Contraction of human umbilical artery, but not vein, by oxygen.

McGrath, J.C.; MacLennan, S. J.; Mann, A C; Stuart-Smith, K.; Whittle, Martin

doi:10.1113/jphysiol.1986.sp016299

Cited by 32 publications

(16 citation statements)

References 8 publications

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“…As such, the oxygen tension of the umbilical arterial flow may be expected to be higher than in the lung. This has been established by measurement in utero as 15 Torr (McGrath et al, 1986). Direct measurement of the pO 2 of fetal lung tissue at 10-12 Torr is consistent with these considerations.…”

Section: Discussionsupporting

confidence: 69%

On the pulmonary toxicity of oxygen: III. The induction of oxygen dependency by oxygen use

Shanklin

2010

Experimental and Molecular Pathology

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Oxygen is central to the development of neonatal lung injury. The increase in oxygen exposure of the neonatal lung during the onset of extrauterine air breathing is an order of magnitude, from a range of 10-12 to 110-120 Torr. The contributions of oxygen and the volume and pressure relationships of ventilatory support to lung injury are not easily distinguished in the clinical setting. Sequential changes in inspired air or 100% oxygen were studied in 536 newborn rabbits without ventilatory support. Bilateral cervical vagotomies (BCV) were performed at 24 hours post natal to induce ventilatory distress which eventuates in hyaline membrane disease. The sequences applied yielded evidence for an induced state of oxygen dependency from oxygen use which was reflected in differences in survival and the extent of pulmonary injury. The median survival for animals kept in air throughout was 3 hours. Oxygen before vagotomy or during the first 3 hours afterwards extended the survival significantly but produced more extensive, more severe, and more rapid lung lesions. Returning animals to air after prior oxygen exposure reduced the number of survivors past 10 hours and shortened the maximum survival in those groups. These features indicate the development of a dependency of the defense mechanisms on the availability of oxygen at the higher level for metabolic and possibly other aspects of the pulmonary and systemic response to injury, beyond the usual physiological need.Subset analysis revealed additive and latent effects of oxygen and demonstrated a remarkable rapidity in onset of severe lesions under some circumstances, illustrating the toxicity of oxygen per se.

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Section: Discussionsupporting

confidence: 69%

On the pulmonary toxicity of oxygen: III. The induction of oxygen dependency by oxygen use

Shanklin

2010

Experimental and Molecular Pathology

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“…Following birth umbilical vein stays open and umbilical arteries constrict with increasing oxygen saturation, which allows the placental blood to flow towards the infant's circulation as demonstrated in the clinic (McGrath et al, 1986;Mercer and Skovgaard, Fig. 5.…”

Section: Placental Transfusion Improves Ventricular Function and Hemomentioning

confidence: 95%

Transition from fetal to neonatal circulation: Modeling the effect of umbilical cord clamping

Yigit

Kowalski

Hutchon

et al. 2015

Journal of Biomechanics

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Hemodynamics of the fetal to neonatal transition are orchestrated through complex physiological changes and results in cardiovascular adaptation to the adult biventricular circulation. Clinical practice during this critical period can influence vital organ physiology for normal newborns, premature babies and congenital heart defect patients. Particularly, the timing of the cord clamping procedure, immediate (ICC) vs. delayed cord clamping (DCC), is hypothesized to be an important factor for the transitory fetal hemodynamics. The clinical need for a quantitative understanding of this physiology motivated the development of a lumped parameter model (LPM) of the fetal cardio-respiratory system covering the late-gestation to neonatal period. The LPM was validated with in vivo clinical data and then used to predict the effects of cord clamping procedures on hemodynamics and vital gases. Clinical time-dependent resistance functions to simulate the vascular changes were introduced. For DCC, placental transfusion (31.3 ml) increased neonatal blood volume by 11.7%. This increased blood volume is reflected in an increase in preload pressures by ~20% compared to ICC, which in turn increased the cardiac output (CO) by 20% (COICC=993 ml/min; CODCC=1197 ml/min). Our model accurately predicted dynamic flow patterns in vivo. DCC was shown to maintain oxygenation if the onset of pulmonary respiration was delayed or impaired. On the other hand, a significant 25% decrease in oxygen saturations was observed when applying ICC under the same physiological conditions. We conclude that DCC has a significant impact on newborn hemodynamics, mainly because of the improved blood volume and the sustained placental respiration.

