Vessels Resistance

7/29/2019 Vessels Resistance

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Lecture 8 Control of Resistance Vessels

1. What is meant by resistance vessels?- Arteries or arterioles that contribute most substantially to TPR-

VESSEL TYPE DIAMETER (mm) FUNCTION

Aorta 25 Pulse dampening and distribution

Large Arteries 1.0 - 4.0 Distribution of arterial blood

Small Arteries 0.2 - 1.0 Distribution and resistance

Arterioles 0.01 - 0.20 Resistance (pressure & flow regulation)

Capillaries 0.006 - 0.010 Exchange

Venules 0.01 - 0.20 Exchange, collection, and capacitance

Veins 0.2 - 5.0 Capacitance function (blood volume)

Vena Cava 35 Collection of venous blood

- Large arteries branching off the aorta (e.g., carotid, mesenteric, renal arteries) distributethe blood flow to specific organs. These large arteries, although capable of constricting

and dilating, serve virtually no role in the regulation of pressure and blood flow under

normal physiological conditions. Once the distributing artery reaches the organ to which

it supplies blood, it branches into smaller arteries that distribute blood flow within the

organ. These vessels continue to branch and become arterioles. Together, the small

arteries and arterioles represent the primary vessels that are involved in the regulation

of arterial blood pressure as well as blood flow within the organ

2. Flow Principles


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- Blood flow is the volume of blood flowing through a vessel, organ, or the entirecirculation in a given period and may be expressed as ml/min (blood flow of the entire

circulation is equal to cardiac output)

- Blood pressure is the force per unit area exerted by the blood against a vessel wall and isexpressed in millimeters of mercury (mm Hg)

- Resistance is a measure of the friction between blood and the vessel wall, and arisesfrom three sources: blood viscosity, blood vessel length, and blood vessel diameter. The

variable with the greatest effect on resistance is the diameter (or radius, 1/2 the

diameter) of a particular vessel - resistance drops exponentially as the radius increases.

- TPR is total peripheral resistance - resistance throughout the entire systemic circulation.


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3. Control of Resistance

- Blood pressure varies with changes in blood volume, TPR, and cardiac output, which aredetermined primarily by venous return and neural and hormonal controls

- Autonomic Factor Vessels are highly innervated by autonomic nerves Both sympathetic and parasympathetic division of autonomic nervous system

control the tone of resistance vessels by opposing actions

Almost all blood vessels receive efferent nerve fibres from sympathetic nervesystem to their smooth muscles.

Even though only a small portion of smooth muscle is innervated by the nerves,once the upper part of smooth cells are fired, the electrical impulse will be

transmitted to the neighbouring cells via the gap junctions.


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Receptors for norepinephrine on heart muscle are mainly beta-adrenergic

Other neurotransmitters for sympathetic nerves such as noradrenaline (aka

norepinephrine) co-transmitters ATP, Neuropeptide Y(NPY)

Sympathetic nerves are tonically active (continuously firing) Parasympathetic nerves- acetylcholine, vasoactive intestinal polypeptide (VIP),

nitric oxide (NO)

They are all responsible for vasodilation and only affect limited number oftissues and plays no significant role in TPR

Parasympathetic nerves are not tonicaly active- Humoral Modulation


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- Autoregulation : a nearly constant flow in the face of changing pressure

Autoregulation is the automatic adjustment of blood flow to each tissue inproportion to its needs, and is controlled intrinsically by modifying the diameterof local arterioles. (Extrinsic influences control MAP.)


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Metabolic controls of autoregulation are most strongly stimulated by a shortageof oxygen at the tissues

There are two mechanisms that control autoregulation. One comprises samemetabolic factors described for active hyperemia.

When arterial pressure reduction lowers blood flow to organ, the supply ofoxygen to the organ diminishes

Extracellular concentrations of CO2, H+ ions, and metabolites all increasebecause blood cannot remove them as fast they are produced.

Unlike hypermia, flow autoregulation is not limited to circumstances in whicharterial pressure decreases.

Initial increase in flow due to increased pressure removes the local vasodilatorchemical factors faster than they are produced and also increases the local

concentration of oxygen

This causes arterioles to constrict, thereby maintaining relatively constant localflow in the face of increased pressure.

