基础医学各论Ⅰ：22-呼吸系统生理2

Respiration2GasexchangeTissuecapillariesTissuecellsCO2CO2O2O2PulmonarycapillaryCO2O2CO2CO2O2O2Pulmonarygasexchange TissuegasexchangePhysicalprinciplesofgasexchangeLawsgoverninggasdiffusionHenry’slaw TheamountofdissolvedgasisdirectlyproportionaltothepartialpressureofthegasBoyle’slawstatesthatthepressureofafixednumberofgasmoleculesisinverselyproportionaltothevolumeofthecontainer.LawsgoverninggasdiffusionGraham'sLaw Whengasesaredissolvedinliquids,therelativerateofdiffusionofagivengasisproportionaltoitssolubilityintheliquidandinverselyproportionaltothesquarerootofitsmolecularmassLawsgoverninggasdiffusionFick’slaw Thenetdiffusionrateofagasacrossafluidmembraneisproportionaltothedifferenceinpartialpressure,proportionaltotheareaofthemembraneandinverselyproportionaltothethicknessofthemembraneD: RateofgasdiffusionT: AbsolutetemperatureA: AreaofdiffusionS: Solubilityofthegas

P: Differenceofpartialpressured: DistanceofdiffusionMW: MolecularweightFactorsaffectinggasexchangeChangesintheconcentrationofdissolvedgasesareindicatedasthebloodcirculatesinthebody.Oxygenisconvertedtowaterincells;cellsreleasecarbondioxideasabyproductoffuelcatabolism.InlungsOxygendiffusionalongthelengthofthepulmonarycapillariesquicklyachievesdiffusionalequilibrium,unlessdiseaseprocessesinthelungsreducetherateofdiffusion.IntissueFactorsthataffectpulmonarygasexchangeThicknessofrespiratorymembraneSurfaceareaofrespiratorymembraneVentilation-perfusionratio(V/Q)RespiratorymembranesurfactantepithelialcellinterstitialspacealveoluscapillaryredbloodcellendothelialcellO2CO2Ventilation-perfusionratioAlveolarventilation(V)=4.2LPulmonarybloodflow(Q)=5LV/Q=0.84(optimalratio)Ventilation-perfusionratioVA/QC

EffectofgravityonV/QGastransportinthebloodFormsofgastransportedPhysicaldissolveChemicalcombinationAlveoli Blood Tissue

O2→dissolve→combine→dissolve→O2CO2←dissolve←combine←dissolve←CO2TransportofoxygenFormsofoxygentransportedPhysicaldissolve:1.5%Chemicalcombination:98.5%Hemoglobin(Hb)isessentialforthetransportofO2bybloodAddinghemoglobintocompartmentBsubstantiallyincreasesthetotalamountofoxygeninthatcompartment,sincetheboundoxygenisnolongerpartofthediffusionalequilibrium.Hb+O2HbO2

HighPO2LowPO2Oxygencapacity ThemaximalamountofO2thatcancombinewithHbathighPO2Oxygencontent

TheamountofO2thatcombineswithHbOxygensaturation (O2content/O2capacity)x100%CyanosisHb>50g/LCarbonmonoxidepoisoningCOcompetesfortheO2sidesinHbCOhasextremelyhighaffinityforHbO2O2O2COCOCOOxygen-hemoglobindissociationcurveTherelationshipbetweenO2saturationofHbandPO2

FactorsthatshiftoxygendissociationcurvePCO2and[H+]Temperature2,3-diphosphoglycerate(DPG)BohrEffectIncreaseddeliveryofoxygentothetissuewhencarbondioxideandhydrogenionsshifttheoxygendissociationcurveChemicalandthermalfactorsthatalterhemoglobin’saffinitytobindoxygenaltertheeaseof“loading”and“unloading”thisgasinthelungsandneartheactivecells.TransportofcarbondioxideFormsofcarbondioxidetransportedPhysicaldissolve:7%Chemicalcombination:93%Bicarbonateion:70%Carbaminohemoglobin:23%tissuecapillariestissuesCO2transportintissuecapillariesCO2+HbHbCO2CO2plasmatissues

capillariesCO2+H2OH2CO3H++HCO3-HCO3-CO2+H2OH2CO3carbonicanhydraseCO2Cl-CO2+R-NH2R-NHCOO-+H+H++HCO3-pulmonarycapillariesCO2+HbHbCO2H++HCO3-HCO3-H2CO3carbonic

anhydraseCO2+H2OplasmaalveoliCl-pulmonarycapillariesCO2transportinpulmonarycapillaries

CO2CO2Cl-CarbonDioxideDissociationCurveHaldaneEffectWhenoxygenbindswithhemoglobin,carbondioxideisreleasedPO2=40mmHgPO2=100mmHgBohreffectandHaldaneeffectH2CO3H++HCO3-HbO2Hb+O2CO2HbCO2HbHBohreffectHaldaneeffectHbO2Hb+O2tissuecapillariesRegulationofrespirationBreathingisautonomicallycontrolledbythecentralneuronalnetworktomeetthemetabolicdemandsofthebodyBreathingcanbevoluntarilychanged,withincertainlimits,independentlyofbodymetabolismRespiratorycenterAcollectionoffunctionallysimilarneuronsthathelptoregulatetherespiratorymovementRespiratorycenterMedullaPonsHigherrespiratorycenter:cerebralcortex,hypothalamus&limbicsystemBasicrespiratorycenterRespiratorycenterDorsalrespiratorygroup(medulla)–mainlycausesinspirationVentralrespiratorygroup(medulla)–causeseitherexpirationorinspirationPneumotaxiccenter(pons)–helpscontroltherateandpatternofbreathingPulmonarymechanoreceptorsA:SlowlyAdaptingReceptor(SAR)B:RapidlyAdaptingReceptor(RAR)C:J-receptors(C-fibers)LocationFibersStimulusEffectSARtrachea-terminalbronchioles(smoothmuscle)largemyelinatedStretch(lungvolume)terminationofinspirationRARtrachea-respiratorybronchioles(epithelium)smallmyelinatedlungvolume,noxiousgases,cigarettesmoke,histamine,lungdeflationbronchocontriction,(rapid&shallowbreathing)C-fibersalveolarcapillarymembranenon-myelinatedvolumeofinterstitialfluidApneafollowedbyarapid&shallowbreathingHR&BPHering-Breuerinflationreflex

(Pulmonarystretchreflex)Thereflexreactionsoriginatinginthelungsandmediatedbythefibersofthevagusnerve:inflationofthelungs,elicitingexpiration,anddeflation,stimulatinginspirationHering-BreuerreflexEndofinspirationFRCFRCChemicalcontrolofrespirationChemoreceptorsCentralchemoreceptorsPeripheralchemoreceptorsCarotidbodyAorticbodyCentralchemoreceptorsChemosensoryneuronsthatrespondtochangesinbloodpHandgascontentarelocatedintheaortaandinthecarotidsinuses;thesesensoryafferentneuronsalterCNSregulationoftherateofventilation.CarotidbodyEffectofcarbondioxideonpulmonaryventilationCO2

respiratoryactivityCentralandperipheralchemosensoryneuronsthatrespondtoincreasedcarbondioxidelevelsinthebloodarealsostimulatedbytheacidityfromcarbonicacid,sothey“inform”theventilationcontrolcenterinthemedullaoblongatatoincreasetherateof