醫(yī)學(xué)教學(xué)課件：心臟之后的血管生理

RegulationofCardiovascularActivitiesNervousRegulationInnervationoftheheartCardiacsympatheticnerveCardiacvagusnerve起源origin節(jié)前纖維preganglionicfiber外周神經(jīng)節(jié)ganglion節(jié)后纖維postganglionicfiber支配distribution遞質(zhì)neurotransmitterCardiacsympatheticactionsPositivechronotropiceffect正性變時(shí)作用Positivedromotropiceffect正性變傳導(dǎo)作用Positiveinotropiceffect正性變力作用CardiacmechanismsofnorepinephrineMechanismsofnorepinephrine—increaseNa+&Ca2+permeabilityIf,phase4spontaneousdepolarization,autorhythmicityCa2+influx(ICa,L),phase0amplitude&velocity,conductivityCa2+influx(ICa,L),Ca2+release,[Ca2+]i,contractility(CICR)

AsymmetricalinnervationofsympatheticnerveCardiacparasympatheticactionsNegativechronotropiceffect負(fù)性變時(shí)作用Negativedromotropiceffect負(fù)性變傳導(dǎo)作用Negativeinotropiceffect負(fù)性變力作用CardiacmechanismsofacetylcholineMechanismsofacetylcholine—increaseK+&decreaseCa2+permeabilityK+outward

,|MRP|

,phase4spontaneousdepolarization,autorhythmicityInhibitionofCa2+channel,phase0amplitude&velocity,conductivity

Ca2+influx,[Ca2+]i,contractilityCardiaceffectofparasympatheticstimulationVagalManeuversValsalvamaneuverAmaneuverinwhichapersontriestoexhaleforciblywithaclosedglottis(thewindpipe)sothatnoairexitsthroughthemouthornoseas,forexample,instrenuouscoughing,strainingduringabowelmovement,orliftingaheavyweight.TheValsalvamaneuverimpedesthereturnofvenousbloodtotheheart.NamedforAntonioMariaValsalva,arenownedItaliananatomist,pathologist,physician,andsurgeon(1666-1723)whofirstdescribedthemaneuver.PhysiologicalresponseinValsalvamaneuverThenormalphysiologicalresponseconsistsof4phasesPhysiologicalresponseinValsalvamaneuverThenormalphysiologicalresponseconsistsof4phasesInitialpressurerise:Onapplicationofexpiratoryforce,pressurerisesinsidethechestforcingbloodoutofthepulmonarycirculationintotheleftatrium.Thiscausesamildriseinstrokevolume.Reducedvenousreturnandcompensation:Returnofsystemicbloodtotheheartisimpededbythepressureinsidethechest.Theoutputoftheheartisreducedandstrokevolumefalls.Thisoccursfrom5toabout14secondsintheillustration.Thefallinstrokevolumereflexivelycausesbloodvesselstoconstrictwithsomeriseinpressure(15to20seconds).Thiscompensationcanbequitemarkedwithpressurereturningtonearorevenabovenormal,butthecardiacoutputandbloodflowtothebodyremainslow.Duringthistimethepulserateincreases.Pressurerelease:Thepressureonthechestisreleased,allowingthepulmonaryvesselsandtheaortatore-expandcausingafurtherinitialslightfallinstrokevolume(20to23seconds)duetodecreasedleftventricularreturnandincreasedaorticvolume,respectively.Venousbloodcanoncemoreenterthechestandtheheart,cardiacoutputbeginstoincrease.Returnofcardiacoutput:Bloodreturntotheheartisenhancedbytheeffectofentryofbloodwhichhadbeendammedback,causingarapidincreaseincardiacoutput(24secondson).Thestrokevolumeusuallyrisesabovenormalbeforereturningtoanormallevel.Withreturnofbloodpressure,thepulseratereturnstowardsnormal.InteractionofsympatheticandparasympatheticnervesPredominanceofautonomicnervesTonus緊張Cardiacvagaltone心迷走緊張Cardiacsympathetictone心交感緊張InnervationofthebloodvesselsVasoconstrictornerve縮血管神經(jīng)Sympatheticvasoconstrictornerve交感縮血管神經(jīng)Vasodilatornerve舒血管神經(jīng)Sympatheticvasodilatornerve交感舒血管神經(jīng)Parasympatheticvasodilatornerve副交感舒血管神經(jīng)Dorsalrootvasodilatornerve脊髓背根舒血管神經(jīng)CardiovascularCenterAcollectionoffunctionallysimilarneuronsthathelptoregulateHR,SV,andbloodvesseltoneVasomotorcenterLocatedbilaterallymainlyinthereticularsubstanceofthemedullaandofthelowerthirdoftheponsVasoconstrictorareaVasodilatorareaCardioinhibitorarea–dorsalnucleiofthevagusnervesandambiguousnucleus

