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SECTION 3 VASCULAR PHYSIOLOGY Ⅰ. Functional properties of different blood vessels 1. Artery: Aorta and large artery Pressure reservoir vessels 1.Elastic reservoir vessels: Systole: store of energy ↑ Elastic fiber elasticity Stretched Distensibility Distole: release of energy recoil maintain distolic←→kinetic energy elastic reservoir pressure intermittent flow → continuous flow Middle artery: carry blood to arterioles distribution vessels Small artery and arteriole: resistance vessels are regulated by neurohumoral factors Control of capillary blood flow 2. Capillary vessels: exchange vessels Exchange of substances between blood and interstitial fluid. Precapillary sphincter. Control of inflow of capillaries A-V shunt (anastomosis) Blood flow from arteriole to venules by passing capillary. 3. Venous Vessels, capacitance vessels: large vein, vena cava. Blood reservoir big compliance, low mean venous pressure, low resistance vessels Venous valve; venule. Ⅱ.Blood flow, resistance to blood flow and pressure Hemodynamics 1.Blood flow: Blood volume passing a given section in the cardiovascular system per unit time (ml/s). (1). P1-P2 F = ———— R (2). Poiseulle’s law for laminar flow. πΔpr4 F = ———— 8ηL Laminar flow Velocity of different layers is different parabolic no vibration no sound Turbulent flow blood flow is in direct proportion to square root of pressure difference Vibration Sound (murmur) Wasteful energy Empirical equation: Reynold’s number: NR=ρDV/η ρ(rho): density of fluid. D: diameter of the tube. V: velocity of flow. NR< 2000 laminar flow NR< 3000 turbulent flow 2. Resistance to blood flow: P1-P2 8η1 F = ——— R = ——— R πr4 Resistance comes from external friction (L, r) ,internal friction (η). Total peripheral resistance is mainly determined by arterioles(60~70%). Resistance and arterial blood pressure affect blood flow of organ and redistribution of blood flow of organs 3.Blood pressure. 1mmHg = 0.133 Kpa. Two requirements for blood pressure formation: (1) Blood filling in cardiovascular system. Mean circulatory filing pressure ∽ blood volume ——————— = 7mmHg vascular volume affect venous return to heart. (2) Heart work Pressure energy + Kinetic energy Pressure (systole) diastolic pressure forward flow Ⅲ. Arterial Blood Pressure 1.Normal value Systolic Pressure:100~120mmHg,13.3~16 kPa Diastolic Pressure: 8~10 kPa, 60~80mmHg Pulse Pressure: 4.0~5.3 kPa, 30~40mmHg. Mean arterial pressure(MAP) = DP + 1/3 (pulse P): 100 mmHg(13.3kPa) Fall of blood pressure is in direct proportion to resistance to blood flow 2. Determinants of arterial blood pressure (1) arterial blood volume (2) arterial compliance ΔVolume/Δpressure If we assume that arterial compliance remains constant, arterial blood pressure will depend on arterial blood volume and vascular volume Blood volume BP ∽ ———————— vascular volume If a vascular volume does not change arterial blood volume → arterial BP ↑ ↑ ↓ ↓ — — Arterial blood volume is determined by the rate of inflow and outflow of arterial system. Rate of inflow:cardiac output Rate of outflow: resistance and BP. AP = F × R = HR×SV×R Inflow outflow → arterial blood AP volume > ↑ ↑ < ↓ ↓ = - 3. Factors affecting arterial pressure (1) stoke volume (2) heart rate (3) peripheral resistance (4) aorta large artery (5)circulatory blood flow Factors results SV HR PR E BV SP DP PP ↑ ↑ ↑ ↓ ↑ Ⅴ.Venous pressure and venous return 1. Central venous pressure 4~12 cm H2O Affect factors: (1) Heart pump action (2) Venous return velocity An index of cardiovascular function 2. Peripheral venous pressure 2. Effect of gravity on venous pressure Orthostatic hypotension 3. Venous return and affecting factors (1) Mean circulatory filling pressure (2) Cardiac contractility (3) Sympathetic nerve (4) Muscle pump (5) Thoracic pump Ⅳ.Microcirculation 1. Architecture of microcirculation. (1) Thoroughfare or preferential channel. (2) A-V anastomosis or A-v shunt. (3) Arteriole →metareriole → precapillary sphincter →true capillary→ venule. 