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 ◽  
...  

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.

1999 ◽  
Vol 276 (2) ◽  
pp. R340-R346 ◽  
Author(s):  
P. Stein ◽  
S. E. White ◽  
J. Homan ◽  
M. A. Hanson ◽  
A. D. Bocking

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.


1992 ◽  
Vol 70 (10) ◽  
pp. 1396-1402 ◽  
Author(s):  
Alicia Sue-Tang ◽  
Alan D. Booking ◽  
A. Nigel Brooks ◽  
Stuart Hooper ◽  
Susan E. White ◽  
...  

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.


1990 ◽  
Vol 259 (4) ◽  
pp. R703-R708 ◽  
Author(s):  
S. B. Hooper ◽  
C. L. Coulter ◽  
J. M. Deayton ◽  
R. Harding ◽  
G. D. Thorburn

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)


1995 ◽  
Vol 268 (3) ◽  
pp. H974-H979
Author(s):  
M. Dalinghaus ◽  
J. W. Gratama ◽  
W. G. Zijlstra ◽  
J. R. Kuipers

Cardiovascular responses to acute hypoxemia are in part mediated through adrenergic and chemoreceptor stimulation. In chronic hypoxemia the response to these stimuli may be blunted. Therefore, we determined whether the cardiovascular responses to acute hypoxemia superimposed on 3–4 wk of chronic hypoxemia were blunted in lambs with an experimental cardiac right-to-left shunt (combination of atrial septal defect and variable pulmonary stenosis). Cardiovascular variables and regional blood flows were determined during chronic hypoxemia and after acutely reducing the arterial oxygen saturation by increasing the cardiac right-to-left shunt. Arterial oxygen saturation decreased (65 +/- 7 to 40 +/- 7%, P < 0.001) and systemic blood flow increased (164 +/- 63 to 233 +/- 100 ml.min-1.kg-1, P < 0.01), maintaining systemic oxygen supply and oxygen uptake. Blood flow to the myocardium (P < 0.01), the adrenals (P < 0.05), and the brain (0.05 < P < 0.10) increased, and oxygen supply to these organs was maintained. Conversely, blood flow to the kidneys and the gastrointestinal tract was unaltered, so that oxygen supply to these organs was decreased. The responses to acute hypoxemia in chronically hypoxemic lambs were similar to those previously reported in normoxemic lambs. We conclude that the cardiovascular responses to acute hypoxemia in chronically hypoxemic lambs are not blunted.


1982 ◽  
Vol 243 (4) ◽  
pp. E278-E286
Author(s):  
C. E. Wood ◽  
L. C. Keil ◽  
A. M. Rudolph

To test the hypothesis that ACTH and vasopressin responses are quantifiable as functions of induced changes in central venous or arterial pressures, we produced various degrees of vena caval obstruction in fetal sheep (118--134 days gestation). In seven experiments, vena caval obstruction increased heart rate 18 +/- 7 beats/min and carotid arterial oxygen saturation 8.4 +/- 2.1%, but did not alter any measured vascular pressure or hormones. More severe vena caval obstruction (n = 10) decreased mean arterial pressure 13 +/- 2 mmHg, central venous pressure 1.3 +/- 0.3 mmHg, and heart rate 47 +/- 12 beats/min, and increased fetal plasma ACTH 1,047 +/- 448 pg/ml, cortisol 4.4 +/- 2.2 ng/ml, and vasopressin 47.9 +/- 24.2 pg/ml, but did not alter 11-deoxycortisol. The stimulus increased plasma cortisol (radioimmunoassay after chromatography) 100% and "corticosteroids" (radiotransinassay without chromatography) 20%, demonstrating the nonlinear relationship between these two variables. End-inflation plasma ACTH and vasopressin concentrations were significantly related to the induced decreases in mean arterial and central venous pressures, suggesting that the hormonal responses to vena caval obstruction were mediated by cardiovascular mechanoreceptors. Plasma vasopressin concentrations were linearly related to plasma ACTH concentrations (4 = 0.94; P less than 0.001), suggesting parallel release of the two hormones.


