Fetal swallowing: response to graded maternal hypoxemia

1991 ◽  
Vol 71 (5) ◽  
pp. 1856-1861 ◽  
Author(s):  
D. J. Sherman ◽  
M. G. Ross ◽  
L. Day ◽  
J. Humme ◽  
M. G. Ervin
Keyword(s):  
Flow Measurement ◽  
Plasma Osmolality ◽  
Fetal Plasma ◽  
Percent Time ◽  
Arterial Ph ◽  
Fetal Breathing ◽  
Computer Based ◽  
Plasma Arginine ◽  
Arterial Po2 ◽  
Fluid Flow Measurement

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.

Intraruminal rehydration of ovine fetuses

1991 ◽  
Vol 261 (6) ◽  
pp. R1381-R1387
Author(s):  
M. G. Ross ◽  
D. J. Sherman ◽  
M. G. Ervin ◽  
L. Day
Keyword(s):  
Blood Pressure ◽  
Glomerular Filtration Rate ◽  
Filtration Rate ◽  
Plasma Osmolality ◽  
Urine Osmolality ◽  
Distilled Water ◽  
Intravascular Volume ◽  
Fetal Plasma ◽  
Arterial Blood ◽  
Arterial Po2

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.

Maternal/fetal dehydration: prolonged effects and responses to oral rehydration

1993 ◽  
Vol 264 (1) ◽  
pp. R197-R203 ◽  
Author(s):  
C. L. Agnew ◽  
M. G. Ross ◽  
Y. Fujino ◽  
M. G. Ervin ◽  
L. Day ◽  
...  
Keyword(s):  
Atrial Natriuretic Factor ◽  
Filtration Rate ◽  
Plasma Osmolality ◽  
Maternal Plasma ◽  
Urine Flow ◽  
Fetal Blood ◽  
Water Access ◽  
Oral Rehydration ◽  
Fetal Plasma ◽  
Plasma Arginine

Dehydration induces marked alterations in maternal-fetal fluid homeostasis and accompanying fetal endocrine responses. We sought to determine if the increase in fetal plasma arginine vasopressin (AVP) levels during maternal dehydration is mediated by fetal plasma hypovolemia in addition to hyperosmolality and to examine maternal and fetal plasma atrial natriuretic factor (ANF) responses to maternal dehydration and oral rehydration. Seven pregnant ewes (127 +/- 1 day) were water deprived for 72-96 h, and five of these were orally rehydrated. Dehydration induced significant increases in maternal plasma osmolality (pOSM) (300 +/- 2 to 325 +/- 8 mosmol/kg) and AVP (3.0 +/- 0.4 to 18.9 +/- 4.0 pg/ml), and decreases in plasma ANF levels (28.1 +/- 3.1 to 19.7 +/- 3.1 pg/ml). Fetal pOSM (293 +/- 3 to 314 +/- 4 mosmol/kg), AVP (2.5 +/- 0.6 to 8.1 +/- 4.8 pg/ml), and urinary fractional sodium excretion increased significantly, whereas plasma ANF and fetal blood volume did not change. After maternal water access maternal plasma AVP decreased rapidly in comparison to the gradual decrease in maternal pOSM. Fetal plasma AVP levels did not change significantly and fetal pOSM decreased more slowly than maternal pOSM. Fetal plasma ANF increased in association with increased urine flow and glomerular filtration rate after maternal rehydration. These data indicate marked differences in fetal and maternal plasma ANF and AVP responses with dehydration-induced increases in fetal plasma AVP being secondary to plasma hyperosmolality, rather than hypovolemia. Rapid suppression of maternal plasma AVP may contribute to the slower equilibration of fetal pOSM during oral, as compared with intravenous, maternal rehydration.

Effect of mild hypocapnia on fetal breathing and behavior in unanesthetized normoxic fetal lambs

1994 ◽  
Vol 76 (4) ◽  
pp. 1476-1480 ◽  
Author(s):  
I. M. Kuipers ◽  
W. J. Maertzdorf ◽  
D. S. De Jong ◽  
M. A. Hanson ◽  
C. E. Blanco
Keyword(s):  
Low Voltage ◽  
Blood Gases ◽  
Electromyographic Activity ◽  
Fetal Life ◽  
Fetal Sheep ◽  
Arterial Ph ◽  
Fetal Breathing ◽  
The Mean ◽  
And Behavior ◽  
Arterial Po2

