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Journal articles on the topic 'Maternal physiology'

Author: Grafiati

Published: 24 June 2021

Last updated: 12 February 2022

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1

Jansson, Lauren M., Martha L. Velez, Krystle McConnell, Lorraine Milio, Nancy Spencer, Hendree Jones, and Janet A. DiPietro. "Maternal buprenorphine treatment during pregnancy and maternal physiology." Drug and Alcohol Dependence 201 (August 2019): 38–44. http://dx.doi.org/10.1016/j.drugalcdep.2019.03.018.

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2

BLECHNER, JACK N. "Maternal-Fetal Acid- Base Physiology." Clinical Obstetrics and Gynecology 36, no. 1 (March 1993): 3–12. http://dx.doi.org/10.1097/00003081-199303000-00004.

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3

STERRETT, MARY. "Maternal and Fetal Thyroid Physiology." Clinical Obstetrics and Gynecology 62, no. 2 (June 2019): 302–7. http://dx.doi.org/10.1097/grf.0000000000000439.

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4

Goulopoulou, Styliani. "Maternal Vascular Physiology in Preeclampsia." Hypertension 70, no. 6 (December 2017): 1066–73. http://dx.doi.org/10.1161/hypertensionaha.117.08821.

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5

Heidemann, Bernhard H., and John H. McClure. "Changes in maternal physiology during pregnancy." BJA CEPD Reviews 3, no. 3 (June 2003): 65–68. http://dx.doi.org/10.1093/bjacepd/mkg065.

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6

Taylor, Lucy, Brenda Kelly, and Paul Leeson. "Maternal Smoking and Infant Cardiovascular Physiology." Hypertension 55, no. 3 (March 2010): 614–16. http://dx.doi.org/10.1161/hypertensionaha.109.146944.

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7

Kadic, Aida Salihagic, and Maja Predojevic. "Fetal and Maternal Physiology and Ultrasound Diagnosis." Donald School Journal of Ultrasound in Obstetrics and Gynecology 7, no. 1 (2013): 9–35. http://dx.doi.org/10.5005/jp-journals-10009-1267.

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ABSTRACT Fetal developmental potential is determined at the moment of conception by genetic inheritance. However, this development is modulated by environmental factors. It is important to recognize that both, the mother and the fetus, actively participate in the maintenance of the physiological intrauterine environment. Unfortunately, the fetus is not entirely protected from harmful influences of the external factors. By altering the intrauterine environment, these factors can have a long-term effect on fetal health. How to cite this article Kadic AS, Predojevic M, Kurjak A. Fetal and Maternal Physiology and Ultrasound Diagnosis. Donald School J Ultrasound Obstet Gynecol 2013;7(1):9-35.

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8

Hauth, John C. "Oral Concurrent Session A Maternal Fetal Physiology." American Journal of Obstetrics and Gynecology 170, no. 1 (January 1994): 268–70. http://dx.doi.org/10.1016/s0002-9378(94)01022-7.

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9

Norwitz, Errol R., Valentine Edusa, and Joong Shin Park. "Maternal Physiology and Complications of Multiple Pregnancy." Seminars in Perinatology 29, no. 5 (October 2005): 338–48. http://dx.doi.org/10.1053/j.semperi.2005.08.002.

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10

Miller, Margaret, and Amanpreet Kaur. "General Management Principles of the Pregnant Woman." Seminars in Respiratory and Critical Care Medicine 38, no. 02 (April 2017): 123–34. http://dx.doi.org/10.1055/s-0037-1602167.

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AbstractPregnancy is a dynamic process that consists of profound physiological changes mediated by hormonal, mechanical, and circulatory pathways. Understanding of changes in physiology is essential for distinguishing abnormal and normal signs and symptoms in a pregnant patient. These physiological changes also have important pharmacotherapeutic considerations for a pregnant patient. Although there are limited data to guide decisions regarding medications and diagnostic procedures in pregnancy, a careful review of risks should be balanced with review of risk of withholding a medication or procedure. Interventional pulmonary procedures can be safely performed in pregnant women while keeping in mind the maternal anatomic and physiologic changes. Furthermore, management of a maternal cardiopulmonary arrest requires important modifications in patient positioning and intravenous access to ensure adequate efficacy of chest compressions, circulation, and airway management. This review will provide an overview of maternal physiologic changes with a focus on cardiopulmonary physiology, pharmacotherapeutic considerations, diagnostic and interventional pulmonary procedures during pregnancy, and cardiopulmonary resuscitation in pregnancy.