1988 ◽  
Vol 65 (6) ◽  
pp. 2420-2426 ◽  
Author(s):  
A. D. Bocking ◽  
R. Gagnon ◽  
K. M. Milne ◽  
S. E. White

Experiments were conducted in unanesthetized, chronically catheterized pregnant sheep to determine the fetal behavioral response to prolonged hypoxemia produced by restricting uterine blood flow. Uterine blood flow was reduced by adjusting a vascular occluder placed around the maternal common internal iliac artery to decrease fetal arterial O2 content from 6.1 +/- 0.3 to 4.1 +/- 0.3 ml/dl for 48 h. Associated with the decrease in fetal O2 content, there was a slight increase in fetal arterial PCO2 and decrease in pH, which were both transient. There was an initial inhibition of both fetal breathing movements and eye movements but no change in the pattern of electrocortical activity. After this initial inhibition there was a return to normal incidence of both fetal breathing movements and eye movements by 16 h of the prolonged hypoxemia. These studies indicate that the chronically catheterized sheep fetus is able to adapt behaviorally to a prolonged decrease in arterial O2 content secondary to the restriction of uterine blood flow.


Author(s):  
Christopher A. Lear ◽  
Laura Bennet ◽  
Benjamin S. A. Lear ◽  
Jenny A. Westgate ◽  
Alistair Jan Gunn

Impaired cardiac preload secondary to umbilical cord occlusion (UCO) has been hypothesized to contribute to intrapartum decelerations, brief falls in fetal heart rate (FHR), through the activation of the Bezold-Jarisch reflex. This cardioprotective reflex increases parasympathetic and inhibits sympathetic outflows triggering hypotension, bradycardia and peripheral vasodilation but its potential to contribute to intrapartum decelerations has never been systematically examined. In this study we performed bilateral cervical vagotomy to remove the afferent arm and the efferent parasympathetic arm of the Bezold-Jarisch reflex. 22 chronically instrumented fetal sheep at 0.85 of gestation received vagotomy (n=7) or sham-vagotomy (control, n=15), followed by three 1-min complete UCOs separated by 4-min reperfusion periods. UCOs in control fetuses were associated with a rapid fall in FHR and reduced femoral blood flow mediated by intense femoral vasoconstriction, leading to hypertension. Vagotomy abolished the rapid fall in FHR (p<0.001), and despite reduced diastolic filling time, increased both carotid (p<0.001) and femoral (p<0.05) blood flow during UCOs, secondary to carotid vasodilation (p<0.01) and delayed femoral vasoconstriction (p<0.05). Finally, vagotomy was associated with an attenuated rise in cortical impedance during UCOs (p<0.05), consistent with improved cerebral substrate supply. In conclusion, increased carotid and femoral blood flows after vagotomy are consistent with increased left and right ventricular output, which is incompatible with the hypothesis that labor-like UCOs impair ventricular filling. Overall, the cardiovascular responses to vagotomy do not support the hypothesis that the Bezold-Jarisch reflex is activated by UCO. The Bezold-Jarisch reflex is therefore mechanistically unable to contribute to intrapartum decelerations.


Perfusion ◽  
2021 ◽  
pp. 026765912110559
Author(s):  
Hoong Lim

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.


1996 ◽  
Vol 271 (1) ◽  
pp. R73-R83 ◽  
Author(s):  
D. A. Giussani ◽  
R. A. Riquelme ◽  
F. A. Moraga ◽  
H. H. McGarrigle ◽  
C. R. Gaete ◽  
...  

We tested the hypothesis that the llama fetus has a blunted cardiovascular chemoreflex response to hypoxemia by investigating the effects of acute hypoxemia on perfusion pressure, heart rate, and the distribution of the combined ventricular output in 10 chronically instrumented fetal llamas at 0.6-0.7 gestation. Four llama fetuses had the carotid sinus nerves sectioned. In the intact fetuses, there was a marked bradycardia, an increase in perfusion pressure, and a pronounced peripheral vasoconstriction during hypoxemia. These cardiovascular responses during hypoxemia in intact fetuses were accompanied by a pronounced increase in plasma vasopressin, but not in plasma angiotensin II concentrations. Carotid denervation prevented the bradycardia at the onset of hypoxemia, but it did not affect the intense vasoconstriction during hypoxemia. Plasma vasopressin and angiotensin II levels were not measured in carotid-denervated fetuses. Our results do not support the hypothesis that the carotid chemoreflex during hypoxemia is blunted in the llama fetus. However, they emphasize that other mechanisms, such as increased vasopressin concentrations, operate to produce an intense vasoconstriction in hypoxemia. This intense vasoconstriction in the llama fetus during hypoxemia may reflect the influence of chronic exposure to the hypoxia of high altitude on the magnitude and gain of fetal cardiovascular responses to a superimposed acute episode of hypoxemia.


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