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Fetal macrophages are not present in the myometrium of women who undergo labor at term
S170 SMFM Abstracts 594 FETAL HEART RATE RESPONSES TO ACUTE MATERNAL HYPO- AND HYPERCAPNIA IN LATE GESTATION DEREK FRASER1, DENNIS JENSEN2, LARRY WOLFE2, PHILIP HAHN1, GREGORY DAVIES1, 1Queen’s University at Kingston, Obstetrics and Gynecology, Kingston, Ontario, Canada, 2Queen’s University at Kingston, Physical and Health Education, Kingston, Ontario, Canada OBJECTIVE: To examine the fetal heart rate (FHR) response to maternal hypo- and hypercapnia in late gestation. STUDY DESIGN: Twenty-seven women with healthy singleton pregnancies performed a modified carbon dioxide rebreathing procedure that included prior hyperventilation and maintenance of hyperoxia (end-tidal oxygen tension = 150 Torr). Prior to rebreathing, subjects hyperventilated for 5minutes to reduce the end-tidal CO2 tension (PETCO2) to less than 23 Torr and then switched to a bag containing a normocapnic-hyperoxic gas mixture. During rebreathing, PETCO2 increased from hypocapnia to hypercapnia (4060 Torr). FHR responses were monitored before, during and after rebreathing and classified using the National Institute of Child Health and Development guidelines. The study protocol was approved by the Queen’s University Health Sciences Research Ethics Board. RESULTS: Baseline FHR increased during hyperventilation (144G9.8 bpm) compared to the pretest period (138G7.9 bpm, p = 0.023). There was a decrease in baseline FHR during rebreathing (134G11.7 bpm) compared to hyperventilation (144G9.8 bpm, p!0.001). Baseline FHR was not significantly different between pretest (138G7.9 bpm) and posttest periods (138G12.2 bpm, p=0.992). There were no significant changes in FHR variability throughout the study (p=0.103). There was no difference in accelerations in the pretest period (5.3G3.4) compared to the posttest period (6.3G2.9, p=0.159). Mild tachycardia of 165 bpm was noted in one tracing during rebreathing and no significant bradycardias were recorded. CONCLUSION: Acute maternal hypo- and hypercapnia during modified rebreathing has no adverse effects on fetal well-being. Changes were noted in baseline FHR during hyperventilation and rebreathing. Although statistically significant, the heart rate parameters remained within normal ranges and are not likely to be clinically significant, making this technique safe for research purposes.
596 FETAL MACROPHAGES ARE NOT PRESENT IN THE MYOMETRIUM OF WOMEN WHO UNDERGO LABOR AT TERM CHONG JAI KIM1, JUNG-SUN KIM1, SOONG DEOK LEE2, YEON MEE KIM1, KARINA RICHANI3, JIMMY ESPINOZA3, ROBERTO ROMERO4, 1 Wayne State University School of Medicine, Department of Pathology, Detroit, Michigan, 2Seoul National University College of Medicine, Department of Forensic Medicine, Seoul, South Korea, 3Wayne State University School of Medicine, Department of Obstetrics and Gynecology, Detroit, Michigan, 4Perinatology Research Branch, NICHD, NIH, DHHS, Bethesda, Maryland OBJECTIVE: A role for surfactant protein-A in the initiation of labor has been proposed in mice (PNAS 2004;101:4978). This protein was postulated to induce migration and subsequent activation of fetal macrophages. Fetal macrophages were proposed to invade the myometrium. The purpose of this study was to determine if fetal macrophages invade the myometrium of women in labor. STUDY DESIGN: Placental bed biopsy specimens were obtained from patients with male fetuses at term with (n = 5) or without (n = 2) labor. Non-placental bed biopsy specimens were also evaluated in three of the cases with labor. Formalin-fixed, paraffin-embedded sections were immunostained for CD68, a marker for macrophages. CD68 (C) macrophages in myometrium were obtained by laser capture microdissection. Sex typing of the microdissected macrophages was done by polymerase chain reaction (PCR) for amelogenin. RESULTS: PCR results demonstrated that the microdissected macrophages from both the placental bed and the non-placental bed specimens were of female origin in all cases. CONCLUSION: These observations do not support the hypothesis that fetal macrophages are present in the myometrium at the time of labor in humans.
