Effects of restricting uteroplacental blood flow on concentrations of corticotrophin-releasing hormone, adrenocorticotrophin, cortisol, and prostaglandin E2 in the sheep fetus during late pregnancy

1992 ◽  
Vol 70 (10) ◽  
pp. 1396-1402 ◽  
Author(s):  
Alicia Sue-Tang ◽  
Alan D. Booking ◽  
A. Nigel Brooks ◽  
Stuart Hooper ◽  
Susan E. White ◽  
...  
Keyword(s):  
Blood Flow ◽  
Umbilical Vein ◽  
Arterial Oxygen Saturation ◽  
Control Level ◽  
Arterial Oxygen ◽  
Prostaglandin E ◽  
Uterine Blood Flow ◽  
Concentration Difference ◽  
Releasing Hormone ◽  
Fetal Plasma

We have examined the effects of reduced uterine blood flow and prolonged fetal hypoxemia on the temporal relationship between changes in hormones associated with the activity of the pituitary–adrenal axis (corticotrophin-releasing hormone (CRH), adrenocorticotrophin (ACTH), cortisol, and prostaglandin E2 (PGE2)) in the ovine fetus at 120–125 days of pregnancy, and we sought evidence for placental secretion of CRH and ACTH during prolonged hypoxemia. Uterine blood flow was reduced by placing an adjustable Teflon clamp around the maternal common internal iliac artery to decrease fetal arterial oxygen saturation from mean values of 59.1 ± 3.3 to 25.7 ± 4.6% (±SEM, n = 10). There was a transient peak in immunoreactive (IR-) CRH at 1–2 h after reducing uterine blood flow. IR-ACTH rose to peak values at +2 h, then gradually decreased to control level by +12 h. Fetal plasma cortisol and PGE2 concentrations were elevated significantly by +2 and +4 h, respectively, and at 20–24 h. The identity of IR-CRH in fetal plasma and in ovine placental extracts was confirmed by HPLC, but there was no consistent umbilical vein – femoral arterial concentration difference for either IR-CRH or IR-ACTH during normoxemia or hypoxemia. We conclude that a sequence of endocrine changes involving CRH, ACTH, PGE2, and cortisol occurs in the fetus during a prolonged reduction in uterine blood flow. However, we did not obtain evidence, for placental secretion of either CRH or ACTH in response to this manipulation.Key words: fetus, adrenocorticotrophin, corticotrophin-releasing hormone, prostaglandin E2, placenta.

scholarly journals Fetal endocrine responses to prolonged reduced uterine blood flow are altered following bilateral sectioning of the carotid sinus and vagus nerves

1998 ◽  
Vol 157 (1) ◽  
pp. 149-155 ◽  
Author(s):  
PE Stein ◽  
SE White ◽  
J Homan ◽  
L Fraher ◽  
HH McGarrigle ◽  
...  
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Carotid Sinus ◽  
Arterial Oxygen Saturation ◽  
Cardiovascular Responses ◽  
Arterial Oxygen ◽  
Uterine Blood Flow ◽  
Vagus Nerves ◽  
Fetal Sheep ◽  
Fetal Plasma

The present study examines the effect of carotid sinus/vagosympathetic denervation on fetal endocrine responses to prolonged reduced uterine blood flow (RUBF). Fetal sheep had vascular catheters inserted following bilateral sectioning of the carotid sinus and vagus nerves (denervated, n = 7) or sham denervation (intact, n = 7). Uterine blood flow was mechanically restricted at 126.1 +/- 0.7 days (mean +/- S.E.M.) for 24 h, decreasing arterial oxygen saturation by 47.3 +/- 2.6% (P < 0.01). Fetal plasma samples were obtained at -1, 3, 6, 12 and 24 h for subsequent analyses of arginine vasopressin (AVP), angiotensin II and catecholamines. The AVP response to prolonged RUBF was markedly attenuated in denervated fetuses (15.6 +/- 3.6 to 34.9 +/- 6.0 pg/ml) when compared with intact (10.0 +/- 1.4 to 127.3 +/- 28.4 pg/ml). In contrast, intact fetuses demonstrated no change in plasma angiotensin II concentrations with RUBF whereas denervated fetuses demonstrated a marked increase from 47.5 +/- 18.9 to 128.7 +/- 34.2 pg/ml. The norepinephrine and epinephrine responses to prolonged RUBF were attenuated in denervated fetuses (950.1 +/- 308.9 and 155.8 +/- 58.5 to 1268.3 +/- 474.6 and 290.6 +/- 160.2 pg/ml respectively) when compared with intact (1558.3 +/- 384.4 and 547.3 +/- 304.7 pg/ml to 3289.2 +/- 1219.8 and 896.8 +/- 467.8 pg/ml respectively). These results support a role for the peripheral chemoreceptors in mediating fetal endocrine responses to prolonged RUBF, which may in part lead to the altered cardiovascular responses observed in denervated fetuses under these conditions.

