Cardio L7 Tissue blood flow

Question 1

• The Key role of the vascular system is to

Answer 1

distribute the cardiac output according to the metabolic needs of the tissues.

Question 2

• The distribution of blood flow is

Answer 2

is not fixed, for example at rest skeletal muscle receives about 20% of the cardiac output. During heavy exercise this may increase to 80%.

Question 3

Arterioles: function

Answer 3

3. Regulate local blood flow according to local metabolic need.
4. Large amount of Smooth muscle
5. Exhibit:
   a. Vasoconstriction
   b. Vasodilation

Question 4

Vascular Smooth Muscle (VSM briefly allow

Answer 4

constriction dilation

Question 5

VSM cell shape

Answer 5

1. Spindle shaped cells
2. Approx 50 nanometers x 4um
3. Thick (myosin) and thin (actin) filaments.
4. Actin → inserts into dense bands (inner membrane and dense bodies (cytoplasm)
5. Function syncytium: cells are linked by gap junctions

Question 6

VSM Contraction: process

Answer 6

1. Calcium (from SR or calcium channels) forms a complex with calmodulin
2. Ca-calmodulin regulates an enzyme called myosin light chain kinase (MLKC)
3. MLCK regulates action myosin interaction by phosphorylating the light chain of the myosin head.
4. Latch state of prolonged crossbridge formation (energy efficient tone).

Question 7

VSM contraction stimuli:

Answer 7

VSM contraction stimuli:

Question 8

VasoConstriction controlled by 3 and process

Answer 8

Noradrenaline (alpha 1 receptor)
Angiotensin (ATII receptors action)
Endothelin (act via ETA receptors)
Act via phosphplipase C (PLC) to produce vasoconstriction

Question 9

Vasodilation controlled by

Answer 9

Adrenaline (Beta2) acts via a cAMP dependent pathway to inhibits MLCK and cause vasodilation

Question 10

Beta 2 receptors

Answer 10

Found on skeletal muscle e.g. during exercise increase vasodilation to increase blood flow

Question 11

Vasodilation controlled by

Answer 11

Endothelium derived relaxing factor (EDRF) and atrial natriuretic peptide (ANP) act via cGMP to produce vasodilation.

Question 12

ANP acts via

Answer 12

Acts via cGMP = vasodilation

Question 13

Alpha 1 receptor is for

Answer 13

Vasoconstriction

Question 14

NO

Answer 14

Acts via cGMP causing relaxation

Question 15

Control of Blood Vessels:

Answer 15

local and global control

Question 16

local control

Answer 16

a. Mechanical
b. Metabolites
c. Autocoids

Question 17

Global control

Answer 17

SNS

Hormones

Question 18

Mechanical

Answer 18

A high external pressure may impede blood flow
E.g.
→ Left coronary flow pattern.
→ Pressure sores

Question 19

Mechanical Process of action in arterioles

Answer 19

Raising the internal pressure in arterioles would initially distend them before they reacting by contracting i.e. myogenic response.

Question 20

Metabolites: action

Answer 20

Many products of metabolism cause vasodilation and allow local blood flow to be matched to local metabolite rate

Question 21

Metabolites: examples

Answer 21

Carbon dioxide
Lactate
Adenosine
Potassium ions
Hypoxia

Question 22

Metabolites: clinical

Answer 22

COPD → increase of Co2 pathologically

1. Bounding pulse
2. Headaches

Question 23

Active hyperaemia

Answer 23

Skeletal muscle during exercise. Metabolites increases and so vasodilation occurs and more blood flow.

Question 24

Reactive hyperaemia

Answer 24

After a period of ischemia. E.g cuff

Build up of metabolites that has occurined during ischemia

Question 25

Autocoids (local hormone) Function

Answer 25

These are vasoactive chemicals that are produce locally, released locally and act locally

Question 26

Autocoids (local hormone) Examples

Answer 26

Histamine Serotonin (5-HT) Bradykinin Prostaglandins

Question 27

Thromboxane

Answer 27

Predominantly produce by platelets → platelet aggregation and vasoconstriction

Question 28

Prostacyclin

Answer 28

Produce by endothelium. Inhibits platelet aggregation and causes vasodilation

Question 29

Aspirin

Answer 29

Inhibit production of thromboxane. Acute treatment of MI

Question 30

Auto-regulation: function

Answer 30

Over a range of perfusion pressures blood flow remains remarkably constant. 2. Brain, kidney, myocardium, intestine → flow doesn’t obey straight line increase pressure increase flow

Question 31

auto-regulation 3. Underlying mechanisms

Answer 31

that changes resistance with change in pressure: Probably involves myogenic response and effects of local metabolites.