595 ALTERED FETO-PLACENTAL GROWTH RATIOS DURING MID-GESTATION UNDERNUTRITION IN RAT DAMS ANDREA JELKS1, LINDA DAY1, STACY BEHARE1, MICHAEL G. ROSS1, MINA DESAI1, 1Harbor-UCLA Med. Ctr. (LA BioMed), Dept. of Ob/Gyn, Torrance, California OBJECTIVE: Human and animal studies have shown that maternal undernutrition during pregnancy is associated with abnormal placental growth. Small for gestational age babies or those with altered placental growth show an increased risk of developing coronary heart disease, hypertension and diabetes during adult life. The placenta functions as a key mediator between the mother and fetus, and hence may adversely affect the nutrient supply to the fetus. Currently the impact of maternal nutrition during different periods of gestation on feto-placental growth is not well understood. We therefore sought to determine the impact of in utero undernutrition during midpregnancy on placental and fetal growth. STUDY DESIGN: Time-dated pregnant Sprague-Dawley rats (n = 8) were fed an ad libitum diet (control) or were subjected to 50% food restriction (FR) relative to controls from day 10 of gestation. On gestational day 16, rat dams were euthanized, and the uterus delivered. For each gestational sac, the weight was determined before and after drainage of the amniotic fluid. The placenta and fetus were separated and weighed. Results (meanGSE) were analyzed using unpaired t-test. RESULTS: FR pregnancies showed no significant difference in the placental weight (0.40G0.01 vs. 0.37G0.02 g) or amniotic fluid volume (0.39G0.01 vs. 0.42G0.02 g) as compared to controls. The fetal weights showed a non significant trend toward smaller size in the FR gestations (0.46G0.01 vs. 0.50G0.02 g). However, the ratio of the placenta to fetal weight was significantly increased in the FR pregnancies (0.86G0.02 vs. 0.74G0.04, p!0.05) relative to controls. CONCLUSION: Although maternal undernutrition during mid-pregnancy does not adversely affect placental growth, it resulted in higher placental/fetal growth ratio. This could potentially have long-term implications as suggested by studies linking higher placental/fetal ratios to increased risk of cardiovascular disease, hypertension and diabetes in adults.
597 TERBUTALINE INHIBITS CRH EXPRESSION IN HUMAN TROPHOBLAST CELLS EFTICHIA KONTOPOULOS (F)1, CHRISTINA CHANDRAS2, KATIA KARALIS3, 1Robert Wood Johnson University Hospital- UMDNJ, Obstetrics, Gynecology and Reproductive sciences, New Brunswick, New Jersey, 2Biomedical research of the Academy of Athens, Department of Endocrinology, Athens, Greece, Greece, 3Childrens Hospital/Harvard Medical School, Endocrinology, Boston, Massachusetts OBJECTIVE: To evaluate the effect of beta adrenergic agonists on the regulation of the expression of the placental corticotropin release hormone (CRH) gene. STUDY DESIGN: Term placentae were collected at the time of elective cesarean section, and were processed for trophoblast cells isolation and culture. The isolated trothoblasts were plated, cultured and were subsequently treated with terbutaline, RU486, and/or vehicle control. The messanger RNA (mRNA) abundance of CRH and of the house-keeping gene beta-actin were evaluated by Northern blot analysis. RESULTS: Exposure of the trophoblasts to terbutaline (10ÿ8M) inhibited the expression of the CRH gene as depicted by Northern blot analysis using a specific riboprobe. Co-addition of terbutaline (10ÿ8M) and RU486 (10ÿ6M),which is a progesterone/glucocorticoid antagonist, did not block the stimulatory effects of RU 486 on placental CRH expression. CONCLUSION: The beta- adrenergic agonist terbutaline inhibits the expression of CRH in human trophoblast cells. This finding may provide insight in the mechanism of action of terbutaline and its clinical applications.
596 FETAL MACROPHAGES ARE NOT PRESENT IN THE MYOMETRIUM OF WOMEN WHO UNDERGO LABOR AT TERM CHONG JAI KIM1, JUNG-SUN KIM1, SOONG DEOK LEE2, YEON MEE KIM1, KARINA RICHANI3, JIMMY ESPINOZA3, ROBERTO ROMERO4, 1 Wayne State University School of Medicine, Department of Pathology, Detroit, Michigan, 2Seoul National University College of Medicine, Department of Forensic Medicine, Seoul, South Korea, 3Wayne State University School of Medicine, Department of Obstetrics and Gynecology, Detroit, Michigan, 4Perinatology Research Branch, NICHD, NIH, DHHS, Bethesda, Maryland OBJECTIVE: A role for surfactant protein-A in the initiation of labor has been proposed in mice (PNAS 2004;101:4978). This protein was postulated to induce migration and subsequent activation of fetal macrophages. Fetal macrophages were proposed to invade the myometrium. The purpose of this study was to determine if fetal macrophages invade the myometrium of women in labor. STUDY DESIGN: Placental bed biopsy specimens were obtained from patients with male fetuses at term with (n = 5) or without (n = 2) labor. Non-placental bed biopsy specimens were also evaluated in three of the cases with labor. Formalin-fixed, paraffin-embedded sections were immunostained for CD68, a marker for macrophages. CD68 (C) macrophages in myometrium were obtained by laser capture microdissection. Sex typing of the microdissected macrophages was done by polymerase chain reaction (PCR) for amelogenin. RESULTS: PCR results demonstrated that the microdissected macrophages from both the placental bed and the non-placental bed specimens were of female origin in all cases. CONCLUSION: These observations do not support the hypothesis that fetal macrophages are present in the myometrium at the time of labor in humans.
