An important set of problems in perinatal biology concern the dynamics and control of placental respiratory gas exchange and fetal oxygenation. The proposed studies will test several hypotheses concerning the control of O2 consumption. For instance, we will test the hypothesis that fetal oxygen consumptioon is constant and unvarying. We will measure for the first time on a continuous basis the placental exchange rate and 02 consumption of the total uterine contents, the fetus, and the placenta plus uterus. We will explore the extent to which 02 consumption of these components are constant vs whether they change spontaneously in a dynamic manner. We will examine the extent to which uterine contractures, contractions, fetal breathing movements, and other factors affect O2 consumption. In addition, we will seek and understanding of whether O2 consumption of the fetus is affected by O2 content, O2 tension, or both. In addition, we will examine the dependency of fetal O2 consumption on increased temperature, resulting from maternal exercise. We will also determine the dose-response relations of fetal 02 consumption on increased temperature, resulting from maternal exercise. We will also determine the dose-response relations of fetal O2 consumption to the circulating concentrations of norepinephrine and triodothyronine infusion. We also will examine the role of both uterine and umbilical blood flows in affecting 02 consumption, the time constants of change, and the extent to which the blood flow on one side of the placental circulation alters to match that of the other. Taken as a whole these studies should markedly increase our understanding of the dynamics and control of placental 02 exchange, and fetal oxygen consumption.

Agency
National Institute of Health (NIH)
Institute
Eunice Kennedy Shriver National Institute of Child Health & Human Development (NICHD)
Type
Research Project (R01)
Project #
5R01HD003807-19
Application #
3310215
Study Section
Human Embryology and Development Subcommittee 2 (HED)
Project Start
1978-02-01
Project End
1989-06-30
Budget Start
1987-12-01
Budget End
1989-06-30
Support Year
19
Fiscal Year
1988
Total Cost
Indirect Cost
Name
Loma Linda University
Department
Type
Schools of Medicine
DUNS #
City
Loma Linda
State
CA
Country
United States
Zip Code
92350
Goyal, Ravi; Goyal, Dipali; Longo, Lawrence D et al. (2016) Microarray gene expression analysis in ovine ductus arteriosus during fetal development and birth transition. Pediatr Res 80:610-8
Vrancken, Kurt; Schroeder, Hobe J; Longo, Lawrence D et al. (2016) Postprandial lipids accelerate and redirect nitric oxide consumption in plasma. Nitric Oxide 55-56:70-81
Blum-Johnston, Carla; Thorpe, Richard B; Wee, Chelsea et al. (2016) Developmental acceleration of bradykinin-dependent relaxation by prenatal chronic hypoxia impedes normal development after birth. Am J Physiol Lung Cell Mol Physiol 310:L271-86
Dobyns, Abigail E; Goyal, Ravi; Carpenter, Lauren Grisham et al. (2015) Macrophage gene expression associated with remodeling of the prepartum rat cervix: microarray and pathway analyses. PLoS One 10:e0119782
Tao, Xiaoxiao; Lin, Mike T; Thorington, Glyne U et al. (2015) Long-term hypoxia increases calcium affinity of BK channels in ovine fetal and adult cerebral artery smooth muscle. Am J Physiol Heart Circ Physiol 308:H707-22
Goyal, Ravi; Longo, Lawrence D (2014) Acclimatization to long-term hypoxia: gene expression in ovine carotid arteries. Physiol Genomics 46:725-34
Goyal, Ravi; Goyal, Dipali; Chu, Nina et al. (2014) Cerebral artery alpha-1 AR subtypes: high altitude long-term acclimatization responses. PLoS One 9:e112784
Goyal, Ravi; Van Wickle, Jonathan; Goyal, Dipali et al. (2013) Antenatal maternal long-term hypoxia: acclimatization responses with altered gene expression in ovine fetal carotid arteries. PLoS One 8:e82200
Longo, Lawrence D; Goyal, Ravi (2013) Cerebral artery signal transduction mechanisms: developmental changes in dynamics and Ca2+ sensitivity. Curr Vasc Pharmacol 11:655-711
Papamatheakis, Demosthenes G; Blood, Arlin B; Kim, Joon H et al. (2013) Antenatal hypoxia and pulmonary vascular function and remodeling. Curr Vasc Pharmacol 11:616-40

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