We hypothesized that the level of arterial PCO2 (PaCO2) affects the incidence of fetal breathing movements and electrocorticographic (ECoG) states in chronically instrumented fetal sheep. Six fetuses of 128–132 days gestational age were instrumented for recording fetal behavior and for later connection to an extracorporeal membrane oxygenation (ECMO) system to change fetal blood gases. Before ECMO fetal arterial pH and blood gases were pH 7.40 +/- 0.01, PaCO2 42.9 +/- 1.5 Torr, and arterial PO2 (PaCO2) 19.2 +/- 1.7 Torr; during ECMO in normocapnia they were pH 7.37 +/- 0.01, PaCO2 46.1 +/- 0.7 Torr, and PaCO2 27.6 +/- 3.0 Torr; and during ECMO in mild hypocapnia they were pH 7.47 +/- 0.01, PaCO2 35.3 +/- 1.7 Torr, and PaCO2 26.6 +/- 1.7 Torr. The overall incidence of breathing movements, the incidence of breathing movements during low-voltage (LV) ECoG activity, and the mean duration of periods of breathing decreased significantly during hypocapnia. Fetal ECoG activity showed normal cycling during the periods of mild hypocapnia, and the mean duration of LV ECoG periods did not change. During mild hypocapnia, eye movements remained associated with LV ECoG activity and nuchal electromyographic activity remained associated with high-voltage ECoG activity. These results suggest that the presence of breathing movements in fetal life is not only dependent on the behavioral state but also on the level of fetal PaCO2.

Hypoxic inhibition of breathing in fetal sheep: relationship to brain adenosine concentrations

1994 ◽  
Vol 77 (6) ◽  
pp. 2734-2739 ◽  
Author(s):  
B. J. Koos ◽  
B. A. Mason ◽  
O. Punla ◽  
A. M. Adinolfi
Keyword(s):  
Brain Stem ◽  
Fetal Brain ◽  
Normal Incidence ◽  
Halothane Anesthesia ◽  
Microdialysis Probe ◽  
Fetal Sheep ◽  
Arterial Ph ◽  
Fetal Breathing ◽  
Fetal Breathing Movements ◽  
Arterial Po2

Because hypoxic inhibition of fetal breathing may be caused by a rise in central adenosine levels, the effects of O2 deficiency on fetal brain adenosine concentrations were determined at levels of hypoxia that inhibited fetal breathing. Under halothane anesthesia, the brains of fetal sheep (0.8 term) were implanted with guide cannulas exteriorized through a Silastic rubber window in the uterus and flank of the ewe. At least 4 days after surgery, a microdialysis probe was inserted into a cannula with the membrane tip placed in the rostral brain stem. During 1 h of isocapnic hypoxia, mean fetal arterial PO2 was reduced from 24.0 +/- 0.9 Torr (control) to 13 +/- 0.6 Torr and arterial pH fell progressively from 7.354 +/- 0.007 to 7.273 +/- 0.023. Hypoxia decreased the incidence of fetal breathing movements from 33 +/- 5.2 to 5 +/- 2.2 min/h, with a normal incidence (29 +/- 3.5 min/h) during the hour after arterial PO2 returned to control values. Adenosine concentrations in microdialysis perfusate under control conditions averaged approximately 35 nM, increased up to 2.3-fold during the hour of O2 deficiency, and fell toward control values when normoxia was restored. We conclude that fetal brain adenosine levels are increased at levels of O2 deficiency that inhibit fetal breathing, which are results consistent with a role for adenosine in hypoxic inhibition of fetal breathing.

Placental and renal control of plasma osmolality in chronically cannulated ovine fetus

1987 ◽  
Vol 253 (3) ◽  
pp. R389-R395 ◽  
Author(s):  
M. K. Towstoless ◽  
M. Congiu ◽  
J. P. Coghlan ◽  
E. M. Wintour
Keyword(s):  
Water Retention ◽  
Water Flux ◽  
Plasma Osmolality ◽  
Maternal Plasma ◽  
Water Transfer ◽  
Osmotic Gradient ◽  
Rapid Infusion ◽  
Fetal Plasma ◽  
Ovine Fetus ◽  
Plasma Arginine