Another mechanism that involve in autoregulation is myogenic response Its a direct response caused by changes in calcium movement into the smooth

muscle cells through stretch-sensitive calcium channels in the plasma

membrane.

Myogenic response in independent of endothelium and nerves.


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the effects of suddenly reducing perfusion pressure from 100 to 70 mmHg


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In a passive vascular bed, that is, one that does not show autoregulation, thiswill result in a rapid and sustained fall in blood flow.

In fact, the flow will fall more than the 30% fall in perfusion pressure because ofpassive constriction as the intravascular pressure falls, which is represented by a

slight increase in resistance in the passive vascular bed.

If a vascular bed is capable of undergoing autoregulatory behavior, then afterthe initial fall in perfusion pressure and flow, the flow will gradually increase(red line) over the next few minutes as the vasculature dilates (resistance

decreases

After a few minutes, the flow will achieve a new steady-state level If a vascular bed has a high degree of autoregulation (e.g., brain and coronary

circulations), then the new steady-state flow may be very close to normal

despite the reduced perfusion pressure.

If an organ is subjected to an experimental study in which perfusion pressure isboth increased and decreased over a wide range of pressures, and the steady-

state autoregulatory flow response measured, then the relationship between

steady-state flow and perfusion pressure can be plotted as shown in the figure

If a vasodilator drug is infused into an organ so that it is maximally dilated andincapable of autoregulatory behavior, the curve labeled "Dilated" is generated

as perfusion pressure is changed. It is non-linear because blood vessels passively

dilate with increasing pressures, thereby reducing resistance to flow

The "Constricted" curve represents the pressure-flow relationship when thevasculature is maximally constricted and when autoregulation is not present.

This figure also shows that there is a pressure below which an organ is incapableof autoregulating its flow because it is maximally dilated. This perfusion

pressure, depending upon the organ, may be between 50-70 mmHg. Below this

perfusion pressure, blood flow decreases passively in response to further

reductions in perfusion pressure. This has clinical implications in coronary,

cerebral, and peripheral arterial disease, where proximal narrowing (stenosis) of

vessels may reduce distal pressures below the autoregulatory range; hence, the

distal vessels will be maximally dilated and further reductions in pressure will

lead to reductions in flow.


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4. . Hypermia

- Active hypermia : increased blood flow subsequent ton an increased metabolism

- Mechanism used : metabolic vasodilation

- Functional hyperaemia is an increase in blood flow to a tissue due to the presence of

metabolites and a change in general conditions. When a tissue increases activity there is

a well-characterized fall in the partial pressure of oxygen and pH, an increase in partial

pressure of carbon dioxide, and a rise in temperature and the concentration of

potassium ions (same situation as reduction arterial pressure in autoregulation)

- When cells within the body are active in one way or another, they use more oxygen

and fuel, such as glucose or fatty acids, than when they are not. Increased metabolic

processes create more metabolic waste. The byproducts of metabolism are vasodilators.

(Vasodilating metabolites: CO2, H+, K+, lactate, adenosine) Local arterioles respond to

metabolism by dilatating, allowing more blood to reach the tissue

- Since most of the common nutrients in the body are converted to carbon dioxide

when they are metabolized, smooth muscle around blood vessels relax in response to

increased concentrations of carbon dioxide within the blood and surrounding interstitial

fluid. The relaxation of this smooth muscle results in vascular dilation and increased

blood flow.

- Mostly developed in skeletal muscle, cardiac muscle and glands.

- Reactive hypermia : the increased blood flow subsequent to release of an

obstruction

- Mechanism used : metabolic and myogenic vasodilation

5. Endothelial mechanisms regulating blood flow

The three most important endothelial-derived substances are: nitric oxide (NO),endothelin (ET-1), and prostacyclin (PGI2). NO and PGI2 act as vasodilators, whereas

ET-1 serves as a vasoconstrictor.

Damage to the vascular endothelium due to atherosclerotic processes or followingischemia and reperfusion alters the formation and release of endothelial factors.

When endothelial damage occurs, the endothelium produces less nitric oxide andprostacyclin, which causes the adrenergic vasoconstrictor tone to be unopposed

This can lead to increased vascular tone and vasospasm. Furthermore, decreasedproduction of both of these endothelial factors can lead to increased platelet

adhesion and aggregation, and therefore enhanced thrombogenesis.

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Vessels Resistance