scholarly journals Roles of parasympathetic outflow and sympathetic outflow in the cardiovascular response to brief umbilical cord occlusion in fetal sheep

PLoS ONE ◽  
2021 ◽  
Vol 16 (7) ◽  
pp. e0254155
Author(s):  
Morgan Recher ◽  
Arthur Lauriot Dit Prevost ◽  
Dyuti Sharma ◽  
Julien De Jonckheere ◽  
Charles Garabedian ◽  
...  
Keyword(s):  
Umbilical Cord ◽  
Early Stage ◽  
Cardiovascular Response ◽  
Blood Gases ◽  
Cord Compression ◽  
Fetal Sheep ◽  
Uterine Contractions ◽  
Baseline Values ◽  
To Receive

Fetal heart rate (FHR) deceleration is the most common change seen during labor. The role of the autonomic nervous system in regulating the fetal cardiovascular response during multiple uterine contractions has been well-established. However, the mechanism underlying the hemodynamic response remains unclear and the specific reflex that mediates the cardiovascular modifications is still controversial. This study aimed to determine the role of the sympathetic and parasympathetic systems on fetal hemodynamics in complete cord occlusion. Chronically instrumented fetal sheep were randomized to receive an intravenous injection of atropine 2.5 mg (n = 8), propranolol 5 mg (n = 7), atropine and propranolol (n = 7), or a control protocol (n = 9), followed by three episodes of 1-minute umbilical cord occlusion repeated every 5 minutes. Cord compression induces a rapid decrease in the FHR and a rapid increase in MAP. The decrease in FHR is caused by an increase in parasympathetic activity, (atropine and atropine-propranolol abolish the FHR response to the occlusion). The change in FHR during occlusion was not modified by propranolol injection, showing no effect of sympathetic tone. The increase in MAP during occlusion was similar in the four protocols. After releasing occlusion, the FHR was still lower than that at baseline due to a sustained parasympathetic tone. Suppression of the parasympathetic output to the cardiovascular system unmasks an increase in the FHR above baseline values. The lower FHR with the propranolol protocol further supports an increase in myocardial β-adrenoceptor stimulation after cord release. The increase in MAP after cord release was similar in the four protocols, except after the early stage of interocclusion period in atropine protocol. Four minutes after cord release, the FHR returned to baseline irrespective of the drugs that were infused, thereby showing recovery of ANS control. Blood gases (pH, PaCO2, PaO2) and plasma lactate concentrations was similar between the four protocols at the end of three applications of UCO. Complete cord compression-induced deceleration is likely due to acute activation of parasympathetic output. β-adrenoceptor activity is involved in the increase in FHR after cord release. Understanding the reflexes involved in FHR deceleration may help us understand the mechanisms underlying fetal autonomic adaptation during cord occlusion.

Umbilical cord occlusion stimulates breathing independent of blood gases and pH

1991 ◽  
Vol 70 (4) ◽  
pp. 1796-1809 ◽  
Author(s):  
S. L. Adamson ◽  
I. M. Kuipers ◽  
D. M. Olson
Keyword(s):  
Prostaglandin E2 ◽  
Umbilical Cord ◽  
Blood Gases ◽  
High Frequency Oscillation ◽  
Breathing Rate ◽  
Fetal Sheep ◽  
Arterial Pco2 ◽  
Arterial Blood Gas ◽  
Arterial Blood

The role of umbilical cord occlusion in the initiation of breathing at birth was investigated by use of 16 unanesthetized fetal sheep near full term. Artificial ventilation with high-frequency oscillation was used to control fetal arterial blood gas tensions. At baseline, PCO2 was maintained at control fetal values and PO2 was elevated to between 25 and 50 Torr. In the first study on six intact and four vagotomized fetuses, arterial PCO2 and PO2 were maintained constant during two 30-min periods of umbilical cord occlusion. Nevertheless, the mean fetal breathing rate increased significantly when the umbilical cord was occluded. In the second study on six intact fetuses, hypercapnia (68 Torr) was imposed by adding CO2 to the ventilation gas. When the umbilical cord was occluded, there was a significantly greater stimulation of breathing (rate, incidence, and amplitude) in response to hypercapnia than in response to hypercapnia alone. During cord occlusion, plasma prostaglandin E2 concentration decreased significantly. Results indicate that cord occlusion stimulates breathing possibly by causing the removal of a placentally produced respiratory inhibitor such as prostaglandin E2 from the circulation.