595 ALTERED FETO-PLACENTAL GROWTH RATIOS DURING MID-GESTATION UNDERNUTRITION IN RAT DAMS ANDREA JELKS1, LINDA DAY1, STACY BEHARE1, MICHAEL G. ROSS1, MINA DESAI1, 1Harbor-UCLA Med. Ctr. (LA BioMed), Dept. of Ob/Gyn, Torrance, California OBJECTIVE: Human and animal studies have shown that maternal undernutrition during pregnancy is associated with abnormal placental growth. Small for gestational age babies or those with altered placental growth show an increased risk of developing coronary heart disease, hypertension and diabetes during adult life. The placenta functions as a key mediator between the mother and fetus, and hence may adversely affect the nutrient supply to the fetus. Currently the impact of maternal nutrition during different periods of gestation on feto-placental growth is not well understood. We therefore sought to determine the impact of in utero undernutrition during midpregnancy on placental and fetal growth. STUDY DESIGN: Time-dated pregnant Sprague-Dawley rats (n = 8) were fed an ad libitum diet (control) or were subjected to 50% food restriction (FR) relative to controls from day 10 of gestation. On gestational day 16, rat dams were euthanized, and the uterus delivered. For each gestational sac, the weight was determined before and after drainage of the amniotic fluid. The placenta and fetus were separated and weighed. Results (meanGSE) were analyzed using unpaired t-test. RESULTS: FR pregnancies showed no significant difference in the placental weight (0.40G0.01 vs. 0.37G0.02 g) or amniotic fluid volume (0.39G0.01 vs. 0.42G0.02 g) as compared to controls. The fetal weights showed a non significant trend toward smaller size in the FR gestations (0.46G0.01 vs. 0.50G0.02 g). However, the ratio of the placenta to fetal weight was significantly increased in the FR pregnancies (0.86G0.02 vs. 0.74G0.04, p!0.05) relative to controls. CONCLUSION: Although maternal undernutrition during mid-pregnancy does not adversely affect placental growth, it resulted in higher placental/fetal growth ratio. This could potentially have long-term implications as suggested by studies linking higher placental/fetal ratios to increased risk of cardiovascular disease, hypertension and diabetes in adults.
597 TERBUTALINE INHIBITS CRH EXPRESSION IN HUMAN TROPHOBLAST CELLS EFTICHIA KONTOPOULOS (F)1, CHRISTINA CHANDRAS2, KATIA KARALIS3, 1Robert Wood Johnson University Hospital- UMDNJ, Obstetrics, Gynecology and Reproductive sciences, New Brunswick, New Jersey, 2Biomedical research of the Academy of Athens, Department of Endocrinology, Athens, Greece, Greece, 3Childrens Hospital/Harvard Medical School, Endocrinology, Boston, Massachusetts OBJECTIVE: To evaluate the effect of beta adrenergic agonists on the regulation of the expression of the placental corticotropin release hormone (CRH) gene. STUDY DESIGN: Term placentae were collected at the time of elective cesarean section, and were processed for trophoblast cells isolation and culture. The isolated trothoblasts were plated, cultured and were subsequently treated with terbutaline, RU486, and/or vehicle control. The messanger RNA (mRNA) abundance of CRH and of the house-keeping gene beta-actin were evaluated by Northern blot analysis. RESULTS: Exposure of the trophoblasts to terbutaline (10ÿ8M) inhibited the expression of the CRH gene as depicted by Northern blot analysis using a specific riboprobe. Co-addition of terbutaline (10ÿ8M) and RU486 (10ÿ6M),which is a progesterone/glucocorticoid antagonist, did not block the stimulatory effects of RU 486 on placental CRH expression. CONCLUSION: The beta- adrenergic agonist terbutaline inhibits the expression of CRH in human trophoblast cells. This finding may provide insight in the mechanism of action of terbutaline and its clinical applications.