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)

Fetal neuromuscular blockade: effect on oxygen demand and placental transport

1989 ◽  
Vol 257 (3) ◽  
pp. H734-H738
Author(s):  
R. B. Wilkening ◽  
D. W. Boyle ◽  
G. Meschia
Keyword(s):  
Blood Flow ◽  
Oxygen Saturation ◽  
Neuromuscular Blockade ◽  
Umbilical Vein ◽  
Oxygen Demand ◽  
Arterial Oxygen ◽  
Uterine Blood Flow ◽  
Umbilical Blood ◽  
Steady State Method ◽  
Umbilical Blood Flow

To study mechanisms by which variations in fetal oxygen demand alter fetal oxygen saturation and PO2, we measured uterine and umbilical blood flow and transplacental oxygen diffusion rate in eight chronically prepared pregnant ewes before and during fetal neuromuscular blockade with pancuronium bromide (0.2 mg/kg). Uterine and umbilical blood flows were measured by applying the steady-state method using ethanol as the test substance. Fetal oxygen uptake decreased 7.5% (P less than 0.05). Umbilical blood flow increased 6% (P less than 0.05), whereas uterine blood flow did not change significantly. Fetal arterial oxygen saturation increased markedly (54.8–60.9%; P less than 0.001). There were also significant increases in umbilical vein oxygen saturation (83.6–86.9%; P less than 0.01), uterine vein oxygen saturation (70.7–72.2%; P less than 0.01), umbilical vein PO2 (29.4–32.1 Torr; P less than 0.001), and uterine vein PO2 (49.4–50.7 Torr; P less than 0.01). The uterine-umbilical venous PO2 difference decreased significantly (20.0–18.6 Torr; P less than 0.001), whereas there was no significant change in the uterine-umbilical venous PCO2 difference or in the umbilical ethanol shunt. The data indicate that follows a small decrease in fetal oxygen demand is caused by two aspects of placental oxygen transport: 1) umbilical and uterine blood flow do not react homeostatically to prevent the rise of PO2 in the placental circulation, and 2) the decrease in oxygen flux from placenta to fetus is associated with a decrease in the transplacental PO2 gradient.

Prostaglandin E2 inhibition of fetal breathing movements is not sustained during prolonged reduced uterine blood flow in sheep

1998 ◽  
Vol 76 (9) ◽  
pp. 858-866 ◽  
Author(s):  
Carole S Watson ◽  
Jacobus H Homan ◽  
Susan E White ◽  
John R Challis ◽  
Alan D Bocking
Keyword(s):  
Blood Flow ◽  
Ethanol Exposure ◽  
Late Gestation ◽  
Prostaglandin E ◽  
Uterine Blood Flow ◽  
Fetal Plasma ◽  
Fetal Breathing ◽  
Fetal Breathing Movements ◽  
Baseline Incidence ◽  
And Control

Fetal breathing movements (FBM) are inhibited by both exogenous prostaglandin E2 (PGE2) and ethanol in sheep. Maternal ethanol exposure in late-gestation sheep also increases fetal [PGE2]. However, during prolonged reduced uterine blood flow (RUBF) when [PGE2] in fetal plasma is already elevated, FBM are not inhibited by ethanol. These experiments were designed, therefore, to test the hypothesis that the FBM response to PGE2 is also diminished during RUBF. PGE2 (594 ± 19 ng·min-1·kg-1 fetal body weight) was infused for 6 h into the jugular vein of RUBF (PO2 = 14 ± 1 mmHg (1 mmHg = 133.3 Pa); n = 7) and control (PO2 = 22 ± 1 mmHg (p < 0.01); n = 7) ovine fetuses, and the effect on FBM, electrocortical (ECoG), and electroocular activities was determined. The infusion of PGE2 increased plasma [PGE2] from 881 ± 162 to 1189 ± 114 pg·mL-1 in RUBF fetuses and from 334 ± 72 to 616 ± 118 pg·mL-1 (p < 0.05) in control fetuses. FBM were initially inhibited by PGE2 from 22.5 ± 9.4 and 17.9 ± 6.5% of the time to 6.9 ± 2.4 and 0.5 ± 0.4% (p < 0.01) in RUBF and control fetuses, respectively. FBM remained inhibited in control fetuses throughout the infusion but returned to baseline incidence in RUBF fetuses in the last 2 h of the infusion. These results are consistent with the hypothesis that one component of the adaptative mechanisms of the fetus to prolonged RUBF is an altered response of FBM to exogenous PGE2. We speculate that the lack of a sustained inhibition in FBM during RUBF with infusion of PGE2 may be a result of an alteration in brainstem receptor function or number or local PGE2 removal.Key words: fetal breathing movements, prostaglandin E2, hypoxia, reduced uterine blood flow, ethanol, fetal behaviour.

