113 MATERNAL FETAL ABO-RH BLOOD ANTIGEN STATUS AND RISK FOR PRETERMPREECLAMPSIA ALISSA CARVER1, ERIKA O’DONNELL1, PATRICK RAMSEY1, JOSEPHBIGGIO JR1, WILLIAM ANDREWS1, 1University of Alabama at Birmingham,Obstetrics/Gynecology, Birmingham, Alabama

OBJECTIVE: Evidence has suggested an association between maternal ABOantigen status and risk for preeclampsia (PRE). We sought to evaluate bothmaternal and fetal ABO-Rh status and maternal-fetal ABO-Rh incompatibilityas potential risk factors for the development of severe PRE !32 wks gestation.

STUDY DESIGN: The study was conducted as a secondary analysis ofa prospective cohort study of 457 maternal-infant pairs with preterm birth!32 wks. Maternal and infant blood types were abstracted. Maternal-infantpairs were subclassified as either being compatible or incompatible to maternalto fetal transfusion (MF comp/incomp) and compatible or incompatible to fetalto maternal transfusion (FM comp/incomp). Severe PRE was defined by ACOGcriteria.

RESULTS: The incidence of severe PRE was 29% in cohort. No differenceswere noted between women with and without PRE with respect to age,gestational age, and race. No association was noted between maternal or fetalABO blood antigen status nor ABO-Rh status with respect to development ofPRE. Overall, no association was noted with respect to maternal-fetal ABO andABO-RH incompatability and PRE. However, among nulliparous women bothFM ABO and ABO-Rh incompatibility was associated with an increased risk ofsevere PRE (TABLE).

Maternal and Fetal ABO-Rh Incompatibility and Severe Preeclampsia (PRE)

M-F Incompatibility No PRE (n = 134) PRE (n = 323) RR (95% CI) p

Nulliparous 23.8% 34.7% 1.7 (0.9-3.1) 0.08Multiparous 26.9% 26.2% 1.0 (0.5-1.9) 0.92

F-M IncompatibilityNulliparous 23.8 43.1 2.4 (1.3-4.4) 0.003Multiparous 26.3 18.0 0.6 (0.3-1.3) 0.20

CONCLUSION: Fetal to maternal ABO-Rh incompatibility is associated withdevelopment of severe preterm PRE in nulliparous women.

114 INTRAVENOUS L-ARGININE IS A NEW ANTI-HYPERTENSIVE AGENT FORR PREGNANTWOMEN ISABELLA NERI1, VALERIO MARIA JASONNI1, GIANFRANCO GORI2,IMMACOLATA BLASI1, FABIO FACCHINETTI FOR ARGININE STUDY GROUP1,1University of Modena and Reggio Emilia, Mother-Infant Dept, Modena,Italy, 2Ospedale Morgagni di Forli, Obstetric and Gynecology Dept, Forli, Italy

OBJECTIVE: Evaluate the antihypertensive efficacy of L-Arginine (L-Arg)repeated infusions in women affected by gestational hypertension (GH).

STUDY DESIGN: In a multicentre, randomized, clinical trial 148 women at 24-34 weeks of pregnancy, admitted for GH with (42%) or without proteinuria wererandomized to receive either L-Arg (20g/500 mL) IV, daily, for 5 days or placebo(PL) infusion, in a double-blind design. Patients also observed bed rest 4 hours/day. Patients requiring an immediate delivery, suffering of chronic hypertension,or renal or cardiovascular diseases were excluded. Blood pressure (BP) wasevaluated every 4 hours from 8 a.m. to 8 p.m., starting the day before till the endof treatment.

RESULTS: Mean gestational age at entry was 30.1 G 4.6 for L-Arg and 30.2G 4.7 for PL groups. Age and BMI were similar between groups. Twenty-eightpatients in L-Arg and 33 in PL group were already using anti-hypertensiveagents. Both systolic and diastolic BP were reduced by treatment, the effect of L-Arg being significantly higher than PL (systolic: �7.7 G 1.4 vs �3.6 G 1.5;diastolic �10.9G 1.8 vs. �6.1G 1.9, P! .0001). The magnitude of L-Arg effectwas significantly higher in Diastolic respect with Systolic values (P ! .0001). Aprogressive reduction of BP values was seen till the 5th day of treatment only inpatients receiving L-Arg. L-Arg while not PL effect was irrespective of theconcomitant anti-hypertensive treatment.

CONCLUSION: Repeated L-Arg infusion has proven effective in reducing BP,namely diastolic values and it is candidate to become an anti-hypertensive agentfor patients with gestational hypertension.

