P: Regional circulation

Question 1

Resting coronary blood flow:

Answer 1

around 225ml/min

Question 2

What is active hyperemia?

Answer 2

vasodilatory metabolites released when levels of O2 in coronary myocytes becoming insufficient.

Question 3

Mediators of active hyperemia and their respective mechanisms?

Answer 3

adenosine and nitric oxide.
Reduction in [ATP]I results in an opening of K channels + hyperpolarisation –> relaxation of vascular smooth muscle.

Question 4

Direct effect of sympathetic nerves on blood vessels :

Answer 4

Vasoconstricts via alpha adrenergic receptors on coronary VSM

Question 5

Indirect effect of sympathetic nerve activity:

Answer 5

increased cardiac activity produces metabolic vasodilatory metabolites –> increases coronary blood flow. So indirectly causes vasodilation.

Question 6

Myocardial infarction:

Answer 6

• Decreased cardiac output
  
  • Pulmonary oedema from buildup of blood
  • Fibrillation of heart
  • Rupture of heart

Question 7

Basal high SN activity:

Answer 7

• Maintains degree of vasoconstriction
  
  • Binds to a and adrenergic receptors on VSM
  • Modulated by baroreceptors

Question 8

Carotid artery occlusion

Answer 8

• Reduces baroreceptor firing
  
  • Increases SN activity immediately reducing muscle blood flow
  • Contributes large increase in MAP

Question 9

Release of carotid artery

Answer 9

• Increases baroreceptor firing
  
  • Vasodilation caused by reduced SN activity increase muscle blood flow
  • Reduction in MAP

Question 10

Vasodilatory metabolites

Answer 10

Adenosine, K+, CO2, lactic acid. Increase blood flow in active muscle.

Question 11

VSM in exercising skeletal muscle in response to adrenaline concentration changing:

Answer 11

At start of exercise, low adrenaline concentrations only bind to B1 and B2 receptors, causing vasodilation and increased blood flow to skeletal muscle.
As exercise gets more intense, adrenaline starts binding to a-adrenergic receptors, producing vasoconstrictor effects.

Question 12

ACh relation to nitric oxide

Answer 12

• Ach can trigger nitric oxide release from endothelial cells
  
  • Activates endothelial nitric oxide synthase
  • Endothelial mediated regulation of blood flow

Question 13

Early stage of exercise

Answer 13

• Ach from neuromuscular junction may also diffuse to local blood vessels promoting NO production, VSM relaxation + vasodilation
  
  • Metabolites in actively contracting muscle induce dilation in microcirculation promoting a pressure gradient with upstream feed arteries.
  • Increase in blood flow elevates shear stress, release of NO and further vasodilation

Question 14

Nitric Oxide during exercise

Answer 14

• NO can cause function sympatholysis –> vasoconstrictor activity blunted as NO inhibits noradrenaline release + opposes a2-mediated constriction of VSM
• Skeletal muscle fibres contain neuronal NOS which increase NO release during contraction which can promote local vasodilation.

Question 15

Cutaneous circulation:

Answer 15

• Arterioles feed blood into capillaries which loop under epidermis
• Blood flows into complex venous plexus which acts as blood reservoir
• Specialised shunts, arteriovenous anastomoses feed blood into plexuses directly from subcutaneous arteries.

Question 16

Cutaneous circulation regulation:

Answer 16

• Requirement for O2 and nutrients is low - circulation is mainly needed to regulate body temperature
• Regulated by SN activity: vessels express mostly a-adrenergic receptors
• At normal temperatures skin circulation is subject to a high degree of adrenergic tone.
• Increase SN activity: vasoconstriction of arterioles and AV anastomoses –> reduction of flow into skin capillaries
• Inhibition of SN: vasodilation, increased blood flow.

Question 17

Reactive hyperaemia:

Answer 17

increased blood flow following ischaemia –> vasodilatory metabolites.

Question 18

Effects of exposure to cold:

Answer 18

• Vasoconstriction of capacitance vessels at that region & other extremities
• Temperature receptors signal to temperature regulating centre of hypothalamus, stimulates SN activity to skin
• Diverts blood from extremities
• With sustained exposure, initial vasoconstriction is following by localized cold vasodilation –> warm blood flows in and skin becomes flushed

Question 19

Cholinergic sympathetic nerve innervations:

Answer 19

innervate sweat glands + stimulate sweat production during exercise/ in response to heat

Question 20

What is bradykinin?