Altered fetal cardiovascular responses to prolonged hypoxia after sinoaortic denervation

1999 ◽  
Vol 276 (2) ◽  
pp. R340-R346 ◽  
Author(s):  
P. Stein ◽  
S. E. White ◽  
J. Homan ◽  
M. A. Hanson ◽  
A. D. Bocking
Keyword(s):  
Blood Flow ◽  
Carotid Sinus ◽  
Arterial Oxygen Saturation ◽  
Cardiovascular Responses ◽  
Arterial Oxygen ◽  
Uterine Blood Flow ◽  
Vagus Nerves ◽  
Fetal Sheep ◽  
Peripheral Chemoreceptors

This study examines the role of the peripheral chemoreceptors in mediating fetal cardiovascular responses to prolonged hypoxia secondary to reduced uterine blood flow (RUBF). Fetal sheep were chronically instrumented for continuous heart rate (FHR), blood pressure (FBP), and carotid blood flow (CBF) measurements after bilateral sectioning of the carotid sinus and vagus nerves (denervated, n = 7) or sham denervation (intact, n = 7). Four days postoperatively, uterine blood flow was mechanically restricted, reducing fetal arterial oxygen saturation by 47.3% ( P < 0.01). An initial bradycardia was observed in intact (184.0 ± 10.7 to 160.5 ± 10.7 beats/min, not significant) but not denervated fetuses, followed by a tachycardia (180.0 ± 2.2 to 193.7 ± 2.7 beats/min, P < 0.05). FHR increased in denervated fetuses (175.5 ± 8.7 to 203.0 ± 17.9 beats/min, P < 0.05). FBP increased transiently in intact fetuses from 45.1 ± 1.0 to 55.4 ± 3.0 mmHg at 2 h ( P < 0.01), whereas denervated fetuses demonstrated a decrease in FBP from 47.1 ± 4.2 to 37.2 ± 3.7 mmHg (not significant). CBF increased ( P < 0.05) in both intact and denervated fetuses from 39.3 ± 2.8 and 29.7 ± 3.8 ml ⋅ min−1 ⋅ kg−1to 47.7 ± 0.4 and 39.1 ± 0.3 ml ⋅ min−1 ⋅ kg−1, respectively, whereas carotid vascular resistance decreased only in denervated fetuses (1.7 ± 0.1 to 1.1 ± 0.02 mmHg ⋅ ml−1 ⋅ min ⋅ kg−1, P < 0.05). We conclude that the peripheral chemoreceptors play an important role in mediating fetal cardiovascular responses to prolonged RUBF.

The physiology of extracorporeal membrane oxygenation: The Fick principle

Perfusion ◽  
2021 ◽  
pp. 026765912110559
Author(s):  
Hoong Lim
Keyword(s):  
Blood Flow ◽  
Extracorporeal Membrane Oxygenation ◽  
Arterial Oxygen Saturation ◽  
Arterial Oxygen ◽  
Fick Principle ◽  
Membrane Oxygenation ◽  
Lung Failure ◽  
Va Ecmo ◽  
The Relationship ◽  
Vv Ecmo

Extracorporeal membrane oxygenation (ECMO) can be delivered in veno-arterial (VA) and veno-venous (VV) configurations based on the cannulation strategy. VA and VV ECMO are delivered primarily for haemodynamic and respiratory support in patients with severe heart and lung failure, respectively. The Fick principle describes the relationship between blood flow and oxygen consumption – key parameters in the physiological management of extracorporeal support. This review will discuss the application of the Fick principle in: (i) recirculation in VV ECMO; (ii) the quantification of oxygen delivery (DO2) in VV ECMO and (iii) the quantification of transpulmonary blood flow and systemic arterial oxygen saturation in VA ECMO.

Effects of Active Preconditioning With Local and Systemic Hypoxia on Submaximal Cycling

2021 ◽  
pp. 1-6
Author(s):  
Olivier Girard ◽  
Romain Leuenberger ◽  
Sarah J. Willis ◽  
Fabio Borrani ◽  
Grégoire P. Millet
Keyword(s):  
Blood Flow ◽  
Arterial Oxygen Saturation ◽  
Lactate Concentration ◽  
Blood Lactate Concentration ◽  
Blood Flow Restriction ◽  
Arterial Oxygen ◽  
Total Occlusion ◽  
Flow Restriction ◽  
Cycling Efficiency ◽  
Systemic Hypoxia