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11

Eaton, Malcolm, Xiang Zhao, Elizabeth Hanly, and James Cross. "Placental Hormones and Adaptability of Feto-maternal Physiology." Placenta 57 (September 2017): 233. http://dx.doi.org/10.1016/j.placenta.2017.07.044.

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12

Allen, D. G. "Notebook of Medical Physiology: Endocrinology with Aspects of Maternal, Fetal and Neonatal Physiology." Postgraduate Medical Journal 61, no. 716 (June 1, 1985): 557–58. http://dx.doi.org/10.1136/pgmj.61.716.557-b.

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13

Amir, Mohammed, Julia A. Brown, Stephanie L. Rager, Katherine Z. Sanidad, Aparna Ananthanarayanan, and Melody Y. Zeng. "Maternal Microbiome and Infections in Pregnancy." Microorganisms 8, no. 12 (December 15, 2020): 1996. http://dx.doi.org/10.3390/microorganisms8121996.

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Pregnancy induces unique changes in maternal immune responses and metabolism. Drastic physiologic adaptations, in an intricately coordinated fashion, allow the maternal body to support the healthy growth of the fetus. The gut microbiome plays a central role in the regulation of the immune system, metabolism, and resistance to infections. Studies have reported changes in the maternal microbiome in the gut, vagina, and oral cavity during pregnancy; it remains unclear whether/how these changes might be related to maternal immune responses, metabolism, and susceptibility to infections during pregnancy. Our understanding of the concerted adaption of these different aspects of the human physiology to promote a successful pregnant remains limited. Here, we provide a comprehensive documentation and discussion of changes in the maternal microbiome in the gut, oral cavity, and vagina during pregnancy, metabolic changes and complications in the mother and newborn that may be, in part, driven by maternal gut dysbiosis, and, lastly, common infections in pregnancy. This review aims to shed light on how dysregulation of the maternal microbiome may underlie obstetrical metabolic complications and infections.

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14

Flannelly, Kevin J., Ernest D. Kemble, D. Caroline Blanchard, and Robert J. Blanchard. "Effects of septal-forebrain lesions on maternal aggression and maternal care." Behavioral and Neural Biology 45, no. 1 (January 1986): 17–30. http://dx.doi.org/10.1016/s0163-1047(86)80002-4.

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15

Petry, Clive J., Ken K. Ong, and David B. Dunger. "Does the fetal genotype affect maternal physiology during pregnancy?" Trends in Molecular Medicine 13, no. 10 (October 2007): 414–21. http://dx.doi.org/10.1016/j.molmed.2007.07.007.

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16

Arens, Ursula. "Nutritional Physiology of Pregnancy; Current Concerns in Maternal Nutrition." Nutrition Bulletin 21, no. 3 (September 1996): 229–31. http://dx.doi.org/10.1111/j.1467-3010.1996.tb00861.x.

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17

Murray, Carson M., Margaret A. Stanton, Kaitlin R. Wellens, Rachel M. Santymire, Matthew R. Heintz, and Elizabeth V. Lonsdorf. "Maternal effects on offspring stress physiology in wild chimpanzees." American Journal of Primatology 80, no. 1 (January 12, 2016): e22525. http://dx.doi.org/10.1002/ajp.22525.

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18

Augustine, Mairin E., and Esther M. Leerkes. "Associations between maternal physiology and maternal sensitivity vary depending on infant distress and emotion context." Journal of Family Psychology 33, no. 4 (June 2019): 412–21. http://dx.doi.org/10.1037/fam0000538.

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19

Keller-Wood, Maureen, Xiaodi Feng, Charles E. Wood, Elaine Richards, Russell V. Anthony, Geoffrey E. Dahl, and Sha Tao. "Elevated maternal cortisol leads to relative maternal hyperglycemia and increased stillbirth in ovine pregnancy." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 307, no. 4 (August 15, 2014): R405—R413. http://dx.doi.org/10.1152/ajpregu.00530.2013.