Role of peripheral and central chemoreceptors in the initiation of fetal respiration

1975 ◽  
Vol 38 (3) ◽  
pp. 407-410 ◽  
Author(s):  
V. Chernick ◽  
E. E. Faridy ◽  
R. D. Pagtakhan
Keyword(s):  
Carotid Sinus ◽  
Blood Gases ◽  
Fetal Sheep ◽  
Peripheral Chemoreceptors ◽  
Central Chemoreceptors ◽  
Bilateral Carotid ◽  
Fetal Respiration ◽  
A Minor ◽  
The Relationship

The relationship between fetal femoral arterial P02 and PC02 was evalulated in 13 fetal sheep with intact and denervated peripheral chemoreceptors. With intact chemoreceptors, a significant relationship was found between fetal Pa02 and PaC02 at the time of the first breath (Pa02 = 2.57 + 0.09 PaC02; r = 0.62, P less than 0.05)mfollowing bilateral carotid sinus nerve section (CSN) or total peripheral chemodenervation (TD), PaC02. Comparison of the intact, CSN, and TD blood gases at the time of the first breath demonstrated that a) severe hypoxemia stimulates fetal respiration even following total peripheral chemodenervation; b) fetal central chemoreceptors do not respond to PaC02; c) PaC02 acting via peripheral chemoreceptors has a minor modulating effect on the degree of hypoxemia required to initiate fetal respiration. At a PaC02 below 40 mmHg this effect is inhibitory, acting via the carotid body. At a PaC02 above 90 mmHg this effect is stimulatory, acting via both carotid and aortic bodies.

Cardiovascular responses to graded degrees of hypoxaemia in the llama fetus

1995 ◽  
Vol 7 (3) ◽  
pp. 549 ◽  
Author(s):  
AJ Llanos ◽  
RA Riquelme ◽  
FA Moraga ◽  
G Cabello ◽  
JT Parer
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Cerebral Blood Flow ◽  
Cardiovascular Response ◽  
Blood Gases ◽  
Cardiovascular Responses ◽  
Fetal Sheep ◽  
Severe Hypoxaemia ◽  
The Central Nervous System ◽  
Blood Flow Redistribution

The fetal llama exposed to an intense degree of hypoxaemia did not increase cerebral blood flow, but showed a marked peripheral vasoconstriction. The same cardiovascular response is observed in fetal sheep submitted to a extremely severe hypoxaemia, when the initial compensatory vasodilatory mechanisms in brain and heart fail. To investigate whether the fetal llama responses to acute hypoxaemia are adaptive, or whether they are the result of a breakdown of mechanisms of blood flow redistribution that favours the central nervous system, we studied seven fetal llamas (0.6-0.7 of gestation) chronically-catheterized during 1 h of graded and progressive hypoxaemia. Fetal ascending aorta blood gases and fetal cardiac output and its distribution (radiolabelled-microspheres) were measured after 60 min of normoxaemia (B) and at the end of 20 min (H20), 40 min (H40) and 60 min (H60) of hypoxaemia. Data were analysed by ANOVA and Newman-Keuls tests. Each treatment resulted in a lower (P < 0.05) percentage of haemoglobin saturation than hypoxaemia; H40 was lower than H20, and H60 was lower than H20 and H40. No statistical difference was observed among treatments for cardiac output or cerebral blood flow. These results demonstrate that fetal cardiac output and brain blood flow are maintained at all degrees of hypoxaemia, indicating that these cardiovascular responses are an adaptive response in the llama fetus, rather than an index of cardiorespiratory decompensation.

POSSIBLE ROLE OF UTERINE CONTRACTIONS IN THE SHORT-TERM FLUCTUATIONS OF PLASMA ACTH CONCENTRATION IN FETAL SHEEP

1985 ◽  
Vol 106 (2) ◽  
pp. R9-R11 ◽  
Author(s):  
S.J. Lye ◽  
M.E. Wlodek ◽  
J.R.G. Challis
Keyword(s):  
Percentage Change ◽  
Plasma Acth ◽  
Short Term ◽  
Fetal Sheep ◽  
Uterine Activity ◽  
Fetal Plasma ◽  
Uterine Contractions ◽  
Intrauterine Pressure ◽  
Acth Concentration

ABSTRACT Uterine contractions, induced by the administration of oxytocin to sheep between d 123-144 of pregnancy, were associated with a mean transient decrease in fetal PaO2 of 2.8 mm Hg within 5 min. These changes were associated with a rapid increase in the concentration of ACTH in fetal plasma. There was a significant (P<0.05) increase in the percentage change (+40 to +47%) over basal ACTH levels in fetal plasma at +5, +15 and +20 min after oxytocin. Administration of saline had no significant effect on intrauterine pressure, fetal PaO2 or fetal plasma ACTH levels. We speculate that increases in uterine activity and/or transient decreases in fetal PaO2 may contribute to short-term fluctuations in plasma ACTH in fetal sheep.

