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Elmoselhi - Special Circulatio
Special Circulation

Additional Physiology Flashcards




Explain local control of blood flow


*acts within seconds or minutes

*special phenomena: reactive hyperemia, active hyperemia and autoregulation

*constriction or relaxation of the arterioles, metarterioles and precapillary sphincters based on rate of metabolism in the local tissue or changes of oxygen availability



*acts within days or weeks

*results in changes of physical sizes and numbers of the blood vessels supplying the tissues

Explain global control of blood flow

*Based on the needs of the body as a whole


*mainly through autonomic nervous system and other neural reflexes

Explain active hyperemia

*The local increase of the blood flow to a tissue when this tissue become active (e.g. muscle during exercise)



Active tissue -> increase local metabolism -> use up more nutrients and release more vasodilator substances (adenosine, NO, CO2, K+) -> increase blood flow e.g. intense exercise -> ↑ muscle blood flow 20 fold

Explain reactive hyperemia

*Transient increase in blood flow (4-7 times normal) after a brief period of arterial occlusion (ischemia)


Mechanism: Temporary blood occlusion -> oxygen deficiency and increase vasodilators in local tissue -> vasodilation and increase blood flow


ex - ischemia of the LV occurs during systole

- during tachycardia ischemia can occur as well

What is autoregulation?

*the intrinsic ability of an organ to maintain a constant blood flow despite changes in perfusion pressure




1) Metabolic theory


2) Myogenic theory

What is the metabolic theory?



a) Vasodilator theory: increase tissues metabolites -> relax vascular smooth muscle -> increase blood flow

CO2, increased adenosine, increased lactic acid increased H+ (decreased pH), increased K+, increased osmolarity


b) O2 lack theory: precapillary sphincters and metarterioles open and close cyclically several times/min (vasomotion) based on availability of O2 and others nutrients

decreased O2, decreased nutrients -> relaxation -> increase blood flow

What is myogenic theory?
Stretch of vascular smooth muscle (high blood pressure) -> contraction of smooth muscle in small vessels
Which circulations rely on autoregulation?

1- Cerebral circulation


2- Coronary circulation


3- Renal circulation


4- Circulation of skeletal muscle during exercise

What are some vasoconstrictor agents?

Vasoconstrictor agents:


Norepenephrine (NE) and epeniphrine -> sympathetic stimulation -> alpha1 receptor in blood vessels -> vasoconstriction beta1 receptors in the heart -> increased heart rate and contractility


Endothelin -> vasoconstriction


Angiotensin II -> vasoconstriction in small arterioles


Serotonin -> vasoconstriction in response to vessel damage (migraine)


Vasopressin or ADH -> vasoconstriction in small vessels increased [Ca2+] -> stimulate smooth muscle contraction

How is endothelin-1 regulated?


*angiotensin II


*growth factors



*oxidized LDL


*shear stress








What are some vasodilator agents?

Nitric oxide (NO) -> vasodilation


Bradykinin: among others kinins family cause vasodilation of blood vessels


Histamine: release mainly from mast cells in damaged tissues and basophils in the blood -> vasodilation of blood vessels


Ions and other substances: increased [K+] inhibit smooth muscle contraction -> vasodilation increased [Mg+] increased [H+] increased CO2

Explain long-term regulation of blood flow

Causes: Increase long-term metabolic demand (overactive tissues for a long period of time)


Effects: Formation of new blood vessels to keep up with the metabolic demand


Mechanisms: Deficiency of tissue O2 and other nutrients -> formation of angiogenic factors such as: *Vascular Endothelial Growth Factor (VEGF) *Fibroblast growth factor


Explain global control

Predominantly neural Arteries, arterioles, and veins are innerved by:


α1 adrenergic receptors -> vasoconstriction


β2 adrenergic receptors -> vasodilation


Muscarinic cholinergic receptors are located on the endothelial cells -> vasodilation of adjacent smooth muscle (NO mediated)


Humoral control: Examples include adrenal medullary catecholamines, angiotensin II, and ADH. Blood volume control includes aldosterone, ANP, erythropoietin


Reflexes: Combination of neural and humoral mechanisms


Reflexes includes:

*Arterial baroreceptor reflex.

*Volume reflexes - atrial stretch receptors mediating HR. ADH, ANP.

*Chemoreceptor reflex (central and peripheral). *Central ischemic response and Cushing’s reflex.

What is special circulation?

*The various tissues and organs have different blood flow requirements, e.g. skin and kidneys need blood flow both for tissue nutrition and an excretion function (heat and urine).


*Blood flow control differs in different tissues and organs, e.g. in brain and heart there is minimal sympathetic vasoconstriction and potent local control.


*Blood volume can be shunted from some tissues and organs to others, e.g. liver and splanchnic blood volume can be mobilized by sympathetic vasoconstriction in exercise.

Explain skeletal muscle circulation

Blood flow: depends on metabolic demands.

*At rest, 750 ml/min, 15-20% of blood flow for 40-50% of body mass.

*During exercise, 20L/min, 80-90% of greatly increased cardiac output.


Blood volume: 700ml-1L, 15-20% of total.