Answer 20

• Produces by sweat
• Potent vasodilator
• Stimulates formation of NO
• Perspiration and increased blood flow to skin happen simultaneously

Question 21

Effects of exercise increasing sympathetic outflow:

Answer 21

• Initial vasoconstriction, diversion of blood to active muscles
• Cholinergic sympathetic promote perspiration + vasodilation

Question 22

Countercurrent heat exchange:

Answer 22

Arteries and veins are very close, so cooled venous blood returning from cold hand can be warmed by arterial blood; can happen in opposite direction if exposed to heat.

Question 23

How is blood circulated into brain?

Answer 23

• Internal carotid and vertebral arteries deliver blood via basilar artery to circle of Willis, which loops around brainstem
• Cerebral arteries carry blood to brain tissue

Question 24

Intracranial pressure increased by:

Answer 24

• Intracranial bleeding
• Cerebral oedema
• Tumour

Question 25

Effect of increase intracranial pressure:

Answer 25

- Collapses veins - Decreases effective cerebral perfusion pressure - Reduces blood flow

Question 26

Cerebral perfusion pressure equation:

Answer 26

MAP-ICP

Question 27

Effect of less than 60mmHg in brain

Answer 27

Fainting

Question 28

Effect of more than 160mmHg in brain

Answer 28

Damage to BBB, can cause cerebral oedema

Question 29

How does CO2 regulate cerebral blood flow:

Answer 29

- Most important vasodilatory factor - Increases in CO2 elicit large increases in cerebral blood flow - CO2 can diffuse across BBB and reduce pH of cerebrospinal fluid - Reduction of pH triggers vasodilation of cerebral arterioles Reduction in CPP also reduces washout of CO2 from brain.

Question 30

Hypercapnia vs hypocapnia

Answer 30

Hypercapnia = increased Pco2 Hypocapnia = decreased pco2

Question 31

ICP > MAP

Answer 31

severe cerebral ischaemia

Question 32

Cushing reflex

Answer 32

Response to increased ICP and decreased cerebral blood flow. 1. Cerebral ischaemia stimulates sympathetic system: a-adrenergic receptors binding causes vasoconstriction of blood vessels --> hypertension. B-adrenergic receptor binding increases HR. 2. Hypertension stimulates baroreceptors --> parasympathetic system decreases HR = tachycardia. 3. Hypertension causes irregular breathing.

Question 33

Cushing's triad:

Answer 33

Hypertension, bradycardia + irregular respirations --> symptoms in a patient with brain trauma & increased ICP.

Question 34

Intestinal circulation

Answer 34

- Extensive vascular network which supplies all layers of GI tract down to tips of villi - Countercurrent exchange of O2 from arterioles to venules in villi - Blood is shunted directly from arterioles to venules at base of microvilli - reduces O2 supply to mucusal cells at tip and can result in necrosis of villi

Question 35

Regulation of intestinal blood flow:

Answer 35

- Increased by functional hyperaemia (increase in functional activity of tissue increases blood supply) - Digestive hormones such as gastrin have vasodilatory properties - Absorption of biomolecules in GI increases metabolic activity of tissue - Adenosine levels increase --> vasodilation - NO produced locally - Parasympathetic nerves only innervate intestinal SM and glands to increase motility and secretions .

Question 36

Hepatic circulation:

Answer 36

- Liver receives 25% of cardiac output - Portal venules and hepatic arterioles enter centre fof acinus and deliver blood into capillary network (sinusoids) - Sinusoidal capillaries are very leaky, permitting rapid exchange - Sinusoids radiate to periphery of acinus and connect with hepatic venules, veins and inferior vena cava.

Question 37

What are ascites and how do they occur?

Answer 37

- Heart failure results in an increase in CVP - Increases hepatic venous + hepatic sinusoidal pressures - Increased hydrostatic pressure and hepatic oedema --> accumulation of fluid in abdominal cavity (ascites) - Can occur as a consequence of liver cirrhosis which causes portal hypertension.

Question 38

Intrinsic mechanisms to control blood flow:

Answer 38

- Myogenic regulation - Endothelial-mediated regulation - Metabolic regulation

Question 39

Extrinsic mechanisms to control blood flow:

Answer 39

- Neural (sympathetic) - Hormonal (adrenaline)