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In normal pregnancy, cortisol increases; however, further pathological increases in cortisol are associated with maternal and fetal morbidities. These experiments were designed to test the hypothesis that increased maternal cortisol would increase maternal glucose concentrations, suppress fetal growth, and impair neonatal glucose homeostasis. Ewes were infused with cortisol (1 mg·kg−1·day−1) from day 115 of gestation to term; maternal glucose, insulin, ovine placental lactogen, estrone, progesterone, nonesterified free fatty acids (NEFA), β-hydroxybutyrate (BHB), and electrolytes were measured. Infusion of cortisol increased maternal glucose concentration and slowed the glucose disappearance after injection of glucose; maternal infusion of cortisol also increased the incidence of fetal death at or near parturition. The design of the study was altered to terminate the study prior to delivery, and post hoc analysis of the data was performed to test the hypothesis that maternal metabolic factors predict the fetal outcome. In cortisol-infused ewes that had stillborn lambs, plasma insulin was increased relative to control ewes or cortisol-infused ewes with live lambs. Maternal cortisol infusion did not alter maternal food intake or plasma NEFA, BHB, estrone, progesterone or placental lactogen concentrations, and it did not alter fetal body weight, ponderal index, or fetal organ weights. Our study suggests that the adverse effect of elevated maternal cortisol on pregnancy outcome may be related to the effects of cortisol on maternal glucose homeostasis, and that chronic maternal stress or adrenal hypersecretion of cortisol may create fetal pathophysiology paralleling some aspects of maternal gestational diabetes.

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20

Witek-Janusek, L. "Maternal ethanol ingestion: effect on maternal and neonatal glucose balance." American Journal of Physiology-Endocrinology and Metabolism 251, no. 2 (August 1, 1986): E178—E184. http://dx.doi.org/10.1152/ajpendo.1986.251.2.e178.

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Liver glycogen availability in the newborn is of major importance for the maintenance of postnatal blood glucose levels. This study examined the effect of maternal ethanol ingestion on maternal and neonatal glucose balance in the rat. Female rats were placed on the Lieber-DeCarli liquid ethanol diet, an isocaloric liquid pair-fed diet, or an ad libitum rat chow diet at 3 wk before mating and throughout gestation. Blood and livers were obtained from dams and rat pups on gestational days 21 and 22. The pups were studied up to 6 h in the fasted state and up to 24 h in the fed state. Maternal ethanol ingestion significantly decreased litter size, birth weight, and growth. A significantly higher mortality during the early postnatal period was seen in the prenatal ethanol exposed pups. Ethanol significantly decreased fed maternal liver glycogen stores but not maternal plasma glucose levels. The newborn rats from ethanol ingesting dams also had significantly decreased liver glycogen stores. Despite mobilizing their available glycogen, these prenatal ethanol exposed pups became hypoglycemic by 6 h postnatal. This was more marked in the fasted pups. Ethanol did not affect maternal nor neonatal plasma insulin levels. Thus maternal ethanol ingestion reduces maternal and neonatal liver glycogen stores and leads to postnatal hypoglycemia in the newborn rat.

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21

CHRISTENSEN, V. L., W. E. DONALDSON, and K. E. NESTOR. "Effect of Maternal Dietary Triiodothyronine on Embryonic Physiology of Turkeys." Poultry Science 72, no. 12 (December 1993): 2316–27. http://dx.doi.org/10.3382/ps.0722316.

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22

Moodley, S., A. Arunamata, K. J. Stauffer, S. E. Nourse, A. Chen, A. Quirin, and E. S. Selamet Tierney. "Maternal arterial stiffness and fetal cardiovascular physiology in diabetic pregnancy." Ultrasound in Obstetrics & Gynecology 52, no. 5 (September 25, 2018): 654–61. http://dx.doi.org/10.1002/uog.17528.

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23

Sha, Xiao-yan, Zheng-fang Xiong, Hui-shu Liu, Xiao-dan Di, and Tong-hui Ma. "Maternal-fetal fluid balance and aquaporins: from molecule to physiology." Acta Pharmacologica Sinica 32, no. 6 (May 23, 2011): 716–20. http://dx.doi.org/10.1038/aps.2011.59.

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24

Haslinger, C., H. Bamert, M. Rauh, T. Burkhardt, and L. Schäffer. "Effect of maternal smoking on stress physiology in healthy neonates." Journal of Perinatology 38, no. 2 (November 9, 2017): 132–36. http://dx.doi.org/10.1038/jp.2017.172.