4. Hemodynamic of microcirculation (1) big cross section area slow velocity of blood flow (2) capillary pressure depends on precapillary resistance / postcapillary resistance: 5:1 (3) alternate opening and closing of capillaries 2. Exchange of substances between blood and interstitial fluid (1) Diffusion: the most important way. Lipid soluble substances: O2, CO2 non-lipid soluble substances: Rate of diffusion =(DA/a)(Co-Ci) D: diffusion coefficient (2) Pinocytosis. (3) Filtration and absorption Outward force > inward force filtration < reabsorption Capillary hydrostatic interstitial pressure hydrostatic pressure Interstitial colloid plasma colloid osmotic pressure osmotic pressure VI Formation of interstitial fluid V = Kf [ ( Pc +if ) – (p + Pif ) ] 3. Factors affecting the formation of interstitial fluid. (1) Capillary hydrostatic pressure. (2) Colloid osmotic pressure. (3) Lymph return. (4) Capillary permeability. SECTION 4 REGULATION OF CARDIOVASCULAR ACTIVITY Significance: To maintain normal blood pressure, blood flow to be relativity constant. To redistribute blood supply to different tissue and organs. To redistribute blood supply to different tissue and organs. Ways of regulation: BP = cardiac out × Resistance 8ηL R = ——— πr4 Neural control: reflex Humoral control; humoral factors Autoregulation: intrinsic regulation Cardiovascular reflex (1) Arterial baroreflexes: Carotid sinus baroreflex Aortic baroreflex (2) Cardiopulmonary reflex (3) Chemoreceptor reflex A. Neural regulation 1. Innervation of the heart dual innervation (1) cardiac sympathetic nerve (2) cardiac parasympathetic nerve Cardiac Symp n Cardiac Vagal n IML1-5 Amgiguus N, Dorsal motor N of vagus Preganglionic f ACh Preganglionic f ACh Postganglionic N N receptor Postganglionic f NE receptor propranolol Effects inotropic chronotropic dromotropic Blocker Postganglionic f Ach M receptor atropine (1) Effects of vagal nerve Vagal nerve ending → ACh. → binds to M cholinergic receptor →↑permeability to K+ results in: ↓automaticity of S-A node: ↓contractility due to : ↑K+ efflux at phase 3 repolarization →↓AP duration → Ca2+ influx ↓ → [Ca2+]i↓; ACh inhibits Ca2+ influx → [Ca2+]i ↓→ ↓contractility. ↓conductivity The left Vagus n:↓conductivity in A-V node The right Vagus n: ↓automaticity in S-A node. (2) Effects of cardiac sympathetic nerve: Cardiac sympathetic nerve ending → noradrenaline → binds to βadrenergic receptor→↑permeability to Ca2+ leads to: ↑Automaticity ↑Conductivity ↑Contractility The left Symp n:↑contractility. The right Symp n:↑HR. 2. Innervation of blood vessels (1) Vasoconstriction fiber Pre ganglionic neurons IML T1-L2 ganglionic neurons adrenergic f cholinergic f. ACh N receptor receptor vasoconstriction receptor vasodilation NE Sympathetic vasoconstrictor tone ↑ vascular tone ↑ vasoconstriction ↓ ↓ vasodilation tonic activity bidirectional regulation In artery vessels: arterioles > arteries > venous > capacitance vessels > precapillary sphincters Density of symp vasoconstriction fiber in organs; Skin > Skeletal > Visceral organs, Cerebral vessels, Coronary vessels. (2) Vasodilation nerve fibebs 1) Sympathetic vasodilation never fibers Cerebral cortex relay in hypothalamus and Midbrain → medulla oblongata→ spinal cord → Sym fiber → ACh → Vasodilation in skeletal M. No tonic activity; defense reaction. 2) Parasymp. vasodilation never fibers.(ACh) Origin in some nuclei in brain stem and IML in sacral segments. Innervation of blood vessels in brain, liver, GI tract, external genitals: Local regulation of blood flow. (3)Non-cholinergic, non-adrenergic fibers NO, peptides B. Cardiovascular center 1.Cardiovascular center in medulla oblongata After transection between pon and medulla oblongata, BP remains normal. Stimulation of sciatic nerve induces the increase in BP. After transection at obex in medulla, BP drops to 40 mmHg, no response of BP to stimulation of sciatic nerve. Medulla can maintain normal BP, and is called basal center of cardiovascular activity integration. (1) Rostral ventrolateral medulla (RVLM) (2) Caudal ventrolateral medulla (CVLM) (3) Nucleus of solitary tract (NTS) (4) Cardiac vagal center (1) Rostral ventrolateral medulla (RVLM) Cardiac sympathetic tone Sympathetic vasoconstriction tone Stimulation of RVLM→↑BP,↑HR. Destruction of RVLM, BP decreases to 40mmHg. RVLM is very important center in maintain normal BP, it has vasomotor tonity. (2) Caudal ventrolateral edulla (CVLM) Receives signals from NTS sends axons to RVLM Inhibition of RVLM (3) Nucleus of solitary tract (NTS) receives signals from arterial baroreceptors and cardiopulmanary receptors