Control: (dual control) only in arteries

Neural control (during REST)

*α1 adrenergic - considerable constriction.

*beta2 adrenergic - dilation, particularly with epinephrine.

*Sympathetic cholinergic dilation (minor role if any) *No parasympathetic


Local control (very important with EXERCISE) Increase local metabolites


Extravascular compression: Most important with isometric contraction. Milking action on veins with rhythmic contractions.

Explain GI (splanchnic) circulation

*Blood flow:

Resting, 1,000ml/min via hepatic portal vein, 500 ml/min via hepatic artery. 20% of cardiac output, 25% of body mass. Minimal, 300 ml/min. Important for uptake of nutrients from GI.


*Blood volume: 20-25%of blood volume at rest, 10-15% with baroreflex response.



Sympathetic - α1 predominates. No cholinergic. Local - intrinsic basal tone in intestine. Hormones important.


*Extravascular compression: Important in exercise, aids venous return.

Explain coronary circulation

*Blood flow: ~ 200 ml/min at rest and ~ 1 L/min maximal 4-5% of cardiac output at rest and during exercise. Tied very closely to cardiac function.


*Blood volume: Not an important reservoir.


*Control: Neural - only for fine tuning


Local - metabolic (dominant factor) and intrinsic basal tone (some) - AUTOREGULATION


*Extraction of oxygen - very high 65-75% at rest and ~ 90% during max. exercise Coronary veins have lowest PO2 level at rest


*Extravascular compression: phasic flow

Explain phasic blood flow during systole and diastole in the right and left coronary arteries

*in both arteries there is a high increase in blood flow during diastole


*during systole there is contraction of the ventricles which compresses the subendocardial arterial plexus


*the high increase in blood flow is due to reactive hyperemia


*left coronary has a higher increase in blood flow than the right because the left side of the heart needs more blood

Explain cerebral circulation

*Blood flow:

Overall brain metabolic activity does not change very much and blood flow is relatively constant. Resting, 12-15% of resting cardiac output, 2.5% of body mass. Overall can increase by 40%, doubling in some areas, and decrease by 20%. Brain death - decrease flow, "hot nose" sign


*Blood volume: small variation, skull limitation, not an important volume reservoir. 1,400g, 75 ml blood, 75 ml CSF.




Neural: minor functional importance.

Sympathetic and parasympathetic innervation.

Both α1 and β2 receptors.

NPY is a powerful vasoconstrictor (protects against sudden increases in arterial pressure),

5HT is a powerful vasoconstrictor (vasospasm with subarachnoid hemorrhage).

Parasympathetic function unknown.


Local: predominates - PCO2 very important. May be an important myogenic component to autoregulation. increases PC02, decreased pH -> increased blood flow


*Extravascular compression: Very important in pathological conditions - hemorrhage, increased intracranial pressure, cerebral edema.

Explain cutaneous circulation

*Blood flow: 5% of cardiac output at rest, <0.5% in the cold. ~ 200- 600 ml/min at rest, may be > 5L/min in extremely hot environment.


*Blood volume: Fairly large capacity, mostly in venous plexus. Increase by 40% with sympathectomy, decrease by 50% with maximum sympathetic tone.



Neural tone dominates. α1 adrenergic receptors. Sympathetic cholinergic stimulation of sweat glands - bradykinin causes secondary vasodilation.


Local: intrinsic basal tone. Temperature also has a direct effect.

Explain temperature regulation

*Normal body temperature set point - 37°C or 98.6°F


*Temperature-regulated center is located in anterior hypothalamus.


*Generating-heat and dissipating-heat mechanisms maintain the balance between environmental and body temperatures


*These mechanisms act if the core temperature is above or below the set point temperature

What are the mechanisms that generate heat

Generating-heat Mechanisms: (core temperature is below the set point temperature)


1- Thyroid hormones: thermogenic hormone Stimulates Na+-K+ATPase, increased O2 consumption, increased metabolic rate, increased heat production


2- Sympathetic nervous system:

a) Stimulates metabolic rate and heat production via beta receptor in brown fat,

b) stimulates alpha1 receptors -> vasoconstriction -> reduces heat loss


3- Shivering: most potent mechanism of heat production

What are the mechanisms that dissipate heat?

Dissipating-heat Mechanisms (core temperature is above the set point temperature)


1- decrease sympathetic activity in skin blood vessels


2- increase sympathetic cholinergic stimulation to the sweat glands

Explain fever

*Increase the hypothalamic set point temperature via pyrogens



Pyrogen -> increase interlukin-1 -> increase prostaglandins in ant. hypothalamus -> increase set point temperature


*Treatment: inhibiting prostaglandins synthesis by inhibiting cyclooxygenase enzyme (e.g. aspirin)

Explain heat exhaustion
Increase enviromental temperature -> dissipate heat mechanisms excess sweating -> decreased ECF -> decreased blood volume -> decreased arterial pressure -> fainting
Explain heat stroke
Increase body temperature -> tissues damage
Explain malignant hyperthemia

*Massive increase in the following in skeletal muscle: a) metabolic rate

b) O2 consumption

c) heat production


*Heat-dissipating mechanisms can not keep up


*Caused by inhalation anesthetics

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