P less than 0.01). Blood volume and venous pressure changes were similar in all groups. In the hypertonic groups, plasma ANF and venous pressure returned to control levels within 1 h after the start of the infusion, whereas plasma osmolalities remained elevated. Thus infusions of hypertonic solutions into the ovine fetus caused much greater increases in plasma ANF concentrations compared with those seen with isotonic infusion. The return of plasma ANF levels to control despite maintained hyperosmolality suggests that hyperosmolality stimulated ANF release either by a direct but transient mechanism or by potentiating the effects of vascular volume expansion.

Animals↗
PubMed1989

Modulation of fetal cardiovascular responsiveness to norepinephrine by autonomic nervous system.

To determine the extent to which the autonomic nervous system modifies the fetal cardiovascular responses to exogenous norepinephrine (NE), NE was infused intravenously (0.39-39 micrograms/min) for 30 min into chronically catheterized sheep fetuses averaging 132 days gestation. The resulting changes in arterial pressure, venous pressure, heart rate, and blood volume were compared between fetuses with and without ganglionic blockade. Autonomic blockade did not alter the relationship between the rise in NE concentration and NE infusion rate. In fetuses with a blocked autonomic nervous system, the arterial pressure response to exogenous NE was shifted 0.8 log units to the left when compared with normal fetuses. The venous pressure response to NE infusion was not altered in the blocked fetuses when compared with normal fetuses. Heart rate in the autonomically blocked fetuses increased with plasma NE concentration, which was opposite to the initial suppression of heart rate during NE infusion in control fetuses. Fetal blood volume decreased progressively with increasing NE infusion rate in the blocked fetuses, which was similar in autonomically intact fetuses, except for an increase in blood volume at low NE infusion rates. Thus it appears that the autonomic nervous system modifies the fetal arterial pressure, heart rate, and blood volume responses to exogenous NE but not the response of venous pressure.

Animals↗
PubMed1989

Fetal cardiovascular, endocrine, and fluid responses to atrial natriuretic factor infusion.

The purpose of this study was to determine the effects of atrial natriuretic factor (ANF) in the fetus and to explore the interactions among the fetal cardiovascular, endocrine, and fluid responses to ANF. In 12 chronically catheterized fetal sheep at 130 +/- 1 (SE) days gestation, ANF was infused intravenously for 30 min at 14-300 ng.min-1.kg-1. Fetal arterial plasma ANF concentration increased by 174 to 5,410 pg/ml from a preinfusion value of 163 +/- 13 pg/ml. The clearance of ANF from the circulation was 122 +/- 28 ml.min-1.kg-1 and the half-life was 0.46 +/- 0.07 min. When plasma ANF was greater than 2,000 pg/ml, fetal arterial pressure decreased, venous pressure increased transiently, and heart rate was unchanged. Plasma arginine vasopressin (AVP) concentration and plasma renin activity (PRA) increased with high ANF concentrations, while norepinephrine concentrations were unaffected. Fetal blood volume decreased in all fetuses, and urine flow increased significantly but not in every fetus. Blood and urine osmolalities did not change. On terminating the infusion, venous pressure and urine flow decreased below control, while blood volume and arterial pressure remained reduced. Plasma AVP concentration increased further, and this was accompanied by an increase in urine osmolality. Thus the most consistent effect of ANF in the fetus was a reduction in blood volume, which was independent of urine flow changes. Other cardiovascular, endocrine, and fluid responses to ANF as well as interactions among them appeared to occur largely at supraphysiological concentrations and may be secondary to the changes in blood volume.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Adrenal growth and ontogeny of adrenal substance P, enkephalins and catecholamines in the ovine fetus.

Biologically active peptides have been identified in the adrenal glands of several adult mammalian species. Some of these peptides appear to modulate the nicotine-induced catecholamine release from the adrenal medulla. The present study was carried out to investigate the presence and ontogeny of the peptides substance P, met-enkephalin and leu-enkephalin in the ovine fetal adrenal gland from 70 to 140 days gestation (term = 145-150 days). Concurrently, the growth of the fetal adrenal as well as the gestational changes in catecholamine content were determined. The maternal adrenal glands were also studied for comparison. The ovine fetal adrenal gland increased in weight with advancing gestation at a single exponential rate. Total adrenal substance P content correlated with gestational age, while met-enkephalin, leu-enkephalin and total catecholamine contents correlated with adrenal weight. The adrenal content (normalized as per unit protein) of substance P was highest in the young fetuses at 70 days gestation, decreased progressively towards term and, in the adult levels were significantly lower than those measured in the fetuses. The contents of met-enkephalin and leu-enkephalin were low in the young fetuses at 70 days gestation, but reached high levels at 130 to 140 days gestation. Maternal adrenal contents of the two enkephalins were significantly lower than those measured in the near-term fetal adrenal. Total catecholamine content in the fetal adrenal medulla increased as the fetus matured. Norpinephrine was the primary catecholamine present in the medulla of fetuses at 70 and 80 days gestation, while epinephrine was the major one in the adult.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗
PubMed1988

Fetal hypoxia elevates plasma atrial natriuretic factor concentration.

Acute hypoxia in the fetus is associated with a reduction in fetal blood volume. We hypothesized that atrial natriuretic factor in the fetal circulation may be one of the factors that mediate this blood volume decrease. Thus the present study was designed to determine the effects of hypoxia on circulating concentrations of atrial natriuretic factor in fetal sheep and correlate these changes with fetal blood volume. Hypoxia was induced in chronically catheterized sheep fetuses by infusing nitrogen containing CO2 into the trachea of the ewe for 30 minutes. Fetal arterial PO2 decreased by 10.2 +/- 1.3 (SE) mm Hg. Plasma atrial natriuretic factor concentration rose concurrently with the fall in PO2 such that atrial natriuretic factor increased to 565 +/- 196 pg/ml from a basal level of 127 +/- 13 pg/ml (p less than 0.001). Fetal blood volume was reduced by 7.2% +/- 2.1% and was significantly related to changes in atrial natriuretic factor levels (p less than 0.0001). At the termination of hypoxia, PO2 returned to normal levels before plasma concentrations of atrial natriuretic factor fell to baseline values. Therefore fetal hypoxia appears to be a potent stimulus for elevating plasma concentration of atrial natriuretic factor in the fetus, and this rise in atrial natriuretic factor in the circulation may be partially responsible for the reduction in fetal blood volume observed during hypoxia.

Animals↗