sends axons to vagal center and CVLM (4) Cardiac vagal center nucleus ambiguus, dorsal motor nucleus of vagus receives axons fom NTS NTS →CVLM →RVLM N.ambiguous dorsal motor N of vagus Symp. Preganlionic neurons in IML. 3. Hypothalamus (1) Hypothalamus is higher integrated center of autonomic system, including feeding, regulation of body temperature, fluid balance and endocrine secretion. (2). Anterior hypothalamus Stimulation causes the decrease in BP and HR Sends axons directly to SPN of IML in spinal cord. Receives axons of NTS in medulla. Plays role in arterial baroreflex. NTS → AH → IML → Symp. f. (3) Posterior and lateral hypothalamus Stimulation of defence area cause defensive reaction: Behavior: Rage, attack reaction or fighting associated with hissing, growling, spitting, piloerection, pupil dilation, biting Cardiovascular reactions: ↑BP,↑HR, Vasodilation in skeletal muscle. vasoconstriction in skin and splanchnic organs. 4. Cerebral cortex. (1) Limbic area regulates the activity of lower centers. (2) Motor and premotor area causes vasoconstriction of skin, splanchnic and renal vessels, but vasodilation in skeletal muscles. (3) Responses of BP to pain, anxiety and during exercise. C. cardiovascular reflexes 1. Arterial baroreflexes: Carotid sinus baroreflex Aortic baroreflex (1). Barorecrptor is located in adventitia of carotid sinus and aortic arch Characteristics: a. Response to stretch, not to pressure itself b. Activity is directly related to BP level c. More sensitive to pulsatile pressure than nonpulsatile pressure. (2) Afferent nerve: Buffer nerves Carotid sinus nerve - a branch of glossopharyngeal nerve connected with carotid sinus baroreceptor Aortic nerve-running in vagus n connected with aortic baroreceptor Reflex arc BP Carotid &aortic receptors NTS vagal center CVLM RVLM cardiac vagus HR cardiac symp SV MIL symp vasoconstrictor CO PR BP (3) Function of baroreflex. a.Experimental evidence: (a) Effect of carotid clamping; (b) Buffer nerve cut or stimulated (c) Perfusion of isolated carotid sinus. Method Results: baroreflex function curve. Features of the curve: Anti “S” shape Sinus threshold pressure Sinus saturation pressure working range Equilibrium point or operating point ( Set point ):ISP = arterial pressure. Negative slope (gain) - Negative feedback Slope is no uniform. (4) Functional significances of arterial baroreflex: To keep arterial pressure at normal level To stabilize arterial pressure and prevent arterial pressure from large fluctuation Baroreflex resetting. Operating point and baroreflex function curve shift upward or downward. 2. Cardiopulmonary reflex (1). Atrial volume receptor Location: in the junction of pulmonary vein and left atrium, vena cava and right atrium Reflex action: Tachycardia (bainbridge reflex) 1895. Increase in urine due to↓renal Sympathetic efferent activity and ↓antidiuretic hormone. (2).Left ventricular receptor. a. Mechanoreceptors: Location: Left ventricle. Stimulation of ventricle. Afferent n: vagus n. Reflex action: similar to arterial baroreflex, i.e. decrease in BP and HR. b. Chemoreceptor in ventricle: Coronary chemoreflex (Bezold- Jarisch reflex) Reflex effects: decrease in BP and HR Stimulation: Veratridine, nicotine, bradykinin, prostagladins, myocardial infarction. Vagal afferent n. 2. Chemoreceptor reflex (1) Respiratory depth and frequency increases; (2) Vasoconstriction in skeletal M, splanchnic viscera, kidney. (3) Blood flow in brain and liver increases. BP inceases (4)↑HR, ↑cardiac output due to a.↑respiration rate and depth b.↑catecholamine from adrenal medulla. If respiration rate and depth keep constant→ BP↑ a.↓HR, ↓cardiac output b. vasoconstriction in skeletal M Splanchnic organs and kidneys c. Coronary vosodilation Diving rflex Significances of chemoreceptor reflex Uunder normal condition chemoreflex plays a litte role in control of cardiovascular activity, but in an emergency (asphyxia, hypoxia, acidosis, severe hypotension) blood pressure is maintained by this reflex, because bilateral buffer nerves are cut, blood pressure will drop to very low level. B. Humoral regulation of cardiovascular system 1. Renin - angiotension system. angiotensinogen ( α2-globulin) kidney renin angiotensinⅠ(decapeptide) converting enzyme angiotensinⅡ(octapeptide) angiotensinase A AT1 receptor