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25

Leon, Michael. "The effect of constant light on maternal physiology and behavior." Physiology & Behavior 34, no. 4 (April 1985): 631–33. http://dx.doi.org/10.1016/0031-9384(85)90060-5.

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26

Zhou, Yunqian, Hongbo Qi, and Nanlin Yin. "Adaptations and alterations of maternal microbiota: From physiology to pathology." Medicine in Microecology 9 (September 2021): 100045. http://dx.doi.org/10.1016/j.medmic.2021.100045.

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27

Hocher, Berthold, You-Peng Chen, Ludwig Schlemm, Aline Burdack, Jian Li, Horst Halle, Thiemo Pfab, Philipp Kalk, Florian Lang, and Michael Godes. "Fetal sex determines the impact of maternal PROGINS progesterone receptor polymorphism on maternal physiology during pregnancy." Pharmacogenetics and Genomics 19, no. 9 (September 2009): 710–18. http://dx.doi.org/10.1097/fpc.0b013e328330bc7a.

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28

Viswanathan, N., and Fred C. Davis. "Maternal Entrainment of tau Mutant Hamsters." Journal of Biological Rhythms 7, no. 1 (April 1992): 65–74. http://dx.doi.org/10.1177/074873049200700106.

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29

Dandrea, J., S. Cooper, M. M. Ramsay, M. Keller-Woods, F. Broughton Pipkin, M. E. Symonds, and T. Stephenson. "The Effects of Pregnancy and Maternal Nutrition on the Maternal Renin-Angiotensin System in Sheep." Experimental Physiology 87, no. 3 (May 2002): 353–59. http://dx.doi.org/10.1113/eph8702320.

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30

Cooke, Christy-Lynn M., and Sandra T. Davidge. "Advanced maternal age and the impact on maternal and offspring cardiovascular health." American Journal of Physiology-Heart and Circulatory Physiology 317, no. 2 (August 1, 2019): H387—H394. http://dx.doi.org/10.1152/ajpheart.00045.2019.

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Delaying pregnancy, which is on the rise, may increase the risk of cardiovascular disease in both women and their children. The physiological mechanisms that lead to these effects are not fully understood but may involve inadequate adaptations of the maternal cardiovascular system to pregnancy. Indeed, there is abundant evidence in the literature that a fetus developing in a suboptimal in utero environment (such as in pregnancies complicated by fetal growth restriction, preterm birth, and/or preeclampsia) is at an increased risk of cardiovascular disease in adulthood, the developmental origins of health and disease theory. Although women of advanced age are at a significantly increased risk of pregnancy complications, there is limited information as to whether advanced maternal age constitutes an added stressor on the prenatal environment of the fetus, and whether or not this is secondary to impaired cardiovascular function during pregnancy. This review summarizes the current literature available on the impact of advanced maternal age on cardiovascular adaptations to pregnancy and the role of maternal age on long-term health risks for both the mother and offspring.

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31

Araki, Miyuki, Shota Nishitani, Keisho Ushimaru, Hideaki Masuzaki, Kazuyo Oishi, and Kazuyuki Shinohara. "Fetal response to induced maternal emotions." Journal of Physiological Sciences 60, no. 3 (February 19, 2010): 213–20. http://dx.doi.org/10.1007/s12576-010-0087-x.

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32

Elgendy, Islam Y., Syed Bukhari, Amr F. Barakat, Carl J. Pepine, Kathryn J. Lindley, and Eliza C. Miller. "Maternal Stroke." Circulation 143, no. 7 (February 16, 2021): 727–38. http://dx.doi.org/10.1161/circulationaha.120.051460.

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Maternal mortality rates have been steadily increasing in the United States, and cardiovascular mortality is the leading cause of death among pregnant and postpartum women. Maternal stroke accounts for a significant burden of cardiovascular mortality. Data suggest that rates of maternal stroke have been increasing in recent years. Advancing maternal age at the time of birth and the increasing prevalence of traditional cardiovascular risk factors, and other risk factors, as well, such as hypertensive disorders of pregnancy, migraine, and infections, may contribute to increased rates of maternal stroke. In this article, we provide an overview of the epidemiology of maternal stroke, explore mechanisms that may explain increasing rates of stroke among pregnant women, and identify key knowledge gaps for future investigation in this area.

