ANNALES
UNIVERSITATIS MARIAE CURIE-SKŁODOWSKA
LUBLIN - POLONIA

VOL.LX,SUPPL.XVI,646SECTIOD 2005

KlinikaGinekologii,AkademiaMedycznawGdańsku

DepartmentofGynaecologyofMedicalUniversityofGdańsk,Poland

Dariusz Wydra

Histoclinical analysis of blood-placental barrier in pregnant women
with hypertension

Histokliniczna ocena bariery krwio-łożyskowej u ciężarnych
z nadciśnieniem tętniczym krwi

Inapregnancycomplicatedbyhypertension,bloodflowanalysisinthearteryallowsustoforeseeathreattothefetus.Abnormalbloodflowintheumbilicalarterymakesitpossibletodiscovervascularchangesinplacentawhichcanendangerthelifeofthefetus[7].

Inthesheeppattern,Morrowetal.indicatedthatprogressiveembolizationoftheblood-placentalvesselswasconnectedwiththegradualreductioninapartofthelate-diastolicDopplerwave[10].Theresultsoftheclinicalandexperimentalobservationsshowthatabnormalshapeoffoetalumbilicalarterysuitsincreasedvascularblood-placentalresistance.Somefetuseswithabnormalflowvelocitywaveformsdemonstratehypoxiaandsignsofacidosis.AccordingtoMorrowetal.hypoxiaandacidosisofafetusarenotresponsibleforabnormalityofthewavesform[9].Asuggestedmechanismofincreasedvascularblood-placentalresistanceformationistheclosingoftermvilliarteriolasortheirhypoplasia[2,6].

Materialsandmethods

Fiftythreepregnanciescomplicatedbyhypertensionweretakenintoevaluation.Hypertensionwasrecognizedwhenthepressuretakentwiceinwithinsixhourswashigherthan140/90mmHg.Afteralldeliveries,placentaunderwentmorphologicexaminationintheDepartmentofPathomorphology.Thenumberofepithelialplateandthenumberofvesselsofterminalvilliwerecountedin1mm2ofplacenta.Thefollowingwereestimated:thesurface,theperimeterandthediameterofvilliandthelength,thethicknessandthesurfaceofthinepithelialplateaswellasthesurfaceofvesselsinvilli.Quotientofthenumberofepithelialplatesin1mm2toanaverageplatesthicknesswastakenasanindexofplacentaltransportefficiency.Theanalysisutilizedthemethodforcountingthesurfaceofmetabolicexchangedonebyplateinplacentaaccordingtotheformula(placentalSMEP-surfaceofexchangeofplatesinthemeasuredspecimen,specimensV-specimensvolumeconnectedwiththethicknessofhistologicalspecimensuits5m.)

Accordingtotheanalysisoftheumbilicalarteryflowvelocitywaveformsweredefinedqualitativeindexes-systolic-diastolicindex-A/B;resistanceindex-RI;pulsationindex-PI.ValuesoffetalumbilicalarteryPIinnormalpregnancieswereusedasreferences-PImean+2SDwasconsideredtobenormalwhereasmean+2SDweredefinedasabnormal.Thegravidaswithhypertensionweredividedinto2groupsaccordingtotheresultofbloodflowintheumbilicalartery:thefirstgroup-35patientswithnormalfeto-placentalflow,thesecondgroup–18patientswithabnormalfeto-placentalflow;in2casesweobservedtheabsenceofend-diastolicflowofumbilicalarteryDoppler.Accordingtotheacceptedcriteria,thosevalueswereconsideredcorrectwhichwereinthefollowingrange:averagevalueplustwicethevalueofthestandarddeviationinthecontrolgroup.Theborderingvalueoftheresistanceindexwas0,67.TheT-Studenttestwasusedforstatisticalanalysisoftheresults.Pregnancyweekwhenmeasurementsofbloodflowweredonewas37,42weekofgestationinagroupwithnormalbloodflowand372inpatientswithabnormalbloodflow.

