医学机能实验学报告家兔动脉血压英文

Regulationofarterybloodpressure[PURPOSE]:Learnhowtorecordthebloodpressure(BP)directly.ObservetheeffectofneuralandhumoralfactorsonBP.[ANIMAL]:Rabbit[METHOD]:Anaesthesia:25%urethanesolutionwasinjectedintotheveinintheedgeofanearforanesthesiaandtherabbitwasfixedonoperatingtableonback.Separationofcommoncarotidarteries（CCA）,vagusneverandaorticnerve:Thethreestripsofnervesshouldbedistinguishedcarefully.Thevagusnerveisthethickest,thesympatheticnerveisthinner,andtheaorticnerveisthethinnest.TheleftCCAwasusedtomeasureBPandtherightnerveswereusedtobestimulatedrespectivelyintheexperiment.Arteryintubatton:LigatetheCCAwiththreadattheseparatedsegmentfarfromheart,usethearterialcliptoclipthesegmentneartheheart.Placeathreadundertheseparatedarterywithaslipknotforfurtherstep.Madeaninclinedcuttowardtheheartwithanophthalmologicscissorsatthearterialsegment0.5cmdistancefromtheknot,theninsertthearterialcannulafilledwithhumoralintothecuttowardstheheartandfixwiththethreadprepared,ligatethesurplusthreadonthesideofthecannulatoavoidslippage.Experimentalequipments:Theoutputofpressuretransducerwasconnectedwiththeinputofcomputer.Observationitems:ObservethechangesofBPwhenfollowingeventshappened.LeftCCAwascross-clampedfor10seconds.Aorticnervewasstimulatedbyaprotectiveelectrode.0.3ml1:10000noradrenalinsolutionwasinjectedintravenously.Unilateralvagusnervewasligatedandcutoff(atthedistalendofknot),andtheperipheralendoftheseparatedvagusnervewasstimulated.[Result]:ThenormalBPWhenleftCCAwascross-clampedfor10seconds,accordingtothepictures,BPisincreasing.Whenaorticnervewasstimulatedbyaprotectiveelectrode,BPisdecreasing.When0.3ml1:10000noradrenalinsolutionwasinjectedintravenously,BPisincreasing.Whenunilateralvagusnervewasligatedandcutoffandtheperipheralendoftheseparatedvagusnervewasstimulated,BPisdecreasing.Andthecurvechangessignificantly.[DISCUSSION]:BPandHOMEOSTASISArterialBPisthepressurethatthebloodinarterysqueezesthevessel.ThemostimportantreasonwhyBPformsisthattheventricularcontractsandejectsbloodtoaorticartery.Everyanimal‘sBPisstablerelatively.Itchangedwithinacertainrange.Thehomeostasisisbalancedbyneuralandhumoralregulation.Themostimportantisstaticarterysinus-aorticarchbaroreflex.ThisreflexcandecreaseBP.ItcanalsoincreaseBP.Asaresult,itcanreflexBPbuffering.Thereasonwhywechooserabbitisthataorticnervecanbeseparateeasily.So,thefirstlevelwaveiscausedbythefluctuationsinventricularcontraction.Thesecondlevelwaveiscausedbythefluctuationsinrespiratorymovement.LEFTCCAWASCROSS-CLAMPEDWhenleftCCAwascross-clampedfor10seconds,accordingtothepictures,BPisincreasing.Thereisanarterialbaroreceptor,inittherearelotsofsensorynerveendings.WhenleftCCAwascross-clamped,thecarotidsinusbaroreceptorreceivesstimulationtodrop.So,theratesofefferentimpulsesbecomeslower.Then,thenervousofvagusnervebecomeslowerandsympatheticnerveandthevesselofheartarebecomingmorenervous.Thesechangesmakeaneffectontheheart,sotherateofheartisincreasing.Theoutputofheartincrease,thevesselofbloodcontractsandtheperipheralresistanceofbloodvesselincreases.Atlast,BPisincreasing.AORTICNERVEWASSTIMULATEDBYAPROTECTIVEELECTRODE

Whenaorticnerveisstimulatedbyaprotectiveelectrode,BPisdecreasing.Theaorticnerveofrabbitisafferentnerve.Thefunctionofitisthatitafferentnerveimpulseswhichismadebyaorticarchreceptorstomedullaoblongata.Then,BPdecreasebyreflex.NORADRENALINSOLUTIONWASINJECTEDINTRAVENOUSLYEpinephrineandnorepinephrineinthebloodaremainlysecretedbytheadrenalmedulla.Whenvagusnerveisexciting,itcanpromoteadrenalmedullatosecreteepinephrineandnorepinephrine。Epinephrineandnorepinephrinedependsontheroleofcardiovascularandvascularsmoothmusclecellmembraneofmyocardialadrenergicreceptorsonthetypeanddensity.Adrenergicreceptorhastwokindswhichisαandβ.βreceptorcanbedividedintoβ1,β2andβ3.αreceptorexcite,andvasoconstrictionistheeffect.β1receptorsexciteandhastheeffectof"strongheart".β2receptorsexcitionmakesthevesseldiastole.β3receptorsareinadiposetissue.Epinephrinecanactivatetworeceptorsαandβ,buttheeffectisstrongeronβreceptors.β1receptorsincardiacmembraneiseffectedbyepinephrine,anditisthesamewithcardiacsympatheticnerve.Itmakesheartbeatfaster.Conductionspeedbecomesquicker.Myocardialcontractioncapacityismoreenhancement.Cardiacoutputincreases,andsystolicbloodpressureincreasessignificantly.Thisisduetonorepinephrinecancombinevascularsmoothmuscleαandβ2receptors.Thebloodvesselscontractanddiameterbecomessmall,.Peripheralresistanceincreases.So,BPincrease.Inaddition,norepinephrinecanalsoincreasetheheartrateandmakecardiaccontractilitylarger.Then,Vasoconstrictionismoreevident.UNILATERALVAGUSNERVEWASLIGATEDVagusnervecontainefferentfibersgoingdownf