CORPORATE CHAMPIONS OF EARLY-STAGE PROJECT PROPOSALS AND THE INSTITUTIONALISATION OF ORGANISATIONAL INERTIA

2019 ◽  
Vol 24 (03) ◽  
pp. 2050028
Author(s):  
HEIDI M. J. BERTELS ◽  
MURAD MITHANI ◽  
SIWEI ZHU ◽  
PETER A. KOEN
Keyword(s):  
Product Development ◽  
New Product Development ◽  
Development Process ◽  
Early Stage ◽  
Product Development Process ◽  
Mba Students ◽  
Executive Mba ◽  
Using Data ◽  
To Receive

This study looks at the role of champions in the early stages of the product development process, when employees try to secure initial funding for project proposals. Project proposals that fail to receive funding never become part of the firm’s project pipeline; hence, it is critical to understand the champion’s role early on. Existing research on corporate champions is mostly focused on the later stages of the new product development process and has generally identified corporate champions as key to projects likely to face organisational resistance. However, several recent studies suggest that champions may prefer projects less likely to face organisational resistance. Using data from project proposals of executive MBA students across 78 large organisations, we find that champion support for the team is weaker for project proposals likely to evoke resistance and that such lower champion support further reduces the likelihood of high-resistance early-stage proposals to receive initial funding.

scholarly journals Cholinergic and β-adrenergic control of cardiovascular reflex responses to brief repeated asphyxia in term-equivalent fetal sheep

2016 ◽  
Vol 311 (5) ◽  
pp. R949-R956 ◽  
Author(s):  
Robert Galinsky ◽  
Christopher A. Lear ◽  
Kyohei Yamaguchi ◽  
Guido Wassink ◽  
Jennifer A. Westgate ◽  
...  
Keyword(s):  
Fetal Heart ◽  
Atropine Sulfate ◽  
Adrenergic Blockade ◽  
Adrenergic Stimulation ◽  
Fetal Sheep ◽  
Cholinergic Blockade ◽  
Active Labor ◽  
Baseline Values ◽  
Intravenous Atropine

The role of cholinergic and β-adrenergic activity in mediating fetal cardiovascular recovery from brief repeated episodes of asphyxia, consistent with established labor, remains unclear. In this study, we tested the effect of cholinergic and β-adrenergic blockade on the fetal chemoreflex and fetal heart rate (FHR) overshoot responses during brief repeated asphyxia at rates consistent with early or active labor. Chronically instrumented fetal sheep at 0.85 of gestation received either intravenous atropine sulfate (cholinergic blockade; n = 7) or vehicle ( n = 8) followed by 3 × 1-min umbilical cord occlusions repeated every 5 min (1:5; consistent with early labor), or intravenous propranolol hydrochloride (β-adrenergic blockade; n = 8) or vehicle ( n = 6) followed by 3 × 2-min occlusions repeated every 5 min (2:5; consistent with active labor). In vehicle controls, 1:5 occlusions were associated with rapid and sustained FHR decelerations followed by rapid return of FHR to baseline values after release of the occlusion. Cholinergic blockade abolished FHR decelerations during occlusions and caused FHR overshoot after release of the occlusion ( P < 0.05 vs. control 1:5). In vehicle controls, 2:5 occlusions caused rapid and sustained FHR decelerations followed by FHR overshoot after release of the occlusion. β-adrenergic blockade was associated with greater reduction in FHR during occlusions and attenuated FHR overshoot ( P < 0.05 vs. control 2:5). These data demonstrate that the FHR overshoot pattern after asphyxia is mediated by a combination of attenuated parasympathetic activity and increased β-adrenergic stimulation of the fetal heart.

Randomized phase III trial evaluating the role of erythropoietin in the prevention of chemotherapy-induced anemia.

