326
233
SPO Abstracts
J a n u a r y 1995 A m J O b s t e t Gynecol
BETA CIK,L RESPONSIVENESS IN ADULT RHESUS MONKEYS EXPOSED TO CHRONIC EXOGENOUS HYPERINSULINEMIA IN UTERO. A. LeePanitz', MW ~ r , BHaydon', M. C.ast~, m Susa'. New Emglami Regional Primate Reseamh Center, Southbom, MA, Women and Infant's Hcspital/Rhode Island Hosl~al, Providmce RI. OBJECTIVE:Rhesus monkeys (Macaca mttlatta),that as fetuses were exposed to d u m i c exogences hypefir,sulinemla in utero, eahibited impaired iosulin secn~ion dining irsmvmous glecosc testing (IvoTr) dining pregmncy. Although giucose tdenmee appeared normal, ineremental insulin seer~cn during the IVOTr negafivdy condated with the bl~hweight cf the cffspdng of exlm'~entsl e ~ m l s who were macrosomic compan~ to c~ltrols. The objective of this study was to if these animals have impehed insulin secretion w i r e they are not pregnan~ STUDY DESIGN:A hype~lycemic clamp was performed on 5 ~ m m t a l female mc~keys and 7 weight m~ched feraale controls,during which plasma glucose was m a l n t ~ d at 200 mg/dl for two horns using a variable dextrose infu~on, l~qee~t blood sampling was performed.The incmmmtal area ruder the insulin concantration crave was used to characterize beta cell rcspomiveness to wotc~ged hyperglycemia. Mean plasma insulin conce~ratiora were compared using a t-test. RESULTS:There was no statistical difference in the incremental insulin conce~trsticu under the giycemic curve between the experimental and control groups C/26±439 mU vs. 747±583 mU), although the experimental group tended to have a lower first phase insulin response (174±71 mU vs 215±163 mU).Two distinct groups of subjects were revealed; monkeys who w o e normal insulin respondets end those who were low insulin responders (1080.5±372.1 mU vs 259.4±74.3 mU). These two groups were not c~tingnishable by physiologic or morphomeUic characteristics, nor by phor exposure to exogenous hypefinsulinemia in ~ero. CONCLUSIONS: Exposure to cinwMc exogenous hypednsufinemla in utero does not alter beta cell respc~siveness in the adult nc~-pregna~ Rhesm monkey. Pregnancy may impose an additional stress ca pancreatic fanctic~ to explain the abnolmal insulin sccteti~m exhibited in these animals only during pregnancy.
234 MECHANICALVENTILATION IN PREGNANCY AND POSTPARTUM MINUTE VENTILATION AND WEANING. ~ C. HatveyX, E Ucka~. Dept. OB/GYN, The Uaivemty O f T ~ Hedical Bnmch, Galveston, TX. OHgCTIVE: Limited data exist on matoeal pulmonav funedoe in e~e mechanically ventilaled d~tetdc patient. Toe goal of this stmiy wm to review oex e x ~ in the medmical vsutflmioa ~ pregnat and poetlmmm petlem with scquellae of pregmmcy-ladueedhype~emioa aad to describe tidal volume ON), minute volume (MY), wad embetios pannnae~ STUDY D ~ I G N : We reviewed 9 cases of medumicallyvenfflated peegnant (w--4) md pmtim'tmn (n=5) imicats dkeedy creed for by out obst~xi¢~ intemive cere service dmiag m 18 mmth imied. Om'ts woe affected for ndifional p r e g ~ ' y / deliver7 mscdated data as well as for mode of ventilatioa, lambatiou aad extubatioa
tmmetsr~ bloodgesc~,~ a ~
med~ and hamedyemiclmmete~ All
petiem received Syachroaom Intemlaut Mandatmy Ventilatioa (SIMV) ,I, rates of 10-16 bt~tlm p ~ mimte. RESULTS:Patients stedied iadmied hcepitai4o h o ~ tomders and mbjects creed for in osr l~eaetal systsuL Five paficm w ~ ~ ventilated for cersbmi resusdlafioa and 4 received medma/cal ventilalioa for hypoxic or ventilatcry respirstory fsihwe. InitiaIMV was 10,500.0 (+ 2496.5) mL/min hased upoa aTVgosiof 9.4 (+ 1.0) mL/kg. Initial dyumie Compliaace (Cdya) wm 26.6 (+ 10.0) mL/cm H20 remlting la peak iaslmntot-y im..uurcs (PIP) of 34.2 (+ 10.1) cm H20. Whea MV was ceneded for a ptegnancy-nermsiimd medal C02 (PaC02) of 30 trsr, conectod idealized MV was aot siguificsutlydiffefeat (p <0.01). Eight of the 9 petieats sut rived aad were extnhate& Negative im#rslory force in these patients was 39.7 (+13.9) crs H20. Cdynetextubetionwas37.6(+lS.8)mL/cm H20. Mean time durstionfor medmaical ventilationwas 104.0 (+ 136.7) hour& No Imtientsfeded extuhatioL No palienls had Im'ctmmm, p a ~ , or other comllicatioM of ventiimioa. CONC'LUSIONS: These data su88mt that when eeuventioosl med~aical veetilalios is milized (SIMV with req~ratrsy rstes of 10-16/rain), an initial TV ef 9.4 (+1.0) mL/ kg produces as MV resulting in a Pace2 ~ a t with the normal pt~egnantstste. Rasphatrs'y weaning in pregmmt petients may be similar to weaning in aos-wegmmt p~ients. The relatively shert veatilatioa time ~ i n these patients and the low inddsuce of complicationsmay be attributed to the age sad prlc¢ health histoff of the obstetric patient population.