Sensoryarea–tractussolitariusVasomotorcenterReticularsubstanceoftheponsMesencephalonDiencephalonHypothalamusCerebralcortexCerebellumHighercardiovascularcentersBaroreceptorReflexesArterialbaroreceptorsCarotidsinusreceptorAorticarchreceptorAfferentnerves(Buffernerves)Cardiovascularcenter:medullaEfferentnerves:cardiacsympatheticnerve,sympatheticconstrictornerve,vagusnerveEffector:heart&bloodvesselsBaroreceptorneuronsfunctionassensorsinthehomeostaticmaintenanceofMAPbyconstantlymonitoringpressureintheaorticarchandcarotidsinuses.Characteristicsofbaroreceptors:SensitivetostretchingofthevesselwallsProportionalfiringratetoincreasedstretchingRespondingtopressuresrangingfrom60-180mmHgReceptorswithintheaorticarcharelesssensitivethanthecarotidsinusreceptorsTheactionpotentialfrequencyinbaroreceptorneuronsisrepresentedhereasbeingdirectlyproportionaltoMAP.BaroreceptorneuronsdeliverMAPinformationtothemedullaoblongata’scardiovascularcontrolcenter(CVCC);theCVCCdeterminesautonomicoutputtotheheart.i.e.,MAPisabovehomeostaticsetpoint

i.e.,reducecardiacoutputReflexpathwayTypicalcarotidsinusreflexMaintainingrelativelyconstantarterialpressure,reducingthevariationinarterialpressurePhysiologicalSignificanceHumoralRegulationVasoconstrictoragentsVasodilatoragentsRenin-angiotensinsystemJuxtaglomerularcellReninConstrictsresistancevesselsActsupontheadrenalcortextoreleasealdosteroneStimulatesthereleaseofvasopressinFacilitatesnorepinephrinereleasefromsympatheticnerveendingsStimulatesthirstcenterswithinthebrain

PhysiologicaleffectsofangiotensinIIEpinephrine&NorepinephrineSources Epinephrine---- adrenalmedulla Norepinephrine---- adrenalmedulla sympatheticnervesCatecholaminesNorepinephrineEpinephrine

Effects Epinephrine NorepinephrineReceptor a-adrenoceptor +++++

b-adrenoceptor ++ +Heart heartrate ++(invitro)

－(invivo) cardiacoutput +++ ±Vessels constriction(skin,visceral)++++ relaxation(SM,liver)－+++ totalperipheralresistance±+++Bloodpressure systolic ++++++ diastolic ±++ MAP +++Clinicalapplication positiveinotropicpressoragent agentVasopressin(antidiuretichormone,ADH)

Endothelium-derivedvasoactivesubstancesVasodilatorfactors

PGI2--prostacyclinEDRF,NO--endothelium-derivedrelaxingfactor,nitricoxideEDHF--endothelium-dependenthyperpolarizingfactorVasoconstrictorfactors

EndothelinAtrialnatriureticpeptide(ANP)ProducesnatriuresisanddiuresisDecreasesreninreleaseReducestotalperipheralresistanceviavasodilatationDecreasesheartrate,cardiacoutputAutoregulationDefinition:

Intrinsicabilityofanorgantomaintainaconstantbloodflowdespitechangesinperfusionpressure,independentofanyneuralorhumoralinfluencesMyogenicmechanismThemyogenicmechanismishowarteriesandarteriolesreacttoanincreaseordecreaseofbloodpressuretokeepthebloodflowwithinthebloodvesselconstantThesmoothmuscleofthebloodvesselsreactstothestretchingofthemusclebyopeningionchannels,whichcausethemuscletodepolarize,leadingtomusclecontraction.Thissignificantlyreducesthevolumeofbloodabletopassthroughthelumen,whichreducesbloodflowthroughthebloodvessel.Alternativelywhenthesmoothmuscleinthebloodvesselrelaxes,theionchannelsclose,resultinginvasodilationofthebloodvessel;thisincreasestherateofflowthroughthelumen.From:http://www.umm.uni-heidelberg.de/inst/cbtm/kphys/research-schubert.htmlUniversit?tHeidelberg>Fakult?ten>MedizinischeFakult?tMannheim>CBTM:Kardiovaskul?rePhysiologie>From:AJP-HeartOctober2008vol.295no.4H1505-H1513MetabolicmechanismAnyinterventionthatresultsinaninadequateoxygen(nutrient)supplyforthemetabolicrequirementsofthetissuesresultsintheformationofvasodilatorsubstanceswhichincreasebloodflowtothetissuesMetabolicmechanismLackofoxygen?Formationofvasodilators?Combinationofboth??MetarteriolePrecapillarySphincterCapillaryRelaxationofsmoothmuscleIncreasedBloodFlowMetabolicmechanismHypoxiaTissuemetabolitesandionsAdenosinePotassiumionsCarbondioxideHydrogenionLacticacidInorganicphosphateMaryrosequicklyfromherbedtoanswe