You only get to change two things: the cardiac output and the resistance of the vasculature

Transcription

1 Vsculr Biology 3 Regultion of Flow nd Pressure A. Arteril Pressure (oeriew) 1. Arteril pressure pulse 2. Men rteril pressure 2 MAP 1 P + s P 3 3 d MAP = men rteril pressure, P s = systolic pressure, P d = distolic pressure You only get to chnge two things: the crdic output nd the resistnce of the sculture B. Regultion of Pressure nd Flow : -Arteriolr wlls he ery high rtio of smooth sculr muscle à cn chnge resistnce on commnd. resistnce essels. -Most of the resistnce to flow occurs t the rteriolr leel. Reiew of VSM contrction: 1.Intrinsic regultion: Locl control:

2 . Autoregultion of essels: i. Myogenic mechnism : VSM relxes when the pressure in the essel is reduced nd contrcts when it increses. i.e.- response to mechnicl stimulus(or utocrine). Net effect: mintennce of ner constnt blood flow for prticulr metbolic leel. ii. Endothelil responses ) Endothelium releses sodiltor NO in response to blood flow b) Ionic (C ++ or N ++ ) chnge led to soconstriction or diltion. c) Endothelil Relxtion Fctor.

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4 b. Metbolic regultion : metbolic ctiity produces sodiltors s wste product incresed dimeter lower resistnce greter flow: i. Actie hyperemi (incresed BF s result of incresed metbolic ctiity) ii. constrictors: O 2 (wek) iii. diltors: C0 2, H +, K + (from muscle contrctions), denosine, NO, prostglndins, P i (phsohtes) i. ph is lower becuse of CO2 CO 2 + H 2 O HCO H +. Smooth muscle hs Bsl tone (just like skeletl muscle, except tht it s not independent of neuronl ctiity) c. rectie hyperemi. As rection to ischemi (sudden decrese in flow), the essels will try to mintin the BP constnt een if it mens excesss Blood Flow. bck-propgtion of sodiltion ll the wy to the rteries : i. ccumultion of sodiltor metbolites ii. incresed rteriolr flow incresed sher stress endotherlium relse of EDRF. een more flow. 3. Extrinsic Mechnisms. Centrl nerous system connections descend from medull in brin.

5 i. Sympthetic connections 1. pressor center in medull: (sympthetic / stimultory: soconstriction, increses in hert rte, myocrdic contrctility). 2. Toniclly ctie (see boe) nd modulted by hormones nd locl blood pressures. 3. trnsmitter used is Norepinephine (soconstrictor) 4. Systemic ie- modulted by hormones. 5. Most effectie in enous system. ii. Prsympthetic connections 1. depressor (prsympthetic / inhibitory) res of medull. 2. Acetylcholine (sodiltors), brdykinin 3. Selected orgns iii. Differentition between cpcitnce nd resistnce essels: cpcitnce essels re more pssie, less sensitie to neuronl inputs becuse they lck bet-drenergic receptors ( less bsl tone). More common in muscles. Cpcitnce essels cn still rect to physiologicl conditions (ie- they will contrct in response to hypotension). Resistnce essels re more common in the skin nd ctiely shunt blood towrd where it s needed, b. Arteril Broreceptor responses : Stretch receptors Loction: Crotid sinuses nd ortic rch (min ones, responsible for short term chnges), hert / lungs ( high BP in hert will re-route blood flow to kidneys more urine),

6 1. Inhibit the sympthetic neurl connections

7 : 2. Respond directly to chnces in rteril BP (nd indirectly blood olume, crdic output, TPR) 3. Short term regultion. Venous BP increses better tril filling crdic output b. Arteriole constriction totl peripherl resistnce increses c. Hormonl i. Adrenl glnds ) Norepinephine, epinephrine: lph-drenergic effect: low concentrtion sodiltion, bet-drenergic effect: high concentrtions soconstriction. ii. Angiotensin II (soconstrictor) - Renl hypertension d. Indirect fctors i. E.g. Adenosine Endothelium NO Vsodition e. Chemicl meditors i. Some gents chnge the sensitiity of VSM to C ++ f. chemoreceptors: sme Aortic/crotid sinuses receptors tht regulte respirtory rte he some effect on the soconstriction of VSM, i the

8 medull. (when competing with the broreceptors, though, they lose). Hypercpni, hypoxi, low ph ll cuse peripherl soconstriction. Cerebellum, hypothlmus, skin nd iscer. Pulmonry reflex, centrl chemoreceptors Chemoreceptors in medull produce strongest response Note competition between intrinsic nd extrinsic regultion of blood flow. The more itl/intolernt to hypoxi n orgn is, the more intrinsic control it gets oer its blood flow. Exmples: Dominnt Intrinsic control: brin, hert, ACTIVE skeletl muscle Dominnt Extrinsic control: skin, digestie, RESTING skeletl muscle (brin/hert ) Venous Effects: A. Veins re ery complint, not ery resistie, but there is still enomotor tone. Cerebrl ischemi triggers enous constriction to bring up men blood pressure. B. Unidirectionl les C. Lrge Blood Volume (60% of totl) D. Venous Volume t the Ven C determines how much blood will be ilble for the next stroke olume, but tht olume is function of the stroke olume. Becuse of the wiring, the crdic output dries the enous olume. i.e: idelly: R C C

9 R = ( P P ) / Q V C C C ~ 10xC = V = V / P = V / P r Pretty Good pproximtion in the rel world, but CAREFUL: enous olume hs n effect on the crdic output too! The hert will not pump ny more blood out thn wht it receies. (consider wht hppens with bleeding, edem, dehydrtion... ) Vsculr function cures: ry crdic output rtificilly, wht hppens to enous pressure. reflects lg between crdic output nd enous pressure right fter distole Note the difference in complince between rteries nd eins: Arteriolr responses: constriction, diltion Think of them in terms of chnging resistnce in the circuitry.

10 5. Crdic/sculr coupling:. More output from the hert will rise the pressure through the whole system. b. crdic function cures:) ry enous pressure rtificilly, wht hppens to crdic output c. i. Equilibrium point is where the system normlly opertes, cn t tolerte more thn just smll trnsient chnges. ii. Note the trjectory long the cure when you introduce chnge. iii. e.g: Sympthetic stimultion greter crdic contrctility shift crdic function up.then settle to new equilibrium point. i. e.g.: Bleeding shift sculr function to the left then settle to new equilibrium. e.g: chnge the resistnce chnge the slopes of the cures.

11 d. Crdic output = hert rte x stroke olume BUT, stroke olume is function of hert rte too, i myocrdil contrctility. Non-liner reltionship! 5. Long-term regultion of BP, BV ii. Renl function (though gl response to crdiosculr BP) iii. Fluid intke i. Other fctors relted to fluid retention.