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nitric oxide Flashcards

1
Q

is nitrous oxide a free radical?

A

no

stable and unreactive

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2
Q

what is nitric oxide?

A

mild analgesic and a free radical

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3
Q

what is a free radical?

A

compound with an unpaired electron

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4
Q

what is entonox and what is it made of?

A

medical anaesthesia gas

50% nitrous oxide and 50% oxygen

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5
Q

when is entonox used?

A

pre-hospital care, childbirth and emergency medicine situations

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6
Q

what enzyme is used to make nitric oxide?

A

nitric oxide synthase (NOS)

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7
Q

what does nitric oxide synthase do?

A

NOS converts amino acid I-arginine into citrulline

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8
Q

what condition enhances and inhibits nitric oxide synthase and why?

A

Reaction makes H+ - enhanced in alkali conditions and inhibited in acidic conditions

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9
Q

where is NOS found?

A

in the brain, macrophage and vascular endothelium

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10
Q

what are the isoforms of NOS?

A

NOS type 1
NOS type 2
NOS type 3

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11
Q

what are other names for NOS type 1?

A

bNOS

nNOS

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12
Q

where is NOS type 1 found and what does it depend on?

A

o Central and peripheral neuronal cells

o Calcium dependent

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13
Q

where is NOS type 2 found and what does it depend on?

A

o Most nucleated cells, particularly macrophages – part of the immune system
o Independent of intracellular Ca+2
o Inducible in presence of inflammatory cytokines

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14
Q

where is NOS type 3 found and what does it depend on?

A

o Vascular endothelial cells

o Calcium dependent

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15
Q

what is another name for NOS type 2?

A

iNOS

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16
Q

what is another name for NOS type 3?

A

eNOS

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17
Q

what is the main regulatory factor in endothelial NO synthesis?

A

flowing blood

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18
Q

how does flowing blood activate eNOS?

A
  • Moving blood causes friction (stress) on the endothelial wall – opens Ca2+ channels (maybe by moving a molecule that sits loosely in the Ca2+ channel – called caveolin)
  • Calcium moves into endothelium, binds + activates calmodulin which activates eNOS
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19
Q

name cofactors that help in the oxidation and reduction reactions in NOS?

A

eg biopterinH4, Flavin mononucleotide (FMN), flavin adenine dinucleotide (FAD)

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20
Q

how can ACh activate NO synthesis?

A

Ach (& other factors) in the plasma can also activate NO synthesis by binding Ach receptors or endothelium and opening Ca2+ channels

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21
Q

once nitric oxide is activated in the vascular endothelium, what does it do?

A
  • Nitric oxide diffuses from the endothelium into the surrounding smooth muscle – activates guanylate cyclase
  • Converts guanosine triphosphate to cyclic guanosine monophosphate cGMP (makes muscles relax)
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22
Q

what are main groups of cellular targets for cGMP?

A 
o	cGMP-dependent protein kinases (PKGs)
o	cGMP-gated cation channels
o	Phosphodiesterates (PDE)s.
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23
Q

what do proteins modified by PKG normally do?

A

commonly regulate calcium homeostasis and calcium sensitivity of cellular proteins

24
Q

what is the net effect of raised cGMP?

A

reduce calcium availability in muscles –> inhibit contraction

25
Q

what are the 2 main functions of nitric oxide in the vascular system?

A

1) NO relaxes and dilates arteriolar smooth muscle - lowers vascular resistance (and prevents hypertension) - maintains low PVR and normal BP
2) NO prevents unwanted intravascular coagulation (eg a DVT/VTE)

26
Q

what is the effect of NO in the lungs?

A

relaxes bronchial smooth muscle

27
Q

how can NO help in gas exchange?

A
  • NO released from vascular endothelium during local hypoxia
  • Diffuses into the blood and smooth muscle
  • In RBCs it reacts with oxyhaemoglobin to form nitrosohaemoglobin – displaces O2 from Hb  improves delivery of O2 to hypoxic tissue
28
Q

how does blood flow to different organs in the body change during exercise?

A
  • Blood flow in active muscles increases over TEN FOLD
  • Heart blood flow increases THREE FOLD
  • Kidney blood flow DECREASES by nearly half
  • Skin blood flow increases nearly four-fold
  • Brain blood flow does not change
29
Q

how does the SNS reduce local muscle blood flow?

A

SNS produces general vasoconstriction of arterioles in muscle during exercise mediated by alpha-1 receptors

30
Q

how does redistribution of blood occur during exercise?