This study investigated placental and renal control of plasma osmolality in mature (greater than 120 days, term 142-152 days) and immature (less than 120 days) chronically cannulated ovine fetuses. A transplacental osmotic gradient was generated by the rapid infusion of 20% mannitol (500 ml) into each of 20 pregnant cross-bred Merino ewes on at least two occasions. Maternal plasma osmolality increased by 29.2 +/- 1.0 (n = 29) mosmol/kg water (means +/- SE). Fetal plasma osmolalities increased to the same extent [14.8 +/- 0.9 (n = 29)] in immature and mature fetuses despite significantly higher plasma arginine vasopressin (AVP) concentrations [24.3 +/- 3.6 (n = 13) vs. 13.6 +/- 1.6 (n = 12) pg/ml] and significantly greater renal water retention in mature than immature fetuses (8.7 +/- 1.7 vs. 4.4 +/- 0.8 ml/h, P less than 0.05). Infusion of AVP intravenously to the fetus, at rates of 35-140 ng/h, for 1 h before the maternal mannitol did not alter fetal plasma osmolality. AVP, infused at 35-140 ng/h during the maternal mannitol infusions, did not alter fetal plasma osmolality increases. The conclusions are that 1) placental water transfer is the major determinant of fetal plasma osmolality and 2) the experiments suggest that placental water flux in the sheep is not regulated by endogenous or exogenous AVP.

Fetal endocrine responses to prolonged hypoxemia in sheep

1990 ◽  
Vol 259 (4) ◽  
pp. R703-R708 ◽  
Author(s):  
S. B. Hooper ◽  
C. L. Coulter ◽  
J. M. Deayton ◽  
R. Harding ◽  
G. D. Thorburn
Keyword(s):  
Blood Flow ◽  
Time Course ◽  
Arterial Oxygen Saturation ◽  
Arterial Oxygen ◽  
Plasma Norepinephrine ◽  
Uterine Blood Flow ◽  
Fetal Plasma ◽  
Arterial Ph ◽  
Fetal Breathing ◽  
Fetal Breathing Movements

Our aim was to characterize the pattern of release of epinephrine, norepinephrine, arginine vasopressin (AVP), cortisol (hydrocortisone), and prostaglandin E2 (PGE2) into the fetal circulation during prolonged reductions in uterine blood flow (RUBF). In five sheep RUBF was induced for 24 h, whereas in another five sheep (controls) uterine blood flow was not reduced. Fetal arterial oxygen saturation was decreased from 60.5 +/- 3.6 to 20.3 +/- 1.6% after 2 h of RUBF and remained significantly reduced for the entire RUBF period. The incidence of fetal breathing movements (FBM) and fetal arterial pH were reduced from 36.7 +/- 4.5 min/h and 7.36 +/- 0.01 to 4.3 +/- 1.8 min/h and 7.13 +/- 0.02, respectively, after 2 h of RUBF, but both had returned to control levels after 14 h. Fetal plasma AVP and epinephrine concentrations were increased from 4.4 +/- 0.5 pg/ml and 0.19 +/- 0.05 ng/ml to 333.8 +/- 41.5 pg/ml and 1.5 +/- 0.6 ng/ml, respectively, after 2 h and then declined to near control levels after 12 h of RUBF. Fetal plasma norepinephrine and cortisol concentrations were increased from 1.3 +/- 0.4 and 4.0 +/- 2.2 ng/ml to 6.1 +/- 1.8 and 13.5 +/- 4.1 ng/ml, respectively, after 2 h of RUBF, and both remained significantly elevated throughout the remainder of the RUBF period. Fetal plasma PGE2 concentrations progressively increased (from 1.9 +/- 0.4 to 8.8 +/- 1.7 nmol/l at 12 h) as the duration of RUBF increased and were still significantly elevated after 24 h. The time course for the increase in PGE2 during RUBF was very similar to the increases in arterial pH and in the incidence of FBM.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Increases in Plasma ACTH and Cortisol after Hypertonic Saline Infusion in Patients with Central Diabetes Insipidus

2001 ◽  
Vol 86 (12) ◽  
pp. 5749-5754 ◽  
Author(s):  
Eiji Itagaki ◽  
Sachihiko Ozawa ◽  
Shinya Yamaguchi ◽  
Kenji Ushikawa ◽  
Teruaki Tashiro ◽  
...  
Keyword(s):  
Diabetes Insipidus ◽  
Hypertonic Saline ◽  
Plasma Osmolality ◽  
Central Diabetes Insipidus ◽  
Portal System ◽  
Plasma Acth ◽  
Acth Secretion ◽  
Acth Concentration ◽  
Plasma Arginine ◽  
Hypertonic Saline Infusion