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33

Sherman, D. J., M. G. Ross, L. Day, J. Humme, and M. G. Ervin. "Fetal swallowing: response to graded maternal hypoxemia." Journal of Applied Physiology 71, no. 5 (November 1, 1991): 1856–61. http://dx.doi.org/10.1152/jappl.1991.71.5.1856.

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A computer-based system, incorporating electromyography (EMG) and esophageal fluid flow measurement, was used to determine fetal breathing and swallowing responses to graded maternal hypoxemia. Five chronically prepared ewes with singleton fetuses at a gestational age of 130 +/- 2 (SE) days were subjected to successive 30-min periods of mild and moderate hypoxemia (inspired O2 fraction = 0.16 and 0.13, respectively). Mild and moderate maternal hypoxemia evoked significant reductions in fetal arterial PO2 (21 +/- 1 to 17 +/- 1 and 13 +/- 1 Torr, respectively), while fetal arterial pH, hematocrit, plasma osmolality, heart rate, and mean blood pressure did not change. Moderate hypoxemia was associated with significant increases in fetal plasma arginine vasopressin and renin activity and significant reductions from basal values in percent time breathing (53 +/- 4 to 25 +/- 12%), percent time swallowing (11.5 +/- 3.1 to 1.3 +/- 0.7%), and volume swallowed (21.3 +/- 2.1 to 4.8 +/- 2.7 ml/30 min). Fetal swallowing activity was better correlated with arterial PO2 (r = 0.8) than breathing activity (r = 0.45). We conclude that fetal swallowing is suppressed during mild and moderate hypoxemia. It is suggested that several sites and/or mechanisms may account for the hypoxemic inhibition of fetal activities.

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34

Woods, Lori L. "Maternal glucocorticoids and prenatal programming of hypertension." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 291, no. 4 (October 2006): R1069—R1075. http://dx.doi.org/10.1152/ajpregu.00753.2005.

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Maternal glucocorticoids have been postulated to play an important role in prenatal programming for adult hypertension in the offspring. However, we have shown previously that offspring hypertension caused by maternal dexamethasone subcutaneous administration at 100 μg·kg−1·day−1can be accounted for by the corresponding reduction in food intake that these mothers experience. The present studies were designed to determine whether there is a lower dose of dexamethasone that does not reduce maternal food intake yet still causes hypertension in the adult offspring. Pregnant rats were treated with subcutaneous dexamethasone at 50 (D50) or 25 (D25) μg·kg−1·day−1on days 15–20 of pregnancy. An additional group was untreated or received vehicle injections (control). D25 and D50 dams reduced their food intake by 17% during and after treatment and gained 31% less weight than control over the course of gestation. In adulthood (∼21 wk), chronically instrumented male offspring of D50 and D25 had normal blood pressures (D50: 131 ± 2 mmHg and D25: 127 ± 3 mmHg vs. 127 ± 2 mmHg in control). Qualitatively similar results were found in female offspring. Thus neither dexamethasone per se at these doses nor the accompanying modest reductions in maternal food intake and weight gain have blood pressure programming effects. As far as has been tested, there does not appear to be a dose of dexamethasone that, given over this time period in the rat, programs offspring hypertension without reducing maternal food intake and weight gain. These data do not support the hypothesis that maternal glucocorticoids program offspring hypertension directly.

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35

Mahendru, Amita A., Thomas R. Everett, Carmel M. McEniery, Ian B. Wilkinson, and Christoph C. Lees. "O12. Pre-pregnancy to early pregnancy changes in maternal cardiovascular physiology." Pregnancy Hypertension: An International Journal of Women's Cardiovascular Health 1, no. 3-4 (July 2011): 262–63. http://dx.doi.org/10.1016/j.preghy.2011.08.044.

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36

Dooley, Sharon L. "Oral Concurrent Session D Labor Intrapartum Fetal Evaluation Maternal Fetal Physiology." American Journal of Obstetrics and Gynecology 170, no. 1 (January 1994): 284–86. http://dx.doi.org/10.1016/s0002-9378(94)01026-4.