Results

Theaverageplatesthicknessinthegroupwithabnormalfeto-placentalflowwas1,98±0,31µm,anditwassignificantlyhigherthaninpatientswithhypertensionandwithnormalDopplerexamination-1,76±0,17µm(table1).ResultsshowthatDopplerderivedvascularpatternscorrelatewellwithnormalandadverseperinataloutcome.Inthegroupofgravidaswithhypertensionandabnormalfetoplacentelbloodflowtwicemoreoftenacesareansectionwasmadebecauseoffetalemergencysymptoms.Thestateofanewborninpatientswithhighhypertensionandabnormalfetoplacetalflowwasworsethaninpregnantwomenwithnormalfetoplacentalflow(table2).

Theresultsofourstudyindicatethatthequalityoffeto-placentalflowinpregnantwomenwithhypertensionresultsinparametersoffiltrationareainterminalvilli.Inthecasesofcomplicatedfeto-placentalbloodflowathickerblood-placentalbarrieri.e.epithelialplatewasfound.AnabnormalumbilicalarteryflowtobeapredictorofIUGRandfetaldistressinpregnancycomplicatedbyhypertension.Theanalysisresultsoffetoplacentalbloodflowareoneofthemostimportantprognosticfactorsinpregnanciescomplicatedbyhypertension.

Discussion

Kreczyetal.showthecorrelationbetweenthequalityindexoffeto-placentalflowandthenumberofvesselsinterminalvilliofplacenta[5].Theysuggestedthatthedecreaseofthenumberofvesselscouldbecausedbydelayedangiogenesis.StudiesbyMitrasetal.,whichestimatefeto-bloodflowandcarryoutamorphometricestimationofplacentalvessels,indicateacorrelationbetweenRIandthicknessofplacentalvessels[8].

Gilesetal.noticedastatisticallylowernumberofvesselsinterminalvilliinthegroupof35pregnancieswithhighersystolic-diastolicindex[2].AccordingtotheauthorsprenatalDopplerestimationidentifiesspecificmicrovasculardamagesinplacentawhicharecharacterizedbythevessels’obliterationinterminalvilli.AccordingtoMcCowanetal.thereisanegativecorrelationbetweenPIandthenumberofvesselsinoneterminalvilli[6].TheonlypossibleexplanationforthePIdecreaseis,accordingtotheauthors,obliterationofsmallplacentalvessels.

Incontradistinctiontothementionedauthors,intheanalysedgrouptherewerenotstatisticaldifferencesinthenumberofvesselsinvillimeasuredaccordingtoDopplerexaminationintheplacentasofgravidaswithhypertension(table1).Inbothgroupstheaveragenumberofvesselsinvilliwas2,940,4.Braceroetal.publishedsimilarresultsafteranalysinggroupsofpatientsinwhichgravidaswithhypertensionwereinmajority[1].TheydidnotnoticeastatisticaldifferenceinthenumberofvesselsinvilliinthegroupwithincreasedA/Bintheumbilicalartery.AccordingtoHitscholdetal.thenumberofvesselsinplacentalvilliinthegroupofgravidaswithhypertensionisnotstatisticallydifferentfromthegroupwithanabnormalfeto-placentalflowfromthegroupwithanormalflow[3].Thesameauthorinanotherarticleonfetuseswithlowbirthweightdidnotnoticeanydifferenceinthenumberofvesslesinthegroupwithnormalfeto-placentalflowandinthegroupwithabnormalfeto-placentalflow.However,heproves,asdoesthepresentstudy,theexistenceofawiderblood-bloodbarrier,i.e.athickerplateinfetuses’placentawithapathologicflow.

Likewise,scientistsfromTorontoobservedthickerplates,withoutindicatingdifferencesinthenumberofvesselsinplacentalvilliinthepregnanciesinwhichfetuseshadalowbirthweight[4].Accordingtotheauthorsitisaresultofvesselsdevelopmentdisordercharacterizedbydelayedmaturationblood-bloodbarrier.Allthiscausesnotonlyincreasedfeto-placentalflowresistance(noticedinanearlierstageofpregnancy)butalsoaconsiderablerestrictioninexchangesurfacethroughwhichmaternal-fetalexchangetakesplace.Itcausesadecreaseinplacentaloxygentransportand,asaresult,leadstofetuses’hypoxiaanditsdevelopmentandgrowthdisorder[4].