1997 ◽  
Vol 15 (7) ◽  
pp. 2715-2721 ◽  
Author(s):  
L Del Mastro ◽  
M Venturini ◽  
R Lionetto ◽  
O Garrone ◽  
G Melioli ◽  
...  
Keyword(s):  
Early Stage ◽  
Cost Effective ◽  
Additional Treatment ◽  
Phase Iii ◽  
Control Group ◽  
Breast Cancer Patients ◽  
Clinically Significant ◽  
Few Data ◽  
To Receive

PURPOSE Although erythropoietin (EPO) is known to be useful in treating chemotherapy-induced anemia, few data are available on its potential preventive role. The aim of this study was to evaluate the ability of EPO in preventing the development of clinically significant anemia in patients treated with chemotherapy. PATIENTS AND METHODS Sixty-two early-stage breast cancer patients undergoing accelerated adjuvant chemotherapy were randomized to receive EPO 150 U/kg three times a week or no additional treatment. Chemotherapy consisted of six cycles of cyclophosphamide 600 mg/m2, epirubicin 60 mg/m2, and fluorouracil 600 mg/m2 (CEF) intravenously on day 1, every 2 weeks with the support of granulocyte colony-stimulating factor (G-CSF), 5 microg/kg subcutaneously from day 4 to day 11. RESULTS Throughout the six cycles of chemotherapy, EPO-treated patients maintained stable values of hemoglobin, whereas control patients developed a progressive anemia. At the end of chemotherapy, the mean (+/- SD) hemoglobin decrease in the control group was 3.05 g/dL (+/- 1.0; 95% confidence interval [CI], 2.6 to 3.5), whereas in the EPO group it was 0.8 (+/- 1.4; 95% CI, 0.3 to 1.4). Clinically significant anemia (hemoglobin < or = 10 g/dL) occurred in 16 patients (52%; 95% CI, 33 to 69) in the control arm and in no patient (0%; 95% CI, 0 to 14) in the EPO arm (P = .00001). CONCLUSION EPO prevents anemia in patients undergoing chemotherapy. Further trials are required to identify subsets of patients in which the preventive use of this drug could be cost-effective.

Dynamics of cardiovascular responses to repeated partial umbilical cord compression in late-gestation sheep fetus

1997 ◽  
Vol 273 (5) ◽  
pp. H2351-H2360 ◽  
Author(s):  
Dino A. Giussani ◽  
Nobuya Unno ◽  
Susan L. Jenkins ◽  
Richard A. Wentworth ◽  
Jan B. Derks ◽  
...  
Keyword(s):  
Blood Flow ◽  
Umbilical Cord ◽  
Cardiovascular Responses ◽  
Cord Compression ◽  
Secondary Response ◽  
Fetal Sheep ◽  
Compression Phase ◽  
Umbilical Blood ◽  
Group I ◽  
Umbilical Blood Flow

We characterized the detailed hemodynamics of fetal blood pressure, heart rate, common umbilical blood flow, and femoral blood flow responses to partial compression of the umbilical cord and tested the hypothesis that repeated cord compression modulates fetal cardiovascular responses in 10 chronically instrumented fetal sheep at ∼130 days of gestation. In five fetuses ( group I), partial compression of the umbilical cord was induced 12 times, each for 5 min at 15-min intervals. Each cord compression reduced common umbilical blood flow by 50% and produced modest falls in fetal pH (7.33 ± 0 to 7.29 ± 0) and arterial [Formula: see text] (21.1 ± 0.2 to 16.8 ± 0.2 mmHg) and a mild increase in arterial[Formula: see text] (49.9 ± 0.5 to 54.9 ± 0.4 mmHg). Sham experiments were performed in five other fetuses ( group II). Second-by-second analysis of group I fetal cardiovascular data revealed a clear biphasic response to partial cord compression. Phase I (1st min of cord compression) was characterized by a rapid bradycardia and a rapid femoral vasoconstriction (primary response); phase II ( minutes 2–5of cord compression) was characterized by a delayed bradycardia and a return of femoral vascular resistance toward baseline (secondary response). Repeated cord compression abolished the primary, but not the secondary, cardiovascular responses. These results demonstrate that fetal cardiovascular responses to stress may be modified by preexposure to repeated intrauterine challenges.

scholarly journals Medullary Noradrenergic Neurons Mediate Hemodynamic Responses to Osmotic and Volume Challenges

