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36 Cards in this Set

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Regulation of Blood Flow by the Peripheral Circulation:
What does blood flow through the vasculature dependent on?
Derive Equations
Dependent on pressure gradient and vascular resistance.
Flow (Q) = DP/R = (MAP-CVP)/TPR
Q ~ MAP/TPR since CVP is negligible; Since R fr Poiseuille Eq can't be measured directly, calc TPR instead: TPR = MAP/Q = 2/3Dias + 1/3 Sys = Dias + 1/3(Pulse Pressure) = Dias + 1/3(Sys – Dias); Rest: 120/80; Q = 5L/min-> 18.6TPR; Exercise (avg!): 180/80; Q = 20L/min-> 6.5TPR?
Poiseuille Equation
Fluid Resistance R = Ln/(r^4), where n = viscosity. R increases with increasing L, increasing n, and especially decreasing r. The radius term is the only factor that changes significantly in is the most important one, as small changes in radius can lead to large changes in resistance. However usually TPR (=MAP/Q) is calculated since R cannot be measured directly.
What influences the rate at which a fluid flows through a tube?
Tube Radius
Tube Length
Magnitude of Pressure Drop causing flow
Resistance to Flow offered by fluid itself, given by Poiseuille’s Equation R = Ln/(r^4)
What is the regulation of vascular tone modulated by?
The regulation of vascular tone is modulated by the integrated response of:
1)Neural factors
2)Humoral factors
3)Local factors (including metabolic factors, endothelial factors & myogenic factors)
4)Resistance vessels (i.e. arterioles), which regulate BP, tend to operate at rest in a state of partial contraction called TONE.
NEURAL REGULATION OF BLOOD FLOW: NE, E, ACh
-Tonically active (some firing at rest) SNS nerve->NE->a1AdrR on vascular smooth muscle->vasodilation
-Test: aR blocker->a1AdrR->dec BP
-b2R more common in heart; a1R in splanchnic area (liver, intestines)
-NE doesn’t reach b2R, but circulating E does.
-PNS nerve->ACh + NO->NO causes more NO release->+GC->inc cGMP->vascular SM relaxation, usu at ext genitalia, the only signif area of cholinergic innervation
-Sildenafil->inhibits cGMP breakdown-Tx erectile dsyfxn
HUMORAL REGULATION OF PERIPHERAL BLOOD FLOW & VASCULAR SMOOTH MUSCLE: E, NE
-Adrenal Glands->E->SKM w/ biphasic effect
-low E->bR->vasodilation
-high E->aR->vasoconstriction
-redist’s blood flow during exercise->inc E->vasodilate working SKM, vasconstrict others
-Little from Adrenal Glands but mostly from SNS nerve->NE
-Other hormones released: ADH, serotonin, Ang II, histamine
LOCAL REGULATION OF BLOOD FLOW: GENERAL MECHANISMS
The sensitivity of a given substance varies in the different organ beds. For example, reduced tissue O2 tension tends to cause ____ in systemic vessels but ____ in pulmonary vessels.
For metabolic regulation, adenosine is important in the ____.
1) Metabolic
2) Myogenic
3) Paracrine
vasodilation, vasoconstriction
coronary circulation
LOCAL REGULATION OF BLOOD FLOW: METABOLIC REGULATION
-Metabolites released to change resistance: lactic acid, adenosine, high CO2, high K+, high H+ (low pH), low O2
-inc’d metabolic activity or dec’d O2 supply->parenchymal & endothelial cells release local factors->diffuse to nearby arteriolar SMC’s->relaxation->inc diameter & blood flow->inc O2 + nutrients
-Tissue PO2 decreases w/ inc’d use of O2; when arteriolar wall PO2 also dec, this contributes to vasodilation
-dec arterial PO2->dec O2 delivery->metabolites released->normal flow
-inc tissue metabolism->inc blood flow->restore PO2
LOCAL REGULATION OF BLOOD FLOW: MYOGENIC REGULATION
-physical distension->vascular SM responds to stretch; stretch degree is a function of both the compliance of and pressure gradient across the vessel wall.
-myogenic response counteracts effects of transmural pressure changes on arterial diameter
-inc blood flow->inc BP->inc stretch->vascular SM contraction->inc R->lower blood flow
-dec blood flow->dec BP->dec stretch->vascular SM dilation->dec R->higher blood flow
LOCAL REGULATION OF BLOOD FLOW: ENDOTHELIAL/PARACRINE FACTORS: ENDOTHELIAL CELLS
-produce vasoactive substances that regulate vascular tone: EDRF (NO), PGI2, endothelin (ET-1).
