594 FETAL HEART RATE RESPONSES TO ACUTE MATERNAL HYPO- AND HYPERCAPNIAIN LATE GESTATION DEREK FRASER1, DENNIS JENSEN2, LARRY WOLFE2,PHILIP HAHN1, GREGORY DAVIES1, 1Queen’s University at Kingston, Obstetricsand Gynecology, Kingston, Ontario, Canada, 2Queen’s University at King-ston, Physical and Health Education, Kingston, Ontario, Canada

OBJECTIVE: To examine the fetal heart rate (FHR) response to maternalhypo- and hypercapnia in late gestation.

STUDY DESIGN: Twenty-seven women with healthy singleton pregnanciesperformed a modified carbon dioxide rebreathing procedure that includedprior hyperventilation and maintenance of hyperoxia (end-tidal oxygentension = 150 Torr). Prior to rebreathing, subjects hyperventilated for 5-minutes to reduce the end-tidal CO2 tension (PETCO2) to less than 23 Torrand then switched to a bag containing a normocapnic-hyperoxic gas mixture.During rebreathing, PETCO2 increased from hypocapnia to hypercapnia (40-60 Torr). FHR responses were monitored before, during and after rebreathingand classified using the National Institute of Child Health and Developmentguidelines. The study protocol was approved by the Queen’s University HealthSciences 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 adecrease in baseline FHR during rebreathing (134G11.7 bpm) compared tohyperventilation (144G9.8 bpm, p!0.001). Baseline FHR was not signifi-cantly different between pretest (138G7.9 bpm) and posttest periods(138G12.2 bpm, p=0.992). There were no significant changes in FHRvariability throughout the study (p=0.103). There was no difference inaccelerations 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 tracingduring rebreathing and no significant bradycardias were recorded.

CONCLUSION: Acute maternal hypo- and hypercapnia during modifiedrebreathing has no adverse effects on fetal well-being. Changes were noted inbaseline FHR during hyperventilation and rebreathing. Although statisticallysignificant, the heart rate parameters remained within normal ranges and arenot likely to be clinically significant, making this technique safe for researchpurposes.

595 ALTERED FETO-PLACENTAL GROWTH RATIOS DURING MID-GESTATION UNDER-NUTRITION IN RAT DAMS ANDREA JELKS1, LINDA DAY1, STACY BEHARE1, MI-CHAEL 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 under-nutrition during pregnancy is associated with abnormal placental growth.Small for gestational age babies or those with altered placental growth showan increased risk of developing coronary heart disease, hypertension anddiabetes during adult life. The placenta functions as a key mediator betweenthe mother and fetus, and hence may adversely affect the nutrient supply to thefetus. Currently the impact of maternal nutrition during different periods ofgestation on feto-placental growth is not well understood. We therefore soughtto determine the impact of in utero undernutrition during midpregnancy onplacental and fetal growth.

STUDY DESIGN: Time-dated pregnant Sprague-Dawley rats (n = 8) werefed 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 damswere euthanized, and the uterus delivered. For each gestational sac, the weightwas determined before and after drainage of the amniotic fluid. The placentaand fetus were separated and weighed. Results (meanGSE) were analyzedusing unpaired t-test.

RESULTS: FR pregnancies showed no significant difference in the placentalweight (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 nonsignificant 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 wassignificantly increased in the FR pregnancies (0.86G0.02 vs. 0.74G0.04,p!0.05) relative to controls.

CONCLUSION: Although maternal undernutrition during mid-pregnancydoes not adversely affect placental growth, it resulted in higher placental/fetalgrowth ratio. This could potentially have long-term implications as suggestedby studies linking higher placental/fetal ratios to increased risk of cardiovas-cular disease, hypertension and diabetes in adults.

596 FETAL MACROPHAGES ARE NOT PRESENT IN THE MYOMETRIUM OF WOMEN WHOUNDERGO LABOR AT TERM CHONG JAI KIM1, JUNG-SUN KIM1, SOONG DEOK LEE2,YEON MEE KIM1, KARINA RICHANI3, JIMMY ESPINOZA3, ROBERTO ROMERO4,1Wayne State University School of Medicine, Department of Pathology, De-troit, Michigan, 2Seoul National University College of Medicine, Departmentof Forensic Medicine, Seoul, South Korea, 3Wayne State University School ofMedicine, Department of Obstetrics and Gynecology, Detroit, Michigan, 4Per-inatology Research Branch, NICHD, NIH, DHHS, Bethesda, Maryland

OBJECTIVE: A role for surfactant protein-A in the initiation of labor hasbeen proposed in mice (PNAS 2004;101:4978). This protein was postulated toinduce migration and subsequent activation of fetal macrophages. Fetalmacrophages were proposed to invade the myometrium. The purpose of thisstudy was to determine if fetal macrophages invade the myometrium of womenin labor.

STUDY DESIGN: Placental bed biopsy specimens were obtained frompatients 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 caseswith labor. Formalin-fixed, paraffin-embedded sections were immunostainedfor CD68, a marker for macrophages. CD68 (C) macrophages in myometriumwere obtained by laser capture microdissection. Sex typing of the micro-dissected macrophages was done by polymerase chain reaction (PCR) foramelogenin.

RESULTS: PCR results demonstrated that the microdissected macrophagesfrom both the placental bed and the non-placental bed specimens were offemale origin in all cases.

CONCLUSION: These observations do not support the hypothesis that fetalmacrophages are present in the myometrium at the time of labor in humans.

597 TERBUTALINE INHIBITS CRH EXPRESSION IN HUMAN TROPHOBLAST CELLSEFTICHIA KONTOPOULOS (F)1, CHRISTINA CHANDRAS2, KATIA KARALIS3, 1RobertWood Johnson University Hospital- UMDNJ, Obstetrics, Gynecology andReproductive sciences, New Brunswick, New Jersey, 2Biomedical research ofthe 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 theregulation of the expression of the placental corticotropin release hormone(CRH) gene.

STUDY DESIGN: Term placentae were collected at the time of electivecesarean section, and were processed for trophoblast cells isolation andculture. The isolated trothoblasts were plated, cultured and were subsequentlytreated with terbutaline, RU486, and/or vehicle control. The messanger RNA(mRNA) abundance of CRH and of the house-keeping gene beta-actin wereevaluated by Northern blot analysis.

RESULTS: Exposure of the trophoblasts to terbutaline (10�8M) inhibitedthe expression of the CRH gene as depicted by Northern blot analysis usinga specific riboprobe. Co-addition of terbutaline (10�8M) and RU486(10�6M),which is a progesterone/glucocorticoid antagonist, did not blockthe stimulatory effects of RU 486 on placental CRH expression.

CONCLUSION: The beta- adrenergic agonist terbutaline inhibits the expres-sion of CRH in human trophoblast cells. This finding may provide insight inthe mechanism of action of terbutaline and its clinical applications.

S170 SMFM Abstracts