2021 ◽  
Vol 12 ◽  
Author(s):  
Stefanne Madalena Marques ◽  
Lara Marques Naves ◽  
Talita de Melo e Silva ◽  
Keilah Valéria Naves Cavalcante ◽  
Juliana Milan Alves ◽  
...  
Keyword(s):  
Cardiovascular Response ◽  
Electrolyte Balance ◽  
Noradrenergic Neurons ◽  
Catecholaminergic Neurons ◽  
Blood Flows ◽  
Arterial Blood ◽  
Male Wistar Rats ◽  
Baseline Values ◽  
Hypertonic Saline Infusion

Despite being involved in homeostatic control and hydro-electrolyte balance, the contribution of medullary (A1 and A2) noradrenergic neurons to the hypertonic saline infusion (HSI)-induced cardiovascular response after hypotensive hemorrhage (HH) remains to be clarified. Hence, the present study sought to determine the role of noradrenergic neurons in HSI-induced hemodynamic recovery in male Wistar rats (290–320 g) with HH. Medullary catecholaminergic neurons were lesioned by nanoinjection of antidopamine-β-hydroxylase–saporin (0.105 ng·nl−1) into A1, A2, or both (LES A1; LES A2; or LES A1+A2, respectively). Sham rats received nanoinjections of free saporin in the same regions (SHAM A1; SHAM A2; or SHAM A1+A2, respectively). After 15 days, rats were anesthetized and instrumented for cardiovascular recordings. Following 10 min of stabilization, HH was performed by withdrawing arterial blood until mean arterial pressure (MAP) reaches 60 mmHg. Subsequently, HSI was performed (NaCl 3 M; 1.8 ml·kg−1, i.v.). The HH procedure caused hypotension and bradycardia and reduced renal, aortic, and hind limb blood flows (RBF, ABF, and HBF). The HSI restored MAP, heart rate (HR), and RBF to baseline values in the SHAM, LES A1, and LES A2 groups. However, concomitant A1 and A2 lesions impaired this recovery, as demonstrated by the abolishment of MAP, RBF, and ABF responses. Although lesioning of only a group of neurons (A1 or A2) was unable to prevent HSI-induced recovery of cardiovascular parameters after hemorrhage, lesions of both A1 and A2 made this response unfeasible. These findings show that together the A1 and A2 neurons are essential to HSI-induced cardiovascular recovery in hypovolemia. By implication, simultaneous A1 and A2 dysfunctions could impair the efficacy of HSI-induced recovery during hemorrhage.

Effect of graded umbilical cord compression in fetal sheep at 0.6-0.7 gestation

1991 ◽  
Vol 261 (4) ◽  
pp. H1268-H1274 ◽  
Author(s):  
H. S. Iwamoto ◽  
E. Stucky ◽  
C. M. Roman
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Umbilical Cord ◽  
Cord Compression ◽  
Plasma Norepinephrine ◽  
Fetal Sheep ◽  
Umbilical Blood ◽  
Arterial Blood ◽  
Arterial Ph ◽  
Umbilical Blood Flow

To define responses of immature fetuses to asphyxia, we occluded the umbilical cord of 11 chronically instrumented fetal sheep at 82-94 days gestation and measured hemodynamic and catecholamine responses. The fetuses became acidemic, hypoxemic, and hypercarbic: arterial pH and PO2 decreased from 7.36 +/- 0.04 and 22 +/- 3 Torr to 7.10 +/- 0.04 (mean +/- SD, P less than 0.01) and 15 +/- 4 Torr (P less than 0.01), respectively, and PCO2 increased from 56 +/- 5 to 86 +/- 8 Torr (P less than 0.01) when umbilical blood flow was reduced by 75-88%. This degree of reduction in umbilical blood flow decreased cardiac output from 606 +/- 101 to 247 +/- 67 ml.min-1.kg-1 (P less than 0.01) and blood flow to hepatic, renal, musculoskeletal, and pulmonary vascular beds. Plasma norepinephrine concentrations increased from 1,557 +/- 975 to 16,718 +/- 14,672 pg/ml (P less than 0.05) with a 75-88% reduction, but mean arterial blood pressure did not increase. The absence of a hypertensive response probably relates to the decrease in cardiac output. These data indicate that asphyxia severely compromises cardiac output and organ perfusion in the midgestation fetus.

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