To clarify the mechanism for the potentiation of CRH-induced ACTH response by the infusion of hypertonic saline, we investigated changes in plasma ACTH concentration after infusion of 5% hypertonic saline in five patients with untreated central diabetes insipidus (DI). Basal levels of plasma ACTH and cortisol in the DI group were not significantly different from those in normal control subjects. The infusion of hypertonic saline produced an increase in plasma arginine vasopressin (AVP) in controls, but did not elevate ACTH. However, in patients with DI, the plasma AVP concentration did not change, but circulating ACTH increased 3.6-fold (7.7 ± 1.5 to 23.0 ± 2.7 pmol/liter; P < 0.01), and plasma cortisol also increased significantly (298 ± 99 to 538 ± 124 nmol/liter; P < 0.05). Moreover, a positive correlation was observed between plasma ACTH and osmolality (r = 0.72; P < 0.005). These results indicate that ACTH secretion in DI patients is regulated by a mechanism distinct from that in healthy subjects. It seems possible that the increase in plasma osmolality promotes ACTH secretion in DI patients through AVP and/or urocortin via the hypophyseal portal system, independent of the AVP secretion from magnocellular neurons.

Acid-base balance and plasma composition in the aestivating lungfish (Protopterus)

1977 ◽  
Vol 232 (1) ◽  
pp. R10-R17 ◽  
Author(s):  
R. G. DeLaney ◽  
S. Lahiri ◽  
R. Hamilton ◽  
P. Fishman
Keyword(s):  
Plasma Osmolality ◽  
Respiratory Acidosis ◽  
Electrolyte Balance ◽  
Plasma Composition ◽  
Total Plasma ◽  
Acid Base Balance ◽  
Acid Base ◽  
Plasma Bicarbonate ◽  
Arterial Ph ◽  
Base Balance

Upon entering into aestivation, Protopterus aethiopicus develops a respiratory acidosis. A slow compensatory increase in plasma bicarbonate suffices only to partially restore arterial pH toward normal. The cessation of water intake from the start of aestivation results in hemoconcentration and marked oliguria. The concentrations of most plasma constituents continue to increase progressively, and the electrolyte ratios change. The increase in urea concentration is disproportionately high for the degree of dehydration and constitutes an increasing fraction of total plasma osmolality. Acid-base and electrolyte balance do not reach a new equilibrium within 1 yr in the cocoon.

Prompt recovery of plasma arginine vasopressin in diabetic coma after intravenous infusion of a small dose of insulin and a large amount of fluid

1990 ◽  
Vol 122 (4) ◽  
pp. 455-461 ◽  
Author(s):  
San-e Ishikawa ◽  
Toshikazu Saito ◽  
Koji Okada ◽  
Shoichiro Nagasaka ◽  
Takeshi Kuzuya
Keyword(s):  
Blood Volume ◽  
Serum Protein ◽  
Arginine Vasopressin ◽  
Small Dose ◽  
Plasma Osmolality ◽  
Diabetic Coma ◽  
Diabetic Patients ◽  
Volume Depletion ◽  
Circulating Blood Volume ◽  
Plasma Arginine

Abstract. We studied the changes in plasma arginine vasopressin in 5 patients with diabetic ketoacidosis and one patient with non-ketotic hyperosmolar coma who had marked hyperglycemia (36.6 ± 4.6 mmol/l, mean ± sem) and dehydration. Plasma osmolality (Posm) was 342.2 ± 11.4 mOsm/kg H2O, and hematocrit, serum protein, and blood urea nitrogen were also elevated at hospitalization. Circulating blood volume was decreased by approximately 21% as compared with that on day 7. Plasma AVP level was increased to 8.5 ± 1.6 pmol/l at hospitalization. When hyperglycemia was improved by iv infusion of a small dose of insulin plus fluid administration, plasma AVP level promptly decreased to 2.4 ± 0.4 pmol/l within six hours. When plasma AVP level had normalized, Posm was still as high as 305 mOsm/kg H2O, but the loss of circulating blood volume was only 4.2% of the control state. Plasma AVP level was positively correlated with change in hematocrit (plasma AVP = 3.58 + 0.45 · hematocrit, r = 0.468, p < 0.01), serum protein (r = 0.487, p < 0.01), Posm (r = 0.388, p < 0.01), and blood glucose (r = 0.582, p < 0.01). Plasma AVP level was negatively correlated with the change in circulating blood volume (plasma AVP = 3.6 – 0.14 · change in circulating blood volume, r = −0.469, p <0.01). These results indicate that both non-osmotic and osmotic stimuli are involved in the mechanism for AVP release in patients with diabetic coma, and that the non-osmotic control of AVP may contribute to circulating homeostasis, protecting against severe blood volume depletion in diabetic patients suffering from hyperglycemia and dehydration.

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