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PULMONARY CIRCULATION AT HIGH ALTITUDE
Jean COUDERT
Laboratoire de Physiologie – Biologie du SportFaculté de Médecine – Université d’AuvergneCLERMONT-FERRAND, FRANCE
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The most striking changes at High Altitude (HA)
! Pulmonary Arterial Hypertension (PAH)
! In Acclimatized Lowlanders at HA
! In HA natives (Highlanders)
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PLAN1) Values of pulmonary Arterial Pressures (PAP) at HA2) Factors acting upon these values
! Exercise! Ambient temperature (cold, heat)! Individual reactivity! Age! Others
3) Mechanisms involved
3-1 Pulmonary Arteriolar Vasoconstriction (PAV)! Effects of hypoxia! Cellular responses
3-2 Structural changes
4) Effects of Hypoxic PAV and Structural Changes induced by Hypoxia
5) Summary
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Values of PAP at HA
1) Values in LA PAZ (3700m)
2) Values at different altitudes
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Values in LA PAZ (3700m)
67 normal male Highlanders
(Arch. Inst. Biol. Andina, 1971)
Data compared with values obtained in Lima (n = 22)
(Banchero et al, Circulation, 1966)
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Ageyear
Ht%
Hbg%
PaO2mmHg
SaO2%
PaCO2mmHg
CaO2vol.%
CvO2vol.%
LA PAZ(3700m)
m
SD
23.6
4.8
48.8
4.1
16.5
2.6
58.5
9.2
28.0
4.6
90.1
4.38
19.3
2.12
15.0
2.09
LIMA(150m)
m
SD
20.7
1.28
44.1
2.59
14.8
0.88
95.7
2.06
19.04
0.998
15.04
1.26
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LA PAZ(3700m)
m
SD
5
1.9
29
6.6
21
4.2
9
2.7
6.43
1.69
3.91
1.09
265
80
148
43
13
3.8
s d m
PaP (mmHg)
RAP(mmHg)
WPP(mmHg)
COl.min-1
CIl.min-1.m-2
PRdynes.sec-1.cm-5
T a
LIMA(150m)
m
SD
2.6
1.3
22
3.5
12
2.2
3.97
0.97
160
46.7
73
24.4
6
2.1
6.5
1.68
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Values at different altitudes
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From GROVES et al, J. Appl. Physiol., 1987
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Factors interfering with PAP at HA
1) Muscular exercise (Lockhart et al, J. Appl. Physiol., 1976)
6 normal male Highlanders in LA PAZ
At rest and during exercise (75W) breathing air (PIO2 = 100mmHg)
and 30% oxygen (PIO2 = 150mmHg)
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2) Ambient temperature (Coudert J., Séminaire CNRS/NSF., 1980)
21 normal male Highlanders in LA PAZ
2–1 Heat exposure (13 subjects)
2–2 Cold exposure (8 subjects)
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2-3 Responses to local cold exposure in pathological chronic hypoxia (COPD)
(Bedu et al, Am. J. Respir. Crit. Care Med., 1996)
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From BIGH J, in « Hypoxia and Cold », Eds. SUTTON JR, HOUSTON CS, COATES G, 1987
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Individual reactivity
Case of Highlander, studied in LA PAZ, one month after HAPO
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oo
O
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AGE
! Foetus, at sea level (SL) and at HA :
! PAP and PVR very high
! Newborn :
! ↓ Adult level
" after 10 days, at SL
" after 1 – 5 months, at HA (Morococha, 4540m)
GAMBOA R. and MARTICORENA E., Arch. Inst. Biol. Andina,1971
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SEX
Possible protection against pulmonary hypertension,in female by sexual hormones
(↓ expression of endotheline-1 by estradiol)
Earley S. et al, Am. J Physiol. Lung Cell Mol Physiol., 2002
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MECHANISMS
1) Pulmonary Arterial Vasoconstriction (PAV)
! Acute hypoxia
! Cellular responses
2) Structural changes
! Chronic hypoxia
" histological changes of the pulmonary arterioles
" cellular and molecular responses
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EFFECTS OF ACUTE HYPOXIA
Pulmonary Arteriolar Vasoconstriction
very short delay of the responses
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N2 and O2 TESTS
Effects of hypoxia and hyperoxia of short duration on the
pulmonary circulation of Highlanders and Lowlanders
living at 3750m
COUDERT J. et al, Prog Resp Res, 1975
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CELLULAR RESPONSES INDUCED BY ACUTE HYPOXIA
Hypoxia inhibits K+ current in an oxygen sensitive potassium channel
! Cellular membrane depolarisation
! Opening of Ca2+ channels
! ↑ Intracellular Ca2+
! Contraction of pulmonary arteriolar smooth muscle cell
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From BRIJ S.O. and PEACOCK A.J., Thorax, 1998
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CONTRACTIONe.g. smooth muscle cell
HYPOXIAmay directly activate theHIF-1 binding sequence
Cellular responses to hypoxia in the pulmonary circulation
?
