Cardio L7 Tissue blood flow Flashcards Preview

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Flashcards in Cardio L7 Tissue blood flow Deck (54):
1

• The Key role of the vascular system is to

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

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• The distribution of blood flow is

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

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Arterioles: function

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

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Vascular Smooth Muscle (VSM briefly allow

constriction dilation

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VSM cell shape

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

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VSM Contraction: process

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).

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VSM contraction stimuli:

VSM contraction stimuli:

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VasoConstriction controlled by 3 and process

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

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Vasodilation controlled by

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

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Beta 2 receptors

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

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Vasodilation controlled by

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

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ANP acts via

Acts via cGMP = vasodilation

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Alpha 1 receptor is for

Vasoconstriction

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NO

Acts via cGMP causing relaxation

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Control of Blood Vessels:

local and global control

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local control

a. Mechanical
b. Metabolites
c. Autocoids

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Global control

SNS
Hormones

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Mechanical

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

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Mechanical Process of action in arterioles

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

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Metabolites: action

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

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Metabolites: examples

Carbon dioxide
Lactate
Adenosine
Potassium ions
Hypoxia

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Metabolites: clinical


COPD → increase of Co2 pathologically
1. Bounding pulse
2. Headaches

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Active hyperaemia

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

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Reactive hyperaemia

After a period of ischemia. E.g cuff
Build up of metabolites that has occurined during ischemia

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Autocoids (local hormone) Function

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

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Autocoids (local hormone) Examples

Histamine
Serotonin (5-HT)
Bradykinin
Prostaglandins

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Thromboxane

Predominantly produce by platelets → platelet aggregation and vasoconstriction

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Prostacyclin

Produce by endothelium. Inhibits platelet aggregation and causes vasodilation

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Aspirin

Inhibit production of thromboxane. Acute treatment of MI

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Auto-regulation: function

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

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auto-regulation 3. Underlying mechanisms

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

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Endothelial Derived Relaxing factor (EDRF):

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.

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Patho: of EDRF

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

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NO vasodilators

GTN (increased production of NO and so vasodilation).

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Sympathetic Nervous system:

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

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4. A fall in sympathetic tone =

dilation

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5. A rise in sympathetic tone =

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

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Hormones:

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

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Renin-Angiotensin-Aldosterone Important in

Control of ECF and blood volume

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Renin-Angiotensin-Aldosterone Function

Decreased afferent arteriolar pressure
Increased renal sympathetic tone

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Renin-Angiotensin-Aldosterone Important in

Response to haemorrhage

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Renin-Angiotensin-Aldosterone Secreted by

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

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Renin-Angiotensin-Aldosterone Process

ACE converts Angiotensin 1 to angiotensin 2

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Angiotensin 2

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

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Vasopressin (ADH) Produced by

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

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Vasopressin (ADH) Released from

The posterior lobe of the pituitary

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Vasopressin (ADH) Stiimulated by

Increased osmoarity or fall in BP

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Vasopressin (ADH) Outcome

Vasoconstriction (except cerebral and coronary vessles)
Renal water retention

49

Adrenaline vs Noradrenaline Both function

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

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Adrenaline vs Noradrenaline Both Cause

Arteriolar vasoconstriction via the alpha 1 adrenoceptor

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Adrenaline alone

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

52

Local Anaesthetics:

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).

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Coronary Circulation:

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

54

Lewis Triple Response:

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

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