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37

Van Mieghem, T., R. van Bree, E. Van Herck, R. Pijnenborg, J. Deprest, and J. Verhaeghe. "Maternal Apelin Physiology during Rat Pregnancy: The Role of the Placenta." Placenta 31, no. 8 (August 2010): 725–30. http://dx.doi.org/10.1016/j.placenta.2010.06.001.

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38

Sakala, Carol, Amy M. Romano, and Sarah J. Buckley. "Hormonal Physiology of Childbearing, an Essential Framework for Maternal–Newborn Nursing." Journal of Obstetric, Gynecologic & Neonatal Nursing 45, no. 2 (March 2016): 264–75. http://dx.doi.org/10.1016/j.jogn.2015.12.006.

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39

Sakala, Carol, Amy M. Romano, and Sarah J. Buckley. "Hormonal Physiology of Childbearing, an Essential Framework for Maternal–Newborn Nursing." Journal of Obstetric, Gynecologic & Neonatal Nursing 45, no. 2 (March 2016): e3-e4. http://dx.doi.org/10.1016/j.jogn.2016.01.003.

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40

Reiter, Russel J., Dun Xian Tan, Ahmet Korkmaz, and Sergio A. Rosales-Corral. "Melatonin and stable circadian rhythms optimize maternal, placental and fetal physiology." Human Reproduction Update 20, no. 2 (October 16, 2013): 293–307. http://dx.doi.org/10.1093/humupd/dmt054.

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41

Donovan, Wilberta L., and Lewis A. Leavitt. "Maternal Self-Efficacy and Infant Attachment: Integrating Physiology, Perceptions, and Behavior." Child Development 60, no. 2 (April 1989): 460. http://dx.doi.org/10.2307/1130990.

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42

Mahendru, A. A., C. C. Lees, T. R. Everett, I. B. Wilkinson, and C. M. McEniery. "P5.01 PRE-PREGNANCY TO EARLY PREGNANCY CHANGES IN MATERNAL CARDIOVASCULAR PHYSIOLOGY." Artery Research 5, no. 4 (2011): 162. http://dx.doi.org/10.1016/j.artres.2011.10.058.

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43

Wilding, Martin, Loredana Di Matteo, and Brian Dale. "The maternal age effect: a hypothesis based on oxidative phosphorylation." Zygote 13, no. 4 (November 2005): 317–23. http://dx.doi.org/10.1017/s0967199405003382.

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The ‘maternal age effect’ in human reproduction, characterized by a negative relationship between maternal age and reproductive efficiency, remains a poorly understood phenomenon. Current data suggest that oocyte physiology determines this relationship. In this review, we present a hypothesis of a mitochondrial role in the physiology of ageing in human oocytes. We suggest that the efficiency of oxidative phosphorylation in the ageing human oocyte is degraded by free radical attack on the primordial oocytes residing in the ovary. Although deficiencies in oxidative phosphorylation can be accounted for in the short term by anaerobic respiration, we suggest that, in the long term, the level of oxidative phosphorylation strongly influences oocyte quality.

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44

Firth, E. C., C. W. Rogers, M. Vickers, P. R. Kenyon, C. M. C. Jenkinson, H. T. Blair, P. L. Johnson, D. D. S. Mackenzie, S. W. Peterson, and S. T. Morris. "The bone-muscle ratio of fetal lambs is affected more by maternal nutrition during pregnancy than by maternal size." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 294, no. 6 (June 2008): R1890—R1894. http://dx.doi.org/10.1152/ajpregu.00805.2007.

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Bone formation and loss are related to the strain imposed on bone by muscle forces. Bone mineral content (BMC) and lean mass (LM) of fetal lambs was determined at day 140 of pregnancy in 8 groups of ewes, which were of either large or small body size, on either high (ad libitum) or maintenance pasture intake from day 21 of pregnancy, or carrying either singletons or twins. BMC and LM (using DXA scanning) of fetal hindquarters/spine were corrected to leg length. BMC and LM were less in twin than singleton groups ( P < 0.001). Large ewes on high intake produced single fetuses with a (group mean) BMC/LM ratio that was higher ( P < 0.002) than that in fetuses of large ewes with singletons on maintenance intake or twins on either high or maintenance intakes, the ratios of which were not different. In single fetuses from small ewes on high intake, the BMC/LM ratio was higher than those from small ewes with singletons on maintenance intake or twins on either high or maintenance intakes, the ratios of which were not different. The ratio was not different in singleton fetuses of ewes on high intake, whether they were large or small. Different fetal environments resulted in a given amount of muscle being associated with a higher or lower bone mass. Dietary intake during pregnancy was more important than maternal size in affecting the ratio. We conclude that intrauterine environmental factors may be important in determining bone mass postnatally, and possibly later in life.

