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Blood, Blood Vessels & Circulation.

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Presentation on theme: "Blood, Blood Vessels & Circulation."— Presentation transcript:

1 Blood, Blood Vessels & Circulation

2 Cardiovascular System
Blood vessels: Types A. Arteries -carry oxygenated blood (most of the time) away from the heart -thicker than veins -three layers: inner endothelium middle smooth muscle outer connective tissue -arteriole = small artery B. Veins -carry deoxygenated blood (most of the time) – toward the heart -same three layers as arteries (less SM and connective tissue) -thinner and more expansive than arteries -contain valves - to help the flow of blood back to heart -small vein = venule C. Capillaries -site of gas exchange with tissues -connect arterioles and venules -network of microscopic vessels (one cell thick) = capillary bed -site of exchange: gases, nutrients, wastes -can be closed off when not needed


4 Arteries Tunica interna (intima) Tunica media Tunica externa
simple squamous epithelium known as endothelium basement membrane internal elastic lamina Tunica media circular smooth muscle & elastic fibers smooth muscle is innervated by sympathetic nervous system decrease in stimulation or presence of certain chemicals causes vasodilation increases diameter of vessel nitric oxide, K+, H+ and lactic acid cause vasodilation increase in stimulation causes muscle contraction or vasoconstriction decreases diameter of vessel Tunica externa elastic & collagen fibers Arteries

5 Blood Distribution – Arterial circuit

6 Blood flow & Pressure gradients
blood flow is fastest in the arteries slows within arterioles slowest rate in capillaries - allows for exchange blood flow becomes faster when vessels merge to form veins flow rate through a vessel is proportional to the pressure gradient and inversely proportional to the vascular resistance (diameter) F = ΔP/R F = flow rate ΔP = pressure gradient R = resistance ΔP is the pressure gradient = difference in P between the beginning and end of a vessel this is what determines flow rate – NOT the absolute pressure! resistance changes as the radius changes R increases as r decreases – F will decrease (if P stays the same) R decreases as r increases – F will increase (if P stays the same) this relationship applies to non-viscous fluids

7 Blood flow & Pressure gradients
frictional losses (resistance) causes a drop in P as the blood travels through a section of vessel caused by friction between the moving fluid and the stationary wall if pressure gradient is unchanged – then increasing R will inhibit blood flow and decrease F R depends on three factors 1. blood viscosity (η) - # of circulating RBCs 2. vessel length (L) 3. vessel radius (r) – major determinant of R R = 1/r4

8 Pouiseuille’s Law (Snooty French Guy Law)
-true description of how blood flow through our vessels – description of viscous fluids Flow rate = η ΔP r4 8 ηL -changing the viscosity (η) of the blood does NOT change the F value (go ahead try it!) -but changing the L value does -this is because thick, viscous blood “sticks” to the blood vessel wall -so the longer the vessel – the more sticking and the slower the blood flows

9 Blood Pressure Pressure exerted by blood on walls of a vessel
depends on the volume of blood within the vessel and the distensibility of the vessel caused by contraction of the ventricles highest in aorta difference between systole and diastole – pulse pressure the volume of blood entering an artery is not the same as the volume leaving it during ventricular systole – the SV leaving the artery is 1/3 of that entering the artery the artery will distend with increasing volumes during diastole – the recoil of the vessel drives the exit of the blood BUT no blood enters the vessel mean arterial pressure – average pressure driving blood forward into the tissues throughout the cardiac cycle at resting heart rate – about 2/3 of the cardiac cycle is spent in diastole MAP = diastolic pressure + 1/3 (systolic pressure – diastolic pressure) MAP falls steadily in systemic circulation with distance from left ventricle 35 mm Hg entering the capillaries 0 mm Hg entering the right atrium

10 our bodies need to control MAP – to keep it in a narrow range
mean arterial pressure – average pressure driving blood forward into the tissues throughout the cardiac cycle at resting heart rate – about 2/3 of the cardiac cycle is spent in diastole MAP = diastolic pressure + 1/3 (systolic – diastolic pressure) MAP is what is regulated by homeostatic mechanisms MAP falls steadily in systemic circulation with distance from left ventricle 35 mm Hg entering the capillaries 0 mm Hg entering the right atrium our bodies need to control MAP – to keep it in a narrow range we do this a few ways 1. elastic arteries help decrease pressure in them by distending 2. muscular arteries can vasodilate and decrease pressure in them by increasing diameter 3. we can also decrease the SV of the heart