References

  1. BraceroLetal.Dopplervelocimetryandplacentaldisease.AmJObstetGynecol1989;161:388-93.
  2. GilesW,TrudingerB,BairdP.Fetalumbilicalarteryflowvelocitywaveformsandplacentalresistance:pathologicalcorrelation.BrJObstetGynecol1985;92:31-8.
  3. HitscholdTetal.Lowtargetbirthweightorgrowthretardation?UmbilicalDopplerflowvelocitywaveformsandhistometricanalysisoffetoplacentalvasculartree.AmJObstetGynecol1993;168:1260-4.
  4. JacksonMetal.Reducedplacentalvillouselaborationinsmall-for-gestational-agepregnancies:relationshipwithumbilicalarteryDopplerwaveforms.AmJObstetGynecol1995;172:518-25.
  5. KreczyA,FusiL,WigglesworthJ.Correlationbetweenumbilicalarteryflowandplacentalmorphology.IntJGynaecolPathol1995;14:306-9.
  6. McCowanL,MullenB,RitchieK.Umbilicalarteryflowvelocitywaveformsandplacentalvascularbed.AmJObstetGynecol1987;157:900-2.
  7. MitraS,SeshanS,RiachiL.PlacentalvesselmorphometryingrowthretardationandincreasedresistanceoftheumbilicalarteryDopplerflow.JMaternFetalMed2000;9:282-6.
  8. MitraSetal.MorphometricstudyoftheplacentalvesselsanditscorrelationwithumbilicalarteryDopplerflow.ObstetGynecol1997;89:238-41.
  9. MorrowRetal.Acutehypoxaemiadoesnotaffectumbilicalarterywaveformsinsheep.ObstetGynecol1990;75:590-3.
  10. MorrowRetal.Theeffectofplacentalembolizationontheumbilicalarterywaveforminsheep.AmJObstetGynecol1989;161:1055-60.7.

Abstract

Objectives:Correlationsbetweenqualityindicesofthebloodflowinthefetalumbilicalarteryinpregnanciescomplicatedbyhypertensionandparametersoflowmolecularexchangeonthelevelofplacentalbarrierwasevaluated.Studydesign:Basedontheresultofumbilicalarteryflow,53pregnanciescomplicatedbyhypertensionweredividedintotwogroups:thefirstgroupof35patientswithnormalvaluesoffoeto-placentalflow,thesecond-18patientswithabnormalresultsoffoeto-placentalflow.Thenumberofepithelialplates,thenumberofepithelialplatesin1mm2ofplacentalvilloustissuesandnumberofvesselsinterminalvilliwerecounted.Thearea,perimeteranddiametersofterminalvilli,length,thicknessandareaofthinepithelialplate,areaofthebloodvesselwereestimated.Results:Themorphometricanalysisindicatesthatthequalityofthefeto-placentalbloodflowinpregnantwomenwithhypertensionresultsinparametersoffiltrationareainterminalvilli.Incasesofcomplicatedfoeto-placentalbloodflow,thickerblood-placentalbarrieri.e.epithelialplatewasfound.Conclusions:.Inthecasesofcomplicatedfeto-placentalbloodflowathickerblood-placentalbarrieri.e.epithelialplatewasfound.