A

• Vasodilation in active muscle and vasoconstriction in inactive skeletal muscle = effective redistribution to active muscles

31
Q

what effect does acidosis have on exercising muscle and how?

A
  • Acidosis triggers vasodilation in exercising muscle
  • Lactic acid is created in exercising muscle caused by decrease in ATP and a shift to anaerobic metabolism –> local acidity for local vasodilation
  • Closed arterioles in the muscle open up
32
Q

which is more important in producing vasodilation in hypoxic muscle; NO or adenosine?

A

NO

33
Q

what happens to NO once it reacts with guanylate cyclase in the muscle?

A

converted to nitroud acid which is then converted to nitrite

34
Q

when can nitrite be converted back to NO?

A

in hypoxic and acid conditions

35
Q

where is nitrite stored and why?

A

Endothelium of the arterioles stores nitrite for when hypoxia occurs

36
Q

what happens to NO in resting and active muscle and why?

A
  • NO synthesised in resting muscle when there’s plenty of O2 and stored as nitrite
  • Active muscle: O2 usage > supply, nitrite is converted back to NO to dilate local arterioles and increase local blood flow
37
Q

why does exercise vasodilation occur?

A

bc of increased NO in pulmonary venous blood

38
Q

why does the pulmonary arteriole endothelium continuously make NO?

A

constantly exposed to PaO2

39
Q

what is nitroglycerin (GTN)?

A

drug to treat angina and MIs

40
Q

what is the effect of nitroglycerin?

A

• Dilates coronary arteries and opens collateral vessels in the heart so blood can get to hypoxic tissue downstream from a blocked coronary artery

41
Q

how does GTN work?

A

• GTN is converted to nitrite by mitochondrial enzymes (e.g. mitochondrial aldehyde dehydrogenase) then some mechanism converts nitrite to NO

42
Q

why do some vasodilators like dipyridamole have a negative effect in ischaemic hearts?

A

bc they increase already open BV size and don’t affect those with an atheroma blockage

Shunts blood away from infarcted regions

43
Q

what is the equation for nitrite to NO?

A

HNO2 + H+ + e-  NO + H2O + ½ [O2]

44
Q

what is needed for the forward reaction of nitrite to NO?

A 
enzyme
reducing agent (electron donor) e.g. ascorbic acid (vitamin C)
45
Q

why do some newborns suffer from hypoxia?

A

reduction in pulmonary arterial resistance following first breath doesn’t happen  suffer from hypoxia bc inadequate lung perfusion

46
Q

how are babies with persistent pulmonary hypertension of the newborn treated?

A

Adding NO to inspired gas dramatically improves the lung function in these children – life saving in some cases

47
Q

why is there a drop in pulmonary arterial resistance when babies take their first breath?

A
  • Pulmonary arterioles are rich in NO synthase, but synthesis needs high PO2
  • When the baby takes their first breath, O2 levels in the lungs rises and triggers massive + rapid synthesis of NO  relaxation of vascular smooth muscle  vasodilation  drop in pulmonary arterial resistance
48
Q

how do adults maintain low resistance in the arterioles?

A

NO is constantly produced in healthy adult lungs

49
Q

why do arterioles constrict in hypoxia?

A

NO production is reduced

50
Q

what changes happen to pulm arterial pressure and pulm arterial resistance during exercise and why?

A

• Pulmonary arterial pressure increases only slightly
• Pulmonary arterial resistance decreases to allow the increased flow
occurs bc all CO passes through the lungs and CO increases 3 fold during exercise

51
Q

why is there decreased pulmonary arterial resistance during exercise?

A
  • thin pulmonary arterial walls can stretch easily
  • increased blood flow in the artrioles increases NO synthesis –> vasodilation = lower resistance
  • SNS acts on beta-2 receptors on bronchial smooth muscle to relax them and increase bronchial diameter. This + increased tidal volume = increased O2 conc in the alveoli
52
Q

how does nitric oxide help anticoagulation?

A

Basal release of NO helps prevent leukocytes and platelets from adhering to the endothelium surface

53
Q

why are green vegetables and beetroot good for you?

A

contains nitrates and ascorbic acid

54
Q

how is nitric oxide made in the stomach?

A
  • Nitrates  nitrites by enzymes in saliva and nitrites enter the stomach
  • In acidic stomach conditions, nitrite + acid = nitric oxide
55
Q

what properties does NO have in strongly acidic conditions?

A

bactericidal - helps kill harmful bacteria in the stomach

56
Q

what happens to nitrites if the stomach pH is too high?

A

nitrites can pass through the stomach into the small intestine where they’re converted to nitrosamines (carcinogenic)

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