11 ΔP = MAP (mean arterial pressure) R = total peripheral resistance
F = ΔP/R applies to the entire circulatory system in addition to a single vessel F = cardiac output ΔP = MAP (mean arterial pressure) R = total peripheral resistance total resistance offered by all systemic peripheral vessels influenced by sympathetic nervous activity rearrange the equation - ΔP = F X R OR MAP = CO X total peripheral resistance

12 1 – CO and total peripheral resistance
2 – CO depends on heart rate and SV 3 & 4– heart rate depends on balance between the parasymp and symp divisions of the ANS 5 – SV increases in response to symp activation (extrinsic control) 6 – SV also increases with increasing venous return (instrinsic control) 7- 10 – venous return is increased by symp induced vasoconstriction (7), skeletal muscle pump (8), respiratory pump (9) and cardiac suction (10) 11 – 13 – venous return is also influenced by how much blood returns to the heart (11), actual blood volume (balance between passive bulk-flow fluid exchange between plasma and ECF (12), water and salt balance (13) and hormonal control (14)

13 15 & 16 – MAP is also determined by radius of the vessel (15) and the number of RBCs (16)
– arteriole radius can be controlled by metabolic factors which control blood need (17) - which leads to vasodilation (18) ALSO by sympathetic activity (19) which can cause vasocontriction (20) OR hormonally (20)

14 Arterioles major resistance vessels in the vascular tree
radius is small enough to offer resistance to flow high arteriolar resistance causes a marked drop in the MAP as blood flows through these vessels MAP arteriole entrance = 93 mm Hg MAP arteriole exit = 37 mm Hg resistance also converts the pulsatile nature of systolic-diastolic pressure to nonpulsatile pressure within the capillaries radius of the arteriole can be adjusted to 1. variably distribute cardiac output among the organs 2. help regulate arterial blood pressure

15 Arterioles and Arteriolar resistance
vasoconstriction and vasodilation presence of a thick layer of smooth muscle sensitive to many systemic, local factors + neurogenic stimulation vascular tone arterioles normally exhibit a state of slight constriction = vascular tone helps establish a baseline of arteriolar resistance tonic activity makes it possible to either vasoconstrict or vasodilate two facets are responsible 1. myogenic activity of smooth muscle layer smooth muscle layer is responsive to neural or hormonal influences – self-induced contractile activity 2. continuous release of NE by sympathetic fibers of the ANS

16 Arteriolar diameter Intrinsic Factors/Local changes – at the tissue, organ specific local chemical factors metabolic factors vasoactive mediators histamine local physical factors hot/cold passive stretch of arteriole shear stress within arteriole Extrinsic factors sympathetic nervous system hormones

17 Chemical influences and arteriole radius = local metabolic changes
most important local chemical influences on arteriolar smooth muscle are local changes in metabolism within that organ local metabolic changes can affect the diameter of an arteriole without neural influence active hyperemia = local arteriolar vasodilation that increases blood flow into an organ arterioles are found within an organ and can be directly affected by that organ’s metabolic needs local metabolic factors decreased/increased oxygen = vasodilation/vasoconstriction increase carbon dioxide = vasodilation increased carbonic acid= vasodilation increased K+ - repeated APs that outpace the Na/K pump’s ability to correct ionic changes = vasodilation increased osmolarity – concentration of solutes accumulates in actively metabolic cells = vasodilation prostaglandin release = vasodilation relative concentration of these factors can determine the state of arteriolar muscle tone

18 Vasoactive Mediators these local chemical changes do not act directly on smooth muscle but act on the endothelial cells ECs – simple squamous epithelia cells found lining the inside of the arteriole and capillary ECs then release chemical factors called vasoactive mediators e.g. endothelin = vasoconstriction e.g. nitric oxide = vasodilation by relaxing arteriolar smooth muscle inhibits entrance of calcium into the smooth muscle which inhibits the opening of the foot proteins on the sarcoplasmic reticulum ECs have multiple roles

19 Histamine NOT released by metabolic changes
NOT produce by endothelial cells released upon pathology released by connective tissue cells within the organ or by circulating white blood cells (mast cells, basophils) usually released in response to organ damage causes vasodilation to increase blood flow and speed healing

20 Local Physical factors
application of heat or cold heat causes localized arteriolar vasodilation increases blood flow cold – counteracts histamine-induced swelling by inducing vasoconstriction shear stress blood flowing over the endothelial lining creates friction = shear stress increase in shear stress can cause increased release of NO – promotes vasodilation increased blood flow now reduces shear stress myogenic response to stretch increased MAP drives more blood into the arteriole which pushes out against the vessel wall = passive stretch leads to vasoconstriction to reduce this blood volume arteriolar smooth muscle responds to passive stretch by increasing its tone through vasoconstriction this increased tone acts to resist the passive stretch done by the release of vasoactive mediators from the EC (e.g. endothelin) arterial occlusion can block blood flow and reduce this stretch arterioles will dilate in response=reactive hyperemia

21 Extrinsic control of arteriolar diameter
includes both neural and hormonal control sympathetic division innervates arteriolar smooth muscle everywhere except the brain NO parasympathetic innervation of arteriolar smooth muscle! (exception – ciltoris and penis) sympathetic activity contributes to arteriolar vascular tone increased sympathetic activity induces vasodilation of arterioles in heart and skeletal muscle– drops arteriolar resistance and changes MAP main area of the brain to adjust sympathetic output = cardiovascular control center other brain regions involved – hypothalamus Hormones: ADH, angiotensin II, epinephrine, norepinephrine

angiotensin II – converted from angiotensin I by the enzyme ACE (produced in the lungs) regulates body’s salt balance causes the release of aldosterone from the adrenal cortex – increased salt reabsorption powerful vasoconstrictor vasopressin (ADH) – released from the posterior pituitary in response to changes in water volume drop in water content, release of vasopressin, decreased urine volume, increased water retention also construction of peripheral vessels = vasoconstrictor plays a role in reducing hemorrhage

23 -Epinephrine and Norepinephrine can be released from the adrenal medulla (sympathetic activity) or NE can be released from neurons (sympathetic) -Ep and NE can cause vasoconstriction or vasodilation!!! depends on receptor and its location -NE binds to a1-adrenergic receptors on ALL arteriolar smooth muscle to increase vasoconstriction -Epi binds to b2-adrenergic receptors on arteriolar smooth muscle in heart and muscles to cause vasodilation -cerebral arterioles do NOT have a1-adrenergic receptors !!! -influenced entirely by local physical and chemical changes (intrinsic changes) -during the “flight or fight” response - Epi is more abundant and has more affinity for the b2-adrenergic receptors which are expressed in large amounts on arteriolar smooth muscle in skeletal and cardiac muscle – so overall effect is vasodilation to heart and skeletal muscles


25 Evaluating Circulation
Pulse is a pressure wave alternate expansion & recoil of elastic artery after each systole of the left ventricle pulse rate is normally between beats/min tachycardia is rate over 100 beats/min/bradycardia under 60 Measuring blood pressure with sphygmomanometer Korotkoff sounds are heard while taking pressure systolic blood pressure from ventricular contraction diastolic blood pressure during ventricular contraction provides information about systemic vascular resistance pulse pressure is difference between systolic & diastolic normal ratio is 3:2:1 -- systolic/diastolic/pulse pressure

26 Measuring Blood pressure

27 the sympathetic nervous system essentially maintains an appropriate driving pressure to each organ (i.e. MAP) but the organ itself controls the amount of blood that actually enters it. sympathetic control over arteriolar vascular tone constricts most vessels to ensure adequate MAP throughout the systemic circuit BUT the organ can override the sympathetic control using local control mechanisms analogy = water pressure in pipes

28 analogy – pipe carrying water
water pressure remains constant differences in the amount of water entering the beaker depends on which valves are open and to what extent these valves are open no water flows when the valve is closed more water flows when the valve is wide open (low resistance) versus when a valve is partially open (high resistance) so the sympathetic NS maintains the “water pressure” (i.e. the MAP), but each organ can control the amount of blood that enters them when increased blood flows into one organ the others must compensate by changing their arteriolar diameter SO THAT MAP IS MAINTAINED WITHIN AN APPROPRIATE RANGE

29 Regulation of BP regulation of mean arterial pressure by the body done mainly through arteriolar diameter Blood pressure = MAP within a small length of blood vessel our body uses BP to immediately determine heart rate and contraction strength BP is measured constantly by baroreceptors changes in pressure within blood vessels initiates either short-term or long-term reflexes two major BRs: carotid sinus & aortic arch baroreceptors (mechanoreceptors) as the BP within the vessels increase –increases the rate of firing of the afferent neurons within these BRs decreasing pressure decreases the rate of firing role of cardiovascular center in the medulla help regulate heart rate & stroke volume integrating center for information sent by the carotid and aortic BRs divided into two centers: vasomotor & cardiac centers (made up of cardioacceleratory, cardioinhibitory divisions) alters the ratio between sympathetic and parasympathetic activity to the heart and BVs Vasomotor center = specific neurons regulate blood vessel diameter - sympathetic vasomotor nerves Cardiac center = signals sent out through vagus & cardiac accelerator nerves - changes heart rate

30 Higher brain centers such as cerebral cortex, limbic system (emotions) & hypothalamus
anticipation of competition increase in body temperature Hypothalamus osmoreceptors control salt and water balance and therefore long-term regulation of BP cerebral cortex-hypothalamus preprograming – fight or flight responses, sexual orgasm, blushing control over cutaneous arterioles for temperature regulation takes control over the cardiovascular center’s control over these vessels for regulation BP therefore BP can fall dramatically as arteries dilate to allow cooling Proprioceptors input during physical activity Chemoreceptors monitor concentration of chemicals in the blood (O2, CO2 and H+ions) also located in the carotid and aortic arteries increase respiratory activity to bring in more O2 or blow off more CO2 also increase BP by sneding excitatory impulses to the cardiovascular center

31 Role of the ANS in Blood pressure

32 Capillaries Continuous capillaries Fenestrated capillaries
skeletal & smooth, connective tissue and lungs Fenestrated capillaries plasma membranes have many holes kidneys, small intestine, choroid plexuses, ciliary process & endocrine glands Sinusoids very large fenestrations incomplete basement membrane liver, bone marrow, spleen, anterior pituitary, & parathyroid gland Microscopic vessels that connect arterioles to venules Found near every cell in the body but more extensive in highly active tissue (muscles, liver, kidneys & brain) entire capillary bed fills with blood when tissue is active lacking in epithelia, cornea and lens of eye & cartilage Function is exchange of nutrients & wastes between blood and tissue fluid Structure is single layer of simple squamous epithelium and its basement membrane

33 capillaries are not open under resting conditions in most tissues
prevents the flow of blood through the capillary bed capillaries branch from a metarteriole or directly from an arteriole metarteriole acts like a thoroughfare connecting a larger arteriole and a venule these MAs are surrounded by spiralling smooth muscle cells – form a precapillary sphincter the sphincters are not innervated by the nervous system by still possess a high degree of myogenic tone to contract in response to chemical factors released by the tissue the more metabolically active the tissue, the greater the number of capillaries e.g. muscle only 10% of the capillaries are open in resting muscle as the muscle increases its activity – local chemical factors change and the precapillary sphincters open to allow more blood flow

34 sizes vary from capillary to capillary
ECs fit together like a jigsaw puzzle with considerable gaps in between the cells = pores sizes vary from capillary to capillary brain capillaries have EC cells held together by tight junctions – no pores most tissue capillaries allow the passage of small water-soluble substances like but glucose, small amino acids and peptides and ions prevents the passage of larger proteins like plasma proteins this transport may actually be regulated by the capillary itself ECs may secrete substances that “tighten” up their junctions histamine increases the gaps by inducing a contractile response in the EC and widening the gaps (actin-myosin interaction in the cytoskeleton) in the liver, the capillary walls have larger pores to allow the passage of proteins liver synthesizes the plasma proteins which must be allowed to pass into the circulatory system

35 Interstitial Fluid or ECF
passive intermediary between blood and cells – not a direct exchange between the blood and the ICF of cells only 20% of the ECF circulates as plasma the remaining 80% is interstitial fluid exchange between the inside of the cell and the interstitial fluid (across the plasma membrane) is passive or active – depending on the cell and the solute being moved BUT exchange between the interstitial fluid and the capillary wall is primarily PASSIVE because the gaps in a capillary wall are quite large, the interstitial fluid and the composition of the blood are essentially the same two ways to exchange materials between the blood and interstitial fluid 1. diffusion 2. bulk-transport

36 Capillary Exchange Movement of materials in & out of a capillary
diffusion (most important method) substances move down concentration gradient all plasma solutes except large proteins pass freely across through lipid bilayer, fenestrations or intercellular clefts blood brain barrier does not allow diffusion of water-soluble materials (nonfenestrated epithelium with tight junctions) transcytosis (vesicular transport) passage of material across endothelium in tiny vesicles by endocytosis and exocytosis large, lipid-insoluble molecules such as insulin or maternal antibodies passing through placental circulation to fetus bulk flow movement of large amount of dissolved or suspended material in same direction move in response to pressure - from area of high pressure to area of low faster rate of movement than diffusion or osmosis regulates relative volumes of blood & interstitial fluid comprised of: filtration (movement of material into interstitial fluid) + reabsorption (movement from interstitial fluid into capillaries)

37 Diffusion diffusion is promoted by several factors:
1. short distance of travel 1. thinness of the capillary wall – 1 um in thickness (simple squamous epithelium + basement membrane) 2. narrowness of the capillary – thinner than the RBC so the cells must pass through one at a time 3. proximity to cells – every cell is approximately 0.01cm from a capillary 2. total surface area – 10 to 40 billion capillaries produces a tremendous surface area for exchange = 600m2 3. velocity of blood through the capillary Slowest blood velocity is found in the capillaries velocity is inversely proportional to the total cross-sectional area of all the capillaries slow velocity of flow allows for sufficient exchange time analogy – river – lake – river flow rate (volume of water) flowing past any point along the river equals that of the lake BUT the speed of the water flowing is slower in the lake

38 most capillary walls solutes cross via diffusion
so the chemical concentration of arterial blood is carefully regulated to promote the diffusion of specific solutes in a specific direction the lungs add oxygen and remove carbon dioxide from the blood, the digestive organs supply glucose the cells use this oxygen and glucose and replace them with waste products the job of the blood is to continuously replace these waste products with fresh O2 and glucose because O2 and glucose pass easily through the walls of the capillary – their movement is dependent upon their specific concentration gradient as cells use more O2, this creates a larger concentration gradient between the cell and the blood – greater movement of O2


40 Bulk-flow a volume of protein-free plasma filters out of the capillary and mixes with the surrounding interstitial fluid and then is reabsorbed = bulk flow the various components are moved in bulk in contrast to the movement of individual components as seen in diffusion when blood pressure inside the capillary exceeds that of the osmotic pressure of the blood – fluid is pushed out through the pores in the capillary wall = ultrafiltration with the fluid comes the movement of multiple other components when inward driving osmotic pressure exceeds the outward blood pressure– net inward movement of fluid and fluid components = reabsorption ultrafiltration and reabsorption are collectively known as bulk flow does NOT play a role in the exchange of individual solutes does play a role in regulating the distribution of ECF between the circulating plasma and interstitial fluid this is the way we establish the composition of our interstitial fluid

41 major factors are Pc and πP
Bulk Flow (Pc + πIF) – (πP + PIF) = outward pressure – inward pressure major factors are Pc and πP

42 factors affecting bulk flow
1. Pc = capillary blood pressure fluid or hydrostatic pressure exerted on the inside of the capillary wall by blood tends to force fluid OUT of the capillaries into the interstitial fluid in general the blood pressure at the arteriolar end of a capillary = 37 mm Hg due to frictional losses in the upstream arterioles - declines to 17 mm Hg at the venous end of a capillary 2. πP = plasma osmotic pressure (oncotic pressure) osmotic pressure encourages inward movement of fluid into the capillary 25 mm Hg – doesn’t change 3. PIF = interstitial fluid hydrostatic pressure fluid pressure exerted on the outside of the capillary wall by interstitial fluid tends to force fluid into the capillaries and into the blood plasma 4. πIF = interstitial fluid-colloid osmotic pressure (πIF is close to zero) does not normally contribute significantly to bulk flow Caused by the osmotic pressure of proteins in the IF - promotes the osmotic movement of water out of the blood and into the fluid but during pathologic conditions – i.e. release of histamine which widens the capillary pores – increased leakage of plasma proteins into the interstitial fluid and πIF can increase

43 Net exchange of fluid across capillaries
Net exchange pressure = (Pc + πIF) – (πP + PIF) = outward pressure – inward pressure two pressures forcing fluid out of the plasma are capillary blood pressure and interstitial fluid-osmotic pressure two pressures forcing fluid into the plasma are plasma-osmotic pressure and interstitial fluid hydrostatic pressure the imbalance between the forces produces a net exchange of fluid at a given point along the capillary wall as the blood enters the capillary – outward forces exceed that of inward and fluid is forced out into the interstitial fluid (no protein movement!) – ultrafiltration forces result at the venular end the inward pressure now exceeds the outward pressure and reabsorption will take place as the blood moves through the capillary – pressure drops so the amount of fluid moving out of the blood drops as the blood travels through the capillary region and progressively increasing amounts of fluid re-enter the blood as the blood reaches the venular end of the capillary BUT these pressure values are controversial

44 Lymph even under normal circumstances – more fluid is filtered from the blood plasma into the interstitial fluid than is reabsorbed back into the blood plasma excess fluid = lymph this excess fluid is directed into a series of vessels that are similar in structure and composition to veins – lymphatic vessels one-way system of vessels that leads back to the circulatory system via the right lymphatic duct and the thoracic duct

45 Veins Proportionally thinner walls than same diameter artery
tunica media less muscle – little inherent myogenic tone lack external elastic lamina tunica externa has more collagen than elastic fibers strong and stretchy but possess poor elastic recoil Still adaptable to variations in volume & pressure Valves are thin folds of tunica interna designed to prevent backflow Venous sinus has no muscle at all coronary sinus or dural venous sinuses

46 Blood Distribution 60% of blood volume at rest is in systemic veins and venules function as blood reservoir often called capacitance vessels venous capacity = volume of blood the veins can accomodate body at rest – much of the blood bypasses the closed capillary beds and enters the venous return circuit – this increases the blood volume in the veins 15% of blood volume in arteries & arterioles

47 Veins & Venules veins & venules have little tone and resistance
the arteriole communicates chemically with the venule to ensure that inflow and outflow surrounding the capillary region matches venous return is enhanced by many extrinsic factors venous return = volume of blood entering the atria from the veins (pulmonary and systemic) much of the driving force on the blood (blood pressure) has been lost as it enters the veins BP averages on 17 mm Hg in the veins but because the pressure of the blood entering the right atrium in o mm Hg – there is still a small driving force that helps to return the blood through the veins clinical note – if atrial pressure becomes pathologically elevated (e.g. leaky AV valves) – this pressure differential can be lost, reducing the venous return

48 sympathetic activity – venous smooth muscle has an abundant nervous innervation by the sympathetic nervous division can produce a small amount of constriction in the veins increasing venous BP and increasing the forces driving blood back to the heart this contraction also decreases the amount of blood that can be held in the veins (decreases venous capacity) by decreasing the diameter of the vein itself so less blood remains in the veins but is returned faster to the heart skeletal muscle activity – contraction of skeletal muscles can push on the vein walls, decreasing their size and decreasing their capacity venous valves – venous vasoconstriction and skeletal muscle contraction also drive blood away from the heart -evolved extensions off the endothelium – valves -these valves can shut off sections of veins to prevent back-flow towards the feet when standing 4. respiratory activity– pressure in the chest is 5 mm Hg less than atmospheric blood flowing through the thoracic cavity on the way back to the heart is exposed to subatmospheric conditions this creates a pressure differential between the pressure in the limb veins and those in the thoracic region veins – drives more blood from the limbs = respiratory pump

49 Veins and gravity - gravity – when lying down, forces of gravity are equally applied to all veins -when standing, vessels below the heart become more subject to gravitational forces -so the veins increase their volume to counteract the increased volume -this reduces the amount of blood returning to the heart – decreases CO -also increases the pressure in the capillaries – forces more fluid out into the tissues from the blood -compensatory mechanisms – fall in MAP triggers the sympathetic NS to induce venous constriction to drive some of the pooled blood up toward the heart + skeletal muscle tone will increase to help propel blood to the heart


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