Question 32

Endothelial Derived Relaxing factor (EDRF):

Answer 32

1. Shear stress, Ach and substance P will cause relaxation of arterial vessels. a. Achieved via: Stimulates endothelial production of EDRF (nitric Oxide) b. EDRF stimulates guanylate cyclase in VSM and produces relaxation.

Question 33

Patho: of EDRF

Answer 33

Septic shock → production of NO is abnormally elevated = abnormal dilation and therefore TPR falls and a fall in blood pressure.

Question 34

NO vasodilators

Answer 34

GTN (increased production of NO and so vasodilation).

Question 35

Sympathetic Nervous system:

Answer 35

3. Tonic activity (noradrenaline release) contributes to the maintenance of vessel tone

Question 36

4. A fall in sympathetic tone =

Answer 36

dilation

Question 37

5. A rise in sympathetic tone =

Answer 37

arteriolar vasoconstriction (raises TPR and afterload) and venoconstriction (raises CVP and preload)→ therefore stroke volume.

Question 38

Hormones:

Answer 38

1. Renin angiotensin aldosterone system 2. Vasopressin (Anti-diuretic hormone 3. Adrenaline 4. ANP

Question 39

Renin-Angiotensin-Aldosterone Important in

Answer 39

Control of ECF and blood volume

Question 40

Renin-Angiotensin-Aldosterone Function

Answer 40

Decreased afferent arteriolar pressure | Increased renal sympathetic tone

Question 41

Renin-Angiotensin-Aldosterone Important in

Answer 41

Response to haemorrhage

Question 42

Renin-Angiotensin-Aldosterone Secreted by

Answer 42

The juxtaglomerular cells (afferent arterioles) in response to: decreased solute NaCL load at the macula densa.

Question 43

Renin-Angiotensin-Aldosterone Process

Answer 43

ACE converts Angiotensin 1 to angiotensin 2

Question 44

Angiotensin 2

Answer 44

Constricts vascular smooth muscle and so increases resistance and increased afterload. Increased water and sodium retention via aldosterone stimulation → Increased preload.

Question 45

Vasopressin (ADH) Produced by

Answer 45

the magnocellular neurones of the supraoptic and paraventricular nuclei of the hypothalamus

Question 46

Vasopressin (ADH) Released from

Answer 46

The posterior lobe of the pituitary

Question 47

Vasopressin (ADH) Stiimulated by

Answer 47

Increased osmoarity or fall in BP

Question 48

Vasopressin (ADH) Outcome

Answer 48

Vasoconstriction (except cerebral and coronary vessles) | Renal water retention

Question 49

Adrenaline vs Noradrenaline Both function

Answer 49

Increases cardiac contractility and hert rate via the Beta 1 adrenoceptor → positive chronotrophs

Question 50

Adrenaline vs Noradrenaline Both Cause

Answer 50

Arteriolar vasoconstriction via the alpha 1 adrenoceptor

Question 51

Adrenaline alone

Answer 51

Has a high affinity for Beta 2 receptors and produces vasodilation in skeletal muscle, myocardial and liver vessels.

Question 52

Local Anaesthetics:

Answer 52

1. A mixture of adrenaline and local anaesthetics is often used to cause vasoconstriction and reduced bleeding but should never be used in distal regions e.g.s fingers/toes (ischemia).

Question 53

Coronary Circulation:

Answer 53

LCA flow is greatest during diastole. | As myocardium contracting → the LCA perforating branches are occluded.

Question 54

Lewis Triple Response:

Answer 54

1. Response to skin trauma → wheel and flare reaction | 2. Abolished by sensory denervation.