Respiratory Gas Exchange in the Placenta

Longo, Lawrence D.

doi:10.1002/cphy.cp030418

Cited by 29 publications

(30 citation statements)

References 269 publications

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“…Moreover, because of increased branching, and thus larger numbers of capillaries per unit of tissue (Figure 3), the surface area available for exchange is greater in fetal cotyledons compared with maternal caruncles during the last trimester (Reynolds et al 2005). As mentioned above, the thickness of the barrier between the fetal and maternal capillaries also may be reduced throughout gestation (Faber and Thornburg 1983;Longo 1987). Taken together, these observations help to explain why the proportion of the nutrients and oxygen taken up by the gravid uterus that is transported to the fetus increases by two-to fourfold from midto late gestation, essentially keeping pace with the rate of fetal growth.…”

Section: Placental Microvascular Architecturementioning

confidence: 77%

“…Based on these and numerous other studies, it seems that increased blood flow, rather than increased extraction, is the primary mechanism of increased transplacental exchange throughout gestation Redmer 1995, 2001;Reynolds et al 2005). In addition, the transport capacity for CO, which is lipid soluble and thus highly permeable across the placental barrier, increases throughout gestation, which indicates not only changes in blood flow but also in the nature of the placental barrier (e.g., increased capillary surface area, decreased thickness of the barrier) during gestation (Faber and Thornburg 1983;Longo 1987).…”

mentioning

confidence: 98%

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Functional Significance of Developmental Changes in Placental Microvascular Architecture

et al. 2005

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Section: Placental Microvascular Architecturementioning

confidence: 77%

mentioning

confidence: 98%

Functional Significance of Developmental Changes in Placental Microvascular Architecture

et al. 2005

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“…5), the surface area available for exchange is greater in fetal cotyledonary villi compared with maternal caruncles during the last third of pregnancy (Reynolds et al, 2005a,b). Additionally, the thickness of the barrier between the fetal and maternal capillaries also may be reduced throughout gestation (Faber and Thornburg, 1983;Longo 1987). Taken together, these observations help to explain why in normal pregnancies the proportion of the nutrients and oxygen taken up by the gravid uterus that is transported to the fetus increases by 2-to 4-fold from mid to late gestation (and, conversely, the proportion that is utilized by the placenta decreases by 2-to 4-4-fold), essentially keeping pace with the rate of fetal growth (Reynolds and Redmer, 1995;Reynolds et al, 2005c).…”

Section: Further Evidence For the Importance Of Placental Angiogenesimentioning

confidence: 99%

Uteroplacental vascular development and placental function: an update

Reynolds¹,

Borowicz²,

Caton³

et al. 2010

Int. J. Dev. Biol.

160

113

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The importance of the placenta and its vascular development to fetal growth and development has been appreciated since ancient times. Based on numerous studies in humans and animal model organisms in the last 2-3 decades, normal placental angiogenesis is critically important to ensure adequate blood flow to the placenta and therefore to provide the substrates that support normal fetal growth. Placental angiogenesis is abnormal at term in compromised pregnancies (those in which fetal growth is altered), including those resulting from maternal nutritional or environmental stress, maternal age, increased numbers of fetuses, maternal or fetal genotype, or the use of assisted reproductive technologies (e.g., cloning by somatic cell nuclear transfer). We and others have recently shown that these defects in placental vascular development occur quite early in pregnancy and may therefore presage compromised fetal growth and development. The challenges will be to find biomarkers of abnormal placental angiogenesis and to develop therapeutic strategies to "rescue" placental vascular development and thus fetal growth in compromised pregnancies. Animal models will be essential in meeting these challenges.

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“…Following birth the PO 2 rises to 70±10 Torr, and then continues to rise to an adult value of ~100±5 Torr [72]. In terms of cerebral O 2 delivery, because of relatively higher values of hemoglobin concentration (~21g/dl) and a lower value of P 50 (O 2 tension at which hemoglobin is 50% saturated, ~20 Torr), the fetus has a similar value of arterial O 2 content, despite its significantly lower arterial O 2 tension [76] (Table 1 ). The fetus also has not only a relatively higher CO 2 tension (44±2 versus 35±2 Torr) [70, 74], but a 30% greater mass of total CO 2 in the blood, compared to the adult [77].…”

Section: Cerebral Blood Flow In the Fetus And Newborn Infantmentioning

confidence: 99%

Cerebral Artery Signal Transduction Mechanisms: Developmental Changes in Dynamics and Ca<sup>2+</sup> Sensitivity

Longo¹,

Goyal²

2013

CVP

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As compared to the adult, the developing fetus and newborn infant are at much greater risk for dysregulation of cerebral blood flow (CBF), with complications such as intraventricular and germinal matrix hemorrhage with resultant neurologic sequelae. To minimize this dysregulation and its consequences presents a major challenge. Although in many respects the fundamental signal transduction mechanisms that regulate relaxation and contraction pathways, and thus cerebrovascular tone and CBF in the immature organism are similar to those of the adult, the individual elements, pathways, and roles differ greatly. Here, we review aspects of these maturational changes of relaxation/contraction mechanisms in terms of both electro-mechanical and pharmaco-mechanical coupling, their biochemical pathways and signaling networks. In contrast to the adult cerebrovasculature, in addition to attenuated structure with differences in multiple cytoskeletal elements, developing cerebrovasculature of fetus and newborn differs in many respects, such as a strikingly increased sensitivity to [Ca2+]i and requirement for extracellular Ca2+ for contraction. In essence, the immature cerebrovasculature demonstrates both “hyper-relaxation” and “hypo-contraction”. A challenge is to unravel the manner in which these mechanisms are integrated, particularly in terms of both Ca2+-dependent and Ca2+-independent pathways to increase Ca2+ sensitivity. Gaining an appreciation of these significant age-related differences in signal mechanisms also will be critical to understanding more completely the vulnerability of the developing cerebral vasculature to hypoxia and other stresses. Of vital importance, a more complete understanding of these mechanisms promises hope for improved strategies for therapeutic intervention and clinical management of intensive care of the premature newborn.

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Respiratory Gas Exchange in the Placenta

Cited by 29 publications

References 269 publications

Functional Significance of Developmental Changes in Placental Microvascular Architecture

Functional Significance of Developmental Changes in Placental Microvascular Architecture

Uteroplacental vascular development and placental function: an update

Cerebral Artery Signal Transduction Mechanisms: Developmental Changes in Dynamics and Ca<sup>2+</sup> Sensitivity

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