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“…Second, they contract when exposed to oxygen. 4,5 Third, they constrict sensitively to endothelin-1. 6,7 Fourth, they are composed of smooth muscle cells with adult phenotype, even during the neonatal period.…”

mentioning

confidence: 99%

Apoptosis and Regulation of Bax and Bcl-X Proteins During Human Neonatal Vascular Remodeling

Kim

Hwang

Seo

et al. 2000

ATVB

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Abstract-To verify that apoptosis is one of the possible mechanisms of neonatal vascular remodeling during the transition from fetal to neonatal circulation, we assayed for apoptosis and evaluated the expression of apoptosis-regulatory proteins in umbilical vessel versus ascending aorta, ductus arteriosus (DA) versus adjacent pulmonary artery and aorta, or aorta versus its branching arteries. Twenty-two umbilical cords (UCs), 6 DAs with adjacent aortas and pulmonary arteries, and 4 aortic arches with their branching great arteries were obtained from neonates. Smooth muscle cell (SMC) apoptosis in umbilical vessels was identified in all UCs. The expressions of Bax and Bcl-X were stronger in umbilical artery than in the neonatal aorta, but Bcl-2 was weak in both arteries in immunohistochemistry. In the immunoblot analysis of UCs, the expression of the proapoptotic short isoform of Bcl-X was stronger than in other tissue, and caspase-3 was selectively activated, whereas it was not in the other components of the cardiovascular system. In contrast, the expression patterns of the FasAg and Fas ligand were similar in umbilical artery and aorta. Regulation of Bcl-2 family proteins was also observed in other vascular sites at which SMCs undergo apoptosis on hemodynamic changes during birth, such as the DA and the branching points of the great arteries from the aortic arch. Apoptosis is involved in the regression of human umbilical vessels and the DA and in the remodeling of the branching great arteries during the neonatal period, when Bcl-2 family proteins are likely to play a key role. A poptosis is a form of programmed cell death that plays a vital role in the maintenance of cell homeostasis in mature organisms, in morphogenesis during development, and in the pathogenesis of various disorders. 1 During perinatal morphogenesis of the cardiovascular system, apoptosis is known to be involved in the molding and shaping of the conduction system, including the atrioventricular node and His bundle, 2 and the remodeling of the vasculature according to perinatal hemodynamic changes such as the regression of the abdominal aorta. 3 The 2 most important changes in the circulation system at birth are the closure of umbilical vessels and the ductus arteriosus. In previous studies of ours and others, it has been demonstrated that certain unique features of umbilical vessels and the ductus arteriosus may contribute to closure after birth. First, they are both arterial systems that close at birth. Second, they contract when exposed to oxygen. 4,5 Third, they constrict sensitively to endothelin-1. 6,7 Fourth, they are composed of smooth muscle cells with adult phenotype, even during the neonatal period. 8 In addition to these physiological properties and phenotypical characteristics, other mechanisms, such as apoptosis, could be involved in the closure of these vessels, a process that is the most dramatic example of vascular remodeling at birth. It has recently been reported that apoptosis of smooth muscle cells was found in areas of cy...

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Contraction of human umbilical artery, but not vein, by oxygen.

Cited by 32 publications

References 8 publications

On the pulmonary toxicity of oxygen: III. The induction of oxygen dependency by oxygen use

On the pulmonary toxicity of oxygen: III. The induction of oxygen dependency by oxygen use

Transition from fetal to neonatal circulation: Modeling the effect of umbilical cord clamping

Apoptosis and Regulation of Bax and Bcl-X Proteins During Human Neonatal Vascular Remodeling

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