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45

Wood, Charles E. "Maternal binge drinking and fetal neuronal damage." Experimental Physiology 92, no. 5 (August 17, 2007): 821. http://dx.doi.org/10.1113/expphysiol.2007.038448.

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46

Osol, George, Nga Ling Ko, and Maurizio Mandalà. "Plasticity of the Maternal Vasculature During Pregnancy." Annual Review of Physiology 81, no. 1 (February 10, 2019): 89–111. http://dx.doi.org/10.1146/annurev-physiol-020518-114435.

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Maternal cardiovascular changes during pregnancy include an expansion of plasma volume, increased cardiac output, decreased peripheral resistance, and increased uteroplacental blood flow. These adaptations facilitate the progressive increase in uteroplacental perfusion that is required for normal fetal growth and development, prevent the development of hypertension, and provide a reserve of blood in anticipation of the significant blood loss associated with parturition. Each woman's genotype and phenotype determine her ability to adapt in response to molecular signals that emanate from the fetoplacental unit. Here, we provide an overview of the major hemodynamic and cardiac changes and then consider regional changes in the splanchnic, renal, cerebral, and uterine circulations in terms of endothelial and vascular smooth muscle cell plasticity. Although consideration of gestational disease is beyond the scope of this review, aberrant signaling and/or maternal responsiveness contribute to the etiology of several common gestational diseases such as preeclampsia, intrauterine growth restriction, and gestational diabetes.

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47

Liu, L. X., and Z. Arany. "Maternal cardiac metabolism in pregnancy." Cardiovascular Research 101, no. 4 (January 20, 2014): 545–53. http://dx.doi.org/10.1093/cvr/cvu009.

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48

Stangenberg, Stefanie, Long The Nguyen, Yik Lung Chan, Amgad Zaky, Carol A. Pollock, Hui Chen, and Sonia Saad. "Maternal L-carnitine supplementation ameliorates renal underdevelopment and epigenetic changes in male mice offspring due to maternal smoking." Clinical and Experimental Pharmacology and Physiology 46, no. 2 (November 22, 2018): 183–93. http://dx.doi.org/10.1111/1440-1681.13038.

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Hillerer, Katharina Maria, Volker Rudolf Jacobs, Thorsten Fischer, and Ludwig Aigner. "The Maternal Brain: An Organ with Peripartal Plasticity." Neural Plasticity 2014 (2014): 1–20. http://dx.doi.org/10.1155/2014/574159.

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Abstract:

The time of pregnancy, birth, and lactation, is characterized by numerous specific alterations in several systems of the maternal body. Peripartum-associated changes in physiology and behavior, as well as their underlying molecular mechanisms, have been the focus of research since decades, but are still far from being entirely understood. Also, there is growing evidence that pregnancy and lactation are associated with a variety of alterations in neural plasticity, including adult neurogenesis, functional and structural synaptic plasticity, and dendritic remodeling in different brain regions. All of the mentioned changes are not only believed to be a prerequisite for the proper fetal and neonatal development, but moreover to be crucial for the physiological and mental health of the mother. The underlying mechanisms apparently need to be under tight control, since in cases of dysregulation, a certain percentage of women develop disorders like preeclampsia or postpartum mood and anxiety disorders during the course of pregnancy and lactation. This review describes common peripartum adaptations in physiology and behavior. Moreover, it concentrates on different forms of peripartum-associated plasticity including changes in neurogenesis and their possible underlying molecular mechanisms. Finally, consequences of malfunction in those systems are discussed.

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Pappas, A. C., E. Zoidis, P. F. Surai, and G. Zervas. "Selenoproteins and maternal nutrition." Comparative Biochemistry and Physiology Part B: Biochemistry and Molecular Biology 151, no. 4 (December 2008): 361–72. http://dx.doi.org/10.1016/j.cbpb.2008.08.009.

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