235 CALCIUM SUPPLEMENTATION AND MATERNAL HEMODYNAMICS. K. Boggess, x B. Schmucker, x J. Wauters,XL. Samuel, x T. Easterling, Dept. of Ob/Gyn, Univ; of WA Seattle,WA. OBJECTIVE: To determine the effect of calcium supplementation on maternal hcmodynamics. STUDY DESIGN: Nonsmoking pregnant women wcre randomized to receive either 1.5 grams of calcium or a placebo for 6 weeks in the third trimester. Cardiac output was measured using Doppler. Hemodynamic measurements were made prior to and two hours following ingestion of the first dose of study drag, and again at the completion of 6 weeks. A sample size of 30 would detect a difference in cardiac output of 0.5 liters with a power of 80% and p<0.05. Data was analyzed by Student's t test (two-tailed). RESULTS: Thirty patients were enrolled in the study. There were no differences in age, parity, weight, dietary intake of calcium, serum calcium, attrition rate, or entry hemodynamics between the two study groups. Urinary calcium excretion increased significantly in the calcium group. There was an 11% increase in cardiac output two hours following ingestion of calcium versus placebo, (p <0.007). Initial results from completed study patients suggest a small reduction in cardiac output after six weeks of calcium. CONCLUSIONS: Calcium supplementation acutely increased cardiac output, suggesting an initial primary cardiac effect.Prolonged therapy with calcium caused a downward trend in cardiac output, perhaps by a differentmechanism. Further study is required to elucidatethe effectof long term calcium supplementation on maternal hemodynamics.
236 P L A T E L E T ACTIVATION IN PREGNANCY. J Star, K Roscnc, M W
Carpenter, L LarsonX,J Ferlandx, G DiLenne~, A Kostin". Brown University, Depts Ob/Gyn/Medicine, Women & Infants/RI Hospital, Providence, RI oBJECTIVE: To assess platelet activation in normal pregnancy using a whole blood flow cytomctric technique measuring antibody binding to platelet membrane 8lYcoprotoin receptors (GMP-140, OPIb and OPIIa/IIIb). STUDY DESIGN: Fivv c¢ of whole blood were obtaineA via atranmmic venipuncture from twanty-six healthy pregnant and six non-pregnant subjects. The samples were stimulated with thrombin or U-46619 (a thmmboxane A2 analogue) at a range from maximal to minimal doses, in parallel with a buffer control. The platelets were fixed and aliquots from each sample were incubated with indicator antibodies (Y251 ( o P m ) or OKM5 (OPIV)) as well as test antibodies: S12 (GMP-140), 6D1 (OPIb) and 7E3 (OPnb/IIIa). A mean value of fluorescence intensity was obtained for 5000 platelets per sample. RESULTS: In the first and second trimesters, platelet activation is not significantly different than in non-pregnant subjects. In the third trimester, baseline and stimulated 7E3 binding is significantly decreased compared to controls. Mean fluorescence intensity with 7E3 (+/- SD) patients controls p value thrembin (units/ml) 0 1543+/-199 2080+/-178 .0005 5 2202+/-195 2880+/-283 .0002 •03 1621 +/-287 2317+/- 152 .0007 U-46619 (units/ml) 0 1539+/-232 2054+/-430 •0054 10 2005+/-245 2813+/-373 .0001 0.5 1702+/-182 2175+/-357 .0023 CONCLUSIONS: Compared to non-pregnant controls, antibody binding to the platelet fibrinogen ~ceptor (OP Hb/IHa) is significantly decreased in the third trimester before and after stimulation. We are investigating possible etiologies including: down-regulation of fibrinogcn receptors in late pregnancy, occupancy of existing receptors by circulating fibrinogen, or a state of chronic activation.