115 RELATIONSHIP BETWEEN BODY MASS INDEX, PREECLAMPSIA, AND SLEEPDISORDERED BREATHING JAMISON MORGAN1, SIG-LINDA JACOBSON2,ROBERT SACK3, GEORGE SAADE1, 1University of Texas Medical Branch atGalveston, Obstetrics and Gynecology, Galveston, Texas, 2Oregon Health &Science University, Obstetrics and Gynecology, Portland, Oregon, 3OregonHealth & Science University, Psychiatry, Portland, Oregon

OBJECTIVE: Preeclampsia has been linked to sleep disordered breathing. Ourobjective was to determine if the relationship between preeclampsia and sleepdisordered breathing is independant of body mass index (BMI), a factor that hasbeen linked to both.

STUDY DESIGN: Six women with preeclampsia by ACOG definition and ninepregnant women without the disease were prospectively enrolled, and underwentone night of respiratory tracings using a pressure transducer in a limited,portable polysomnogram montage provided by the Portable II Plus (ResMed,Inc.). As previously characterized in preeclampsia, flow limitation, labeledFlattening in our recordings, and Apnea-Hypopnea Index (AHI) were used toassess sleep-disordered breathing. Two-way ANOVA, ANCOVA, and multi-variate regression analysis were used to evaluate the relationship between BMI,preeclampsia and sleep-disordered breathing. A P ! .05 was used to denotestatistical significance.

RESULTS: BMI was significantly related flow-limited breathing (P = .04).Slopes of flow-limited breathing versus BMI for the preeclampsia and normalgroups converged. When corrected for BMI, preeclampsia was not related to anyof the sleep disordered breathing variables.

CONCLUSION: The relationship between sleep disordered breathing andpreeclampsia is not independant of BMI. Future mechanistic and therapeuticstudies relating to sleep-disordered breathing and preeclampsia need to haveadequate sample sizes to adjust for this confounder.

Supported by NIH/NCRR grant #5 M01 RR000334.

S42 SMFM Abstracts

116 TRANSFER FUNCTION ANALYSIS OF DYNAMIC CEREBRAL AUTOREGULATION INPREECLAMPSIA KEITH WILLIAMS1, MARIA SMALL2, UGONNA DURU3,MYRIAM FERNANDES3, INNA LANDRES1, SAMUEL RAMSAWAK4, ADESH SIRJUSINGH4,1Yale University, Obstetrics & Gynecology, New Haven, Connecticut, 2YaleUniversity, OB/GYN, New Haven, Connecticut, 3Yale University, Obstetricsand Gynecology, New Haven, Connecticut, 4University of the West Indies,Obstetrics and Gynecology, Mount Hope, Trinidad and Tobago

OBJECTIVE: The cerebral circulatory effects of preeclampsia on the latency(phase) and the efficiency (gain) of the cerebral autoregulatory response isunknown. There is concern that preeclampsia causes a progressive impairment ofthe autoregulatory response which leads to eclampsia. The timing of thisimpairment is unknown. We sought to identify these dynamic cerebral autoregulation changes in preeclampsia.

STUDY DESIGN: We simultaneously measured continuously beat to beatoutputs of mean arterial pressure (MAP) (pilot 9200) and beat to beat, systolic,diastolic, and mean cerebral blood flow (MCBFV) (Nicolet Vascular TCD) for 2minutes with the patient during supine rest. All measurements were stored on anexcel spread sheet for further analysis. 5 preeclampic and 5 matched normoten-sive controls were studied. R-R Intervals, MAP and MCBFV were analyzed inthe frequency domain. Data sets were first fourier transformed and powerspectral densities were calculated. Spectral power was expressed both in the lowand high frequency ranges. We calculated the phase angle (which represents thetemporal relationship between the MAP and mean MCBFV) and the transferfunction (amplitude or gain between changes in the MCBFV signal and theMAP signal). All continuous data was compared between the two groups usingt tests.

RESULTS: We identified a significant difference between (1) the gain betweenthe normotensive and preeclamptic groups. (.29 G .07 vs .10 G .04, P ! .01),and (2) the phase angle (59 G 12 vs 129 G 31, P ! .01). The preeclamptic groupshowed significant decrease in gain but an increase in phase angle)

CONCLUSION: Preeclampsia paradoxically results in a significant improve-ment in dynamic cerebral autoregulation as demonstrated by an increase inphase and a decrease in gain. Clinical studies that can systematically assess theprogression of these dynamic autoregulation changes to identify specific endpoints of impaired autoregulation are needed to understand cerebral function ineclampsia.