Purpose: The authors compared the effects of active preconditioning with local and systemic hypoxia during submaximal cycling. Methods: On separate visits, 14 active participants completed 4 trials. Each visit was composed of 1 preconditioning phase followed, after 40 minutes of rest, by 3 × 6-minute cycling bouts (intensity = 85% of critical power; rest = 6 min). The preconditioning phase consisted of 4 × 5-minute cycling bouts at 1.5 W·kg−1 (rest = 5 min) in 4 conditions: control (no occlusion and normoxia), blood flow restriction (60% of total occlusion), HYP (systemic hypoxia; inspired fraction of oxygen = 13.6%), and blood flow restriction + HYP (local and systemic hypoxia combined). Results: During the preconditioning phase, there were main effects of both systemic (all P < .014) and local hypoxia (all P ≤ .001) on heart rate, arterial oxygen saturation, leg discomfort, difficulty of breathing, and blood lactate concentration. Cardiorespiratory variables, gross efficiency, energy cost, and energy expenditure during the last minute of 6-minute cycling bouts did not differ between conditions (all P > .105). Conclusion: Local and systemic hypoxic stimuli, or a combination of both, during active preconditioning did not improve physiological responses such as cycling efficiency during subsequent submaximal cycling.

Fetal oxygen uptake, oxygenation, and acid-base balance as a function of uterine blood flow

1983 ◽  
Vol 244 (6) ◽  
pp. H749-H755 ◽  
Author(s):  
R. B. Wilkening ◽  
G. Meschia
Keyword(s):  
Blood Flow ◽  
Base Excess ◽  
Umbilical Vein ◽  
Delivery Rate ◽  
Uterine Blood Flow ◽  
O2 Uptake ◽  
Acid Base Balance ◽  
Venous Pco2 ◽  
Base Balance ◽  
O2 Delivery

The rate of O2 delivery to the pregnant uterus (FaO2) was decreased in chronic sheep preparations by mechanical occlusion of uterine blood flow. The relationship of uterine venous O2 saturation (SVO2) to FaO2 was curvilinear with convexity toward the SVO2 axis. As SVO2 decreased, there was a decrease in uterine and umbilical venous O2 tension (PO2), with no appreciable reduction of the PO2 difference between the two veins and a decrease in the umbilical vein O2 delivery rate. Fetal O2 uptake and base excess remained normal as the umbilical vein O2 delivery rate was reduced from 1.1 to 0.6 mmol . min-1 . kg-1 but decreased markedly at an O2 delivery rate less than 0.5. Umbilical venous CO2 tension (PCO2) was higher than, and strongly correlated with, uterine venous PCO2 (R = 0.954). These observations support a venous equilibration model of ovine placental exchange and demonstrate that under normal physiological conditions the O2 supply to the fetal lamb is approximately twice the value necessary to maintain an adequate fetal O2 uptake and a normal fetal base excess.

AN EFFECT OF REDUCED BAROMETRIC PRESSURE ON THE PERIPHERAL CIRCULATION

1957 ◽  
Vol 35 (10) ◽  
pp. 777-783
Author(s):  
F. Girling ◽  
F. A. Sunahara
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Forearm Blood Flow ◽  
Human Subjects ◽  
Arterial Oxygen Saturation ◽  
Barometric Pressure ◽  
Peripheral Circulation ◽  
Arterial Oxygen ◽  
Blood Flows ◽  
The Past

Several groups of investigators have noted in the past that exposure to a reduced barometric pressure results in a decrease in peripheral blood flow.In the present study human subjects were exposed to a pressure of 225 mm. Hg with maintenace of arterial oxygen saturation, and forearm and hand blood flows were measured plethysmographically. Forearm blood flow was not affected by the exposure whereas hand blood flow was reduced in all subjects. Blood pressure and heart rate were also measured and showed no change during the experiment.

Regional blood flow and cardiac output during acute hypoxia in the anesthetized dog

1963 ◽  
Vol 204 (6) ◽  
pp. 963-968 ◽  
Author(s):  
John F. Murray ◽  
I. Maureen Young
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Regional Blood Flow ◽  
Acute Hypoxia ◽  
Arterial Oxygen Saturation ◽  
Head Kidney ◽  
Arterial Oxygen ◽  
Circulatory Effects ◽  
Low Concentrations ◽  
Anesthetized Dogs

The circulatory effects of breathing low concentrations of oxygen were studied in ten anesthetized dogs. Simultaneous measurements were made of cardiac output (indicator dilution technique) and blood flow to the head, kidney, and hind limb (electromagnetic flowmeters). Four experiments were performed with the addition of succinylcholine to inhibit the ventilatory response to hypoxia and maintain pCO2 constant. A rise in cardiac output and mean arterial pressure occurred which was significantly correlated to the decrease in arterial oxygen saturation. No threshold for these responses was found. Blood flow tended to increase during hypoxia in the regions studied but the responses were variable and only the change in renal blood flow had a significant correlation to arterial oxygen unsaturation. Systemic and regional vascular resistances during hypoxia varied both in direction and magnitude of change. The preponderant effects of hypoxia influence cardiac output more than peripheral vascular resistance.

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