-stimulation of the endothelium by Ach, bradykinin, and shear stress of blood on the endothelium itself induces relaxation. NOS itself is controlled by endothelial cell [Ca2+]. The Ca2+-Calmodulin sys is switched on in response to binding of ACh, histamine thrombin, ATP, serotonin, etc to specific endothelial lumenal surface receptors.
LOCAL REGULATION OF BLOOD FLOW: ENDOTHELIAL/PARACRINE FACTORS: ENDOTHELIAL CELL FUNCTIONS
1) maintain vascular tone and structure
2) regulate vascular permeability
3) regulate vascular cell growth
4) regulate thrombotic and fibrinolytic function
5) mediate inflammatory mechanisms
6) modulate lipid oxidation
7) regulate platelet and leukocyte adhesion
LOCAL REGULATION OF BLOOD FLOW: ENDOTHELIAL/PARACRINE FACTORS: OTHER PARACRINE MECHANISMS
-daily aspirin->suppress ability to synthesize thromboxane A2
-vascular SM receives numerous inputs from the SNS from the adventitial side, and both inhibitory (vasodilation, ex NO) and excitatory (vasoconstriction, endothelin) factors produced by the endothelium are present in the blood.
4 ELEMENTS OF LOCAL CONTROL OF BLOOD FLOW IN THE VARIOUS VASCULAR BEDS
1) Active hyperemia (metabolic regulation)
2) Reactive hyperemia (metabolic and myogenic regulation)
3) Autoregulation (metabolic and myogenic regulation)
4) Vascular Response to Injury (paracrine regulation)
For example, in SKM circulation, active hyperemia and perhaps reactive hyperemia are important mechanisms
Some Smooth Muscle Effectors and their Receptors:
NE, E, Angiotensin II, Vasopressin, Serotonin, Endothelin-1, ACh
NE – a1
E – a1/b2
Angiotensin II – AT1, AT2
Vasopressin – V1
Serotonin – S1, S2
Endothelin-1 – ETA, ETB
ACh – M1, M2
REGULATION OF BLOOD FLOW IN THE CORONARY CIRCULATION
Active hyperemia is a must for coronary blood flow. B/C a substantial fraction of arterial O2 is extracted under basal conditions, ANY inc'd O2 req must be met by inc'ing blood flow. Acutely inc’d myocardial metabolism is almost always the result of inc’d SNS nerve activity to the heart. In general, there is a linear relationship b/w coronary blood flow and myocardial metabolism since metabolism normally results in coronary dilation.
REGULATION OF BLOOF FLOW DURING EXERCISE
At rest ~15% of the CO->SKM; 50%->splanchnic area. During exercise, ~80%->SKM; ~5%->splanchnic area. Since CO inc during exercise and BP inc, TPR must dec. Blood redist is due to sympathetic-mediated vasocons to non-working muscle and the release of tissue metabolites causing “metabolic vasodilation”, an effect that outcompetes the effect of inc’d sympathetic drive that occurs during exercise. Also, at rest there is more blood flow to muscles than needed->known b/c est low O2 extraction at rest that inc immediately during exercise, even before the inc in HR and CO.
The tissue distribution (rest/moderate exercise) of blood flow (mL) both at rest and during moderate exercise (CO=12.5L/min) in an individual with a CO of 5L/min at rest.
Splanchnic, Kidney, Skin, Brain, Heart, Skeletal Muscle, Bone
Splanchnic – 1300/600 DEC
Kidney – 1000/550 DEC
Skin – 450/1700 INC
Brain – 650/650 SAME
Heart – 150/550 INC
Skeletal Muscle – 750/8000 INC
Bone – 650/450 DEC
CAPILLARIES
What happens here? What vessel layer is present? What diffuses through?
The capillaries are where the exchange of nutrients take place. There is only an intimal layer for the nutrients (i.e. electrolytes) and water to diffuse through.
What factors are involved in the movement of the nutrients in and out of the capillary?
1) Hydrostatic Pressure (which is BP): forces fluid out of the capillary
2) Osmotic/Oncotic Pressures (due to proteins): tend to pull fluid in; water will move to equalize osmolarity.
Fluid is pushed out at the beginning of the capillary = FILTRATION. Fluid is reabsorbed into the capillary at the end of capillary due to lower hydrostatic pressure, while plasma oncotic pressure remains the same and is higher than the hydrostatic pressure.
Normally, ____ do not leave the capillary and ____ do. When there is an imbalance b/w the ____ and ____, an imbalance b/w the fluid pushed out of the capillaries and reabsorbed may result. This can lead to an _____ in the interstitial space, termed ____. The ____ system is present to absorb excess fluid.
RBC’s, WBC’s, hydrostatic pressure, oncotic pressure, accumulation of fluid, edema, lymphatic capillary
EDEMA
Definition, Variables Inducing Edema
Defined as a swelling of tissue due to an excessive accumulation of interstitial fluid.