Nuclearsynthesis
K+ current inhibition leadsto membrane depolarisation
HIF-1
Gene products e.g.erythropoietin
From Brij S.O. and Peacock A.J., Thorax, 1998
K+
K+
Hypoxia inhibits K+
current in a delayedrectifier K channel
↑CALCIUM Ca2+ Ca2+ influx throughvoltage gated channels
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HIF-1 α + β
Hémoprotéine oxygène Sensor O2
Hémoprotéine oxygène Sensor O2 O2
Phosphorylation des protéines
Factor X
VOIES DE REPONSES A L’HYPOXIE, INDUITES PAR HIF-1
Métabolismeanaérobie
Induction des gènes desenzymes de la glycolyse
Induction du géne dela tyrosine hydroxylase
Induction dugène EPO
Induction dugène vEGF
Angiogénèse Vasodilatation Erythropoïèse Respirationaugmentée
Induction des gènesI-NOS et HO-1
From Coudert J., Urgence pratique, 66, 2004
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STRUCTURAL RESPONSES INDUCED BY CHRONIC HYPOXIA
! Bands of smooth muscle develop in the small pulmonary arteries (arterioles)
! Smooth muscles bonded by internal and external elastic laminae
! Narrowing of the lumen of the pulmonary arterioles and increase of PVR
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From Heath and Williams, 1977
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STRUCTURAL CHANGES : CELLULAR AND MOLECULAR
! Hypoxic proliferation and intracellular signaling (PKC and MAP kinases)
! Hypoxia and the upregulation of growth mitogens
! Nuclear synthesis
! Proliferation and remodelling of all three cell types of the pulmonary arterioles
(Possible regulation by HIF1)
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Cellular responses to hypoxia in the pulmonary circulation
PKC
Nuclearsynthesis
PROLIFERATION and REMODELLINGof all three cell types
?
Phosphorylationevents e.g.MAP kinases
Hypoxia upregulatesthe stress activatedMAP kinases
From Brij S.O. and Peacock A.J., Thorax, 1998
CONTRACTIONe.g. smooth muscle cell
HYPOXIAmay directly activate the HIF-1 binding sequence
?
K+ current inhibition leads to membrane depolarisation
HIF-1
Gene products e.g.erythropoietin
K+
K+
Hypoxia inhibits K+
current in a delayedrectifier K channel
↑CALCIUM Ca2+ Ca2+ influx throughvoltage gated channels
Activationof secondmessengersignal e.g.DAG, IP3
Cell surface receptorvasoconstrictor growth factors e. g. ET-1, PDGF
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EFFECTS OF HYPOXIC PVC AND STRUCTURAL CHANGESINDUCED BY CHRONIC HYPOXIA
Structural changes PAH Right ventricular hypertrophy
PVC Improvement in ventilation perfusion relationships ?
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Regional distribution of pulmonary blood flow, at HA
COUDERT J. et al Respiration, 1975
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SUMMARY
1) At rest : PAP and Pulmonary Resistances (PR)are higher at HA than at SL
! in LL, importance of PVC
! in HL, importance of structural changes
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2) ↑ + + + of PAP and PR
during exercise and cold exposure
↑ + + + in hyperreactive subjects
(triggering factor of HAPE ? and predictive factor of HAPE ?)
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Δ PAPmax=Ex hypoxia-rest normoxia
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3) PAH : useful factor ?
! No improvement of the perfusion of the apex in standing position
! Risk of « chronic pulmonary heart » with right cardiac insufficiency
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Co authors of the studies performed in LA PAZ,in the laboratories of IBBA
ANTEZANA G.BARRAGAN L.BRIANCON L.CUDKOWICZ JDURAND J.LOCKHART A.MENSH-DECHENE J.PAZ-ZAMORA M.SPIELVOGEL H.VARGAS E.ZELTER M.
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