Streszczenie

Poszukiwanokorelacjipomiędzywspółczynnikamijakościowymiprzepływukrwiwtętnicypępowinowejuchorychwciążypowikłanejprzeznadciśnienie,aparametraminiskocząsteczkowejwymianykrew-krewwłożysku.Woparciuowynikprzepływukrwiwtętnicypępowinowejpodzielono53ciężarneznadciśnieniemna2grupy:-35ciężarnychzprawidłowymiwartościamiprzepływupłodowo-łożyskowegoi18ciężarnychzpatologicznymiwartościamiprzepływu.Wkosmkachterminalnychobuanalizowanychgrupobliczanoliczbępłyteknabłonkowych,ichliczbęw1mm2,liczbęnaczyńwkosmkachorazpowierzchnię,obwód,średnicękosmka,jegodługość,grubość,powierzchnięcienkiejpłytkinabłonkowejipowierzchnięnaczyniawkosmku.Przeprowadzonaanalizamorfometrycznawskazuje,żeuciężarnychznadciśnieniemjakośćprzepływupłodowo-łożyskowegoznajdujeswojeodniesieniewparametrachstrefyfiltracyjnejkosmkówIII-rzędowych.Wprzypadkachzaburzonegoprzepływupłodowo-łożyskowegobarierakrwio-łożyskowąbyłaistotnieszerszaapłytkanabłonkowągrubsza.

Table1.Theresultsofmorphometricplacentalexaminationinthegroupofgravidas

withhypertensionwithreferencetotheresultsofumbilicalflow

Feto-placental-bloodvelocimetry
Normaln=35 / Abnormaln=18
Thicknessofthinepithelialplate(µm) / 1,76±0,17 / 1,98±0,31*
Numberofvillisin1mm2 / 145,8±10,0 / 141,2±14,3
Numberofterminalvillisin1mm2 / 67,7±8,0 / 64,4±8,0
Villissurface(µm2) / 1646,0±150,1 / 1698,1±207,1
Villiscircumference(µm) / 148,1±6,0 / 149,1±7,0
Villisdiameter(µm) / 49,0±2,6 / 49,8±1,3
Numberofplatesinmm2 / 124,2±26,4 / 116,2±40,5
Lenghtofplate(µm) / 10,3±1,5 / 9,9±1,9
Platessurface(µm2) / 20,4±3,9 / 22,3±4,7
Numberofplatesinvilli / 1,83±0.31 / 1,79±0,49
Lengthofplatesinvilli(µm) / 18,9±4,6 / 18,3±7,9
Plates’lengthtocircumferenceratio(%) / 12,8±3,0 / 12,2±5,0
Numberofvesselsinvilli / 2,94±0,4 / 2,94±0,4
Vesselssurfaceinvilli(µm2) / 160,0±56,1 / 162,4±73,6
Numberofplatestonumberofvesselsratio(%) / 62,6±10,2 / 60,5±14,7
Vessels’surfacetovillissurfaceratio(%) / 28,4±8,7 / 28,0±10,8
Placentalindex=fetal/placentalweight / 5,85±1,5 / 5,27±1,5
Placentaltransportindex/exponent / 71,8±18,1 / 61,6±28,5
Surfaceofexchangethroughplateinplacenta(m2) / 1,37±0,72 / 1,07±0,86

*significancelevelp<0,05.

Table2.Analysisofcourseofpregnancyandstateofanewbornafterdeliveryincorrelationwithfeto-placentalflowinwomenwithhypertension

parametr / Feto-placental-bloodflow / p
Normal / abnormal
n=35 / %
66 / n=18 / %
34
Operativedeliveryforfetaldistress / 9 / 26 / 10 / 56 / 0.001
Apgarscore7pkt.in1min. / 9 / 26 / 11 / 61 / 0.001
Apgarscore7pkt.w5min. / 8 / 23 / 10 / 56 / 0.001
Maximumvalueofsystolic180mmHganddiastolic>110mmHgbloodpressure / 4
6 / 11
17 / 4
8 / 22
44 / 0.001
0.001
proteinuria(300mg/24h) / 10 / 29 / 9 / 50 / 0.001
Birthweight10percentyl / 7 / 20 / 11 / 61 / 0.001
Birthweight(g) / 3170644 / 1879792 / 0.001
Gestationalageatdelivery(days) / 26414 / 26114 / NS
Apgarscorein1min. / 6,71,4 / 4,92,8 / 0.001
Apgarscorein5min. / 8,20,9 / 7,23,6 / 0.001
Meanarterialpressure / 9513 / 10521 / 0.05

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