angiotensin Ⅲ(heptapeptide) (1).Action a. The increase in BP Arterial constriction→↑total peripheral resistance Venous constriction →↑venous return →↑SV. Stimulation of secretion of aldosterone →renal tubule reabsorption of Na+,H2O →↑blood volume. Facilitation of NE release from adrenergic fiber endings, modulation of sympathetic function. Central effects of angiotensin Ⅱ. Action site: Circumventricular organs; Organum vasoculosum of the lamina terminalis (OVLT), Subfornical organ (SFO), Area postrema (AP). Regulation of renin release a. Renal mechanisms: renal vascular baroreceptor. b.Renal sympathetic n c. Plasm Na+↓,plasm K+↑ Hemorrhage 2.Epinephrine(adrenaline EP) norepinephrine (noradrenaline NE) Origin: adrenal medulla. Secretion: EP 80%, NE 20%. Effect: similar to that of sympathetic nerve. (1)Heart: positive chronotropic and inotropic effect. (2)Blood vessels: α-adrenergic receptor: vasoconstriction. β-adrenergic receptor: vasodilation. The action of EP and NE on cardiovascular system has some differences which depend on the distribution and affinity of α- and β- receptors. 3. Antidiuretic hormone (vasopressin) Synthesis in supraoptic nucleus and paraventricular nucleus. Store in posterior pituitary gland (neurohypophysis). Release ADH to blood stream. Action : V1 receptor: constriction of blood vessel increase in blood pressure. V2 receptor: reabsorption of H2O from collecting duct. Dehydration, hemorrhage:↑AVP 4. Endothelium-derived vasoactive substances. Prostacyclin (PGI2) (1) Endothelium-derived relaxing factor: Nitric oxide (NO) NO synthase L-Argine NO + L-citrulline NO activates guanylyl cyclase which increases cGMP formation. cGMP decreases [Ca2+]i and relaxes vascular smooth muscle. Phosphodiesterase hydrolyses cGMP Factors of activation NOS: ACh, bradykinin, substance P, mechanical stress 3.Endothelin 21 amino acid residues, strong vasoconstrictor iv endothelin causes first decrease in BP and followed by long-term of the increase in BP 5. Atrial natriuretic peptide (ANP) Action: vasodilation, ↓cardiac output ↓HR ↓extracellular fluid volume: ↑excretion of water and Na+ ↓release of renin and aldosterone Factors of releasing ANP: ↑atrial blood volume. 6. Kallikrein-kinin system Kallikreins: proteolytic enzymes kininogens Plasma Kallikrein tissue Kallikrein kinins: bradykinin, lysylbradykinin angiotensin converting enzyme (ACE) Vasodilator, capillary permibility C. Local regulation of blood flow 1. Active hyperemia 2. Blood flow aytoregulation D. Blood volume and long term regulation of blood pressure Renal-body fluid control system SECTION 4 CORONARY CIRCULATION I. Anatomic consideration. II. Feature of coronary flow. ΔP F= R ΔP: perfusion pressure (aortic P atrial P), R: resistance During systole myocardial contraction compress coronary vessels which result in the increase in coronary resistance. During diastole release of compression leads to the decrease in coronary resistance. Therefore, coronary flow depends on: 1.diastolic pressure. 2.duration of diastole. Cyclic change of coronary flow Pressure gradient Ⅲ.Regulation of coronary blood flow. Normal value: 60-80ml/100g.min. Exercise 300-400ml/100g.min O2 consumption 7-9ml/100g.min. O2 extraction 65-70% O2 content in coronary venous blood is 5ml/100ml. O2 content in skeletal muscle venous blood is 17-18ml/100ml. 1. Myocardial metabolic level ↑cardiac activity, ↑cardiac consumption O2 ,↓PO2, adenosine CO2, H+, lactic acid, K+, prostaglandins. Effects of PO2 on coronary flow ATP PO2 ADP AMP 5’nucleotidase adenosine → vasodilation adenosine adenosine Kinase diaminase inosine 2. Neurol control (1).Sympathetic nerve: NE α-receptor → vasoconstriction β-receptor →↑myocardial contraction→ ↑metabolism, coronary vasodilation (2). vagal nerve: ACh → coronary dilation. ↓metabolism→ coronary constriction 3.Hormone regulation NE, EP, thyroxin → coronary dilation AngiotensinⅡ, vasopression → coronary constriction. (2).Regulation of vasopressin release a.Osmotic control; Osmotic receptor in anterioventral third ↑ Ventricle (AV3V) ∣ ↓ ↑plasma osmotic PVN,SON↑ pressure ↓ ADH↑ ↓ Reabsorption of water From collecting ↑ ↓ Blood volume ↑ b. non-osmotic control. * volume receptor ↓ vagal afferent nerve(+) ↓ ADH↓ * arterial baroreceptors (+) ↓ sinus n and aortic n↑ ↓ ADH↓ * Pain, Surgical stress, emotion stress → ADH↑