-increased BP or venous obstruction ( = inc’d hydrostatic pressure)
-increased tissue protein concentration ( = inc’d tissue oncotic pressure)
-decreased plasma protein concentration ( = dec’d plasma oncotic pressure)
-increased capillary permeability
-obstruction of lymphatic vessels (lymphatic clogging)
Variables Inducing Edema: Increased BP or Venous Obstruction ( = increased hydrostatic pressure): CHARACTERISTICS
Increases capillary filtration so that more interstitial fluid is formed at the arteriolar ends of capillaries; example is during exercise, when dilation of additional arterioles occurs and BP increases.
Variables Inducing Edema: Increased Tissue Protein Concentration ( = increased tissue oncotic pressure): CHARACTERISTICS
Decreases diffusion of water into the venous ends of capillaries. Usually localized tissue edema due to leakage of plasma proteins through capillaries during inflammatory, allergic reactions and/or damage to cells which release proteins; fluid will be pulled into the interstitial space.
Variables Inducing Edema: Decreased Plasma Protein Concentration ( = decreased plasma oncotic pressure): CHARACTERISTICS
Decreased reabsorption of fluid back into the venous ends of capillaries. Possible causes: liver disease (insufficient plasma protein production), kidney disease (leakage of plasma proteins into the urine), protein malnutrition.
Variables Inducing Edema: Increased Capillary Permeability: CHARACTERISTICS
Due to inflammatory response/vasodilation; more fluid leaves the capillary as well as lymphocytes and not as much is reabsorbed at the site of inflammation.
Variables Inducing Edema: Obstruction of Lymphatic Vessels (Lymphatic Clogging): CHARACTERISTICS
Infections can block lymphatic drainage and obstruction to further uptake occurs.
HYPERTENSION
Definition
Prevalence
Severe Hypertension is a risk factor for what?
Defined as a BP>140/90 which is associated w/ the inability to maintain BP homeostasis.
It is the most prevalent cardiovascular disease w/ ~50% of individuals over 65 having it.
It is a risk factor for coronary artery disease and stroke (decreased O2 supply to the brain). 2 types of stroke: 1) Hemorrhagic (bursting of brain vessel) & 2) Ischemic (more common blockage of brain vessel)
2 CLASSIFICATIONS OF HYPERTENSION
1) Essential or Idiopathic (primary):
>90% of those w/ hypertension have this type
unknown cause but associated with inc’d peripheral vascular resistance or inc’d plasma volume.
2) Secondary:
<10% of those w/ hypertension
known cause; e.g. an adrenal tumor that increases aldosterone production, lead, etc.
Originally thought that hypertension was part of the aging process, but not so.
Increased resistance underlies the etiology of idiopathic hypertension. This is due to an imbalance b/w vasodilators and vasoconstrictors. Normally there is a finely regulated balance b/w these substances, which include (in hypothesized order or importance):
1)NO
2)Renin-Angiotensin System (RAS)
3)Oxidative Stress
4)Endothelin-1 (ET-1)
5)Increased SNS Activity
6)Anti-Diuretic Hormone (ADH, or vasopressin)
7)Thromboxane A2
Reasons for Increased Resistance in Arterioles: Nitric Oxide
Plays a key role in BP maintenance. Inhibition of NOS results in a precipitous rise in resistance and BP. Normally, increased shear on the endothelium from blood flow increases eNOS activation and NO production
Reasons for Increased Resistance in Arterioles: Oxidative Stress
Free radical production (e.g. O2-, OH-, H2O2) can damage blood vessels, inactivate NO and increase resistance by causing vasoconstriction
Reasons for Increased Resistance in Arterioles: Endothelin-1 (ET-1)
A potent vasoconstrictor produced by the endothelium. Binds to ETA and ETB receptors on vascular SM.
Reasons for Increased Resistance in Arterioles: Increased SNS Activity
Increased NE output will induce vasoconstriction. Stress enhances SNS activity and contributes to the inc’d resistance seen in hypertension. Insulin increases SNS activity, while NO decreases SNS activity.
Reasons for Increased Resistance in Arterioles: Anti-diuretic Hormone (ADH, or vasopressin)
A hormone released by the posterior pituitary to induce volume rentention and vasoconstriction.
Reasons for Increased Resistance in Arterioles: Thromboxane A2
A vasoconstrictor that stimulates platelet aggregation.
MEDIATORS OF VOLUME RETENTION (which can also affect hypertension)
1) RAS
2) Aldosterone (mineralcorticoid): secreted from adrenal gland, which regulates [electrolyte]
3) Atrial Natriuetic Factor (ANF): a peptide released by the atria in response to volume sensed by volume receptors.
4) High-